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Received: 26 November 2019 Revised: 10 January 2020 Accepted: 19 January 2020 DOI: 10.1111/obr.13005 PEDIATRICS/PHYSIOLOGY Adipokines: A gear shift in puberty DesirĂŠe Nieuwenhuis | NatĂ lia Pujol-Gualdo Amanda J. Kiliaan Department of Anatomy, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Preclinical Imaging Center PRIME, Nijmegen, The Netherlands Correspondence Amanda J. Kiliaan, PhD, Associate Professor, Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Preclinical Imaging Center PRIME, Radboud university medical center, 6500 HB Nijmegen, Geert Grooteplein 21N 6525 EZ Nijmegen, The Netherlands. Email: amanda.kiliaan@radboudumc.nl Funding information Europees Fonds voor Regionale Ontwikkeling (EFRO), Grant/Award Number: BriteN 2016 1 | INTRODUCTION The prevalence of obesity in adolescents and children is increasing in | Ilse A.C. Arnoldussen | Summary In this review, we discuss the role of adipokines in the onset of puberty in children with obesity during adrenarche and gonadarche and provide a clear and detailed overview of the biological processes of two major players, leptin and adiponectin. Adipokines, especially leptin and adiponectin, seem to induce an early onset of puberty in girls and boys with obesity by affecting the hypothalamic-pituitary- gonadal (HPG) axis. Moreover, adipokines and their receptors are expressed in the gonads, suggesting a role in sexual maturation and reproduction. All in all, adipokines may be a clue in understanding mechanisms underlying the onset of puberty in child- hood obesity and puberty onset variability. KEYWORDS adipokines, obesity, puberty 1,2 the age of 5 years were overweight or were with obesity in 2016, and 3 Obesity is defined by an excessive accumulation of white adipose tissue (WAT), and it is often indicated by a body mass index (BMI) 4 above 30. Two main types of adipose tissue were described: WAT and brown adipose tissue (BAT), which differ in morphology and func- 5-7 Ilse A.C. Arnoldussen and Amanda J. Kiliaan contributed equally to this work. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. Š 2020 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation Obesity Reviews. 2020;21:e13005. wileyonlinelibrary.com/journal/obr 1 of 10 https://doi.org/10.1111/obr.13005 alarming rates. Specifically, worldwide, 41 million children below this number is expected to increase to 70 million in 2025. obesity is associated with various severe health complications, includ- ing increased risk of diabetes mellitus type 2, hypertension, heart dis- eases, and disturbances in sex hormone levels. 5,6 and mitochondria and plays a role in thermogenesis. Adipocytes in tion. BAT consists of adipocytes containing multiple lipid droplets WAT contain only a few mitochondria and a single lipid droplet. Adipose tissue has several functions including the storage of energy, thermogenesis, and the production and secretion of adipokines Generally, two physiological processes, adrenarche and gonadarche, 11,24 Childhood 5,7,8 a key role in puberty onset. Puberty is known as a period through which the body changes physically, being a physiological process resulting in the maturation of children, i.e. they develop sexual characteristics and obtain reproduc- 9,11 Adipokines are involved in a number of physiological processes including blood pressure, metabo- lism, glucose, and vascular homeostasis and may play amongst others 8-10 (hormones, cytokines, and peptides). tive functions. between obesity and puberty,2,12-23 the biological mechanisms under- lying obesity and puberty onset remain unclear. Hereafter, we review in detail the role of adipokines in the onset of puberty in childhood obesity. Although many studies have shown associations 2 | INITIATION OF PUBERTY PHYSIOLOGICAL PROCESSES IN THE interact to regulate the onset of puberty. During adrenarche, the adrenal cortex secretes steroid hormones (including 2 of 10 NIEUWENHUIS ET AL. androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and cortisol), insulin-like growth factor, and growth hormone, which contribute to the pubertal insights on new genetic loci (e.g. melanocortin-4 receptor, mitochon- drial carrier 2, and mitogen-activated protein kinase 13) and on sev- eral pathways that regulate the timing of puberty; however, it partly 34 9,24,25 Both adrenarche and gonadarche are involved in the development growth spurt, body odor, skin oiliness, and skeletal maturation. explains puberty timing variation. Thereby, defining the role of 25 adipokines is of importance in elucidating the variability in puberty as the expression of adipokines is sex-specific and is altered with body composition, adiposity, and during growth spurts. Moreover, adipokines and their receptors are expressed in gonads and several brain regions suggesting involvement in the onset of puberty and sex- ual maturation. Lastly, adipokines interfere in processes regulating timing and duration of puberty, for instance in the HPA and HPG axes which are both key players during adrenarche and gonadarche. Involvement of adipokines in the onset of puberty and specifically in individuals with obesity will be further reviewed in the next 2,24 3 | Puberty onset in girls is assessed using different markers, such as thelarche (breast development), menarche (the start of of pubic hair. pituitary-gonadal (HPG) axis is activated,2,26 and several hormones have been identified to participate in the activation of the HPG axis During gonadarche (Figure 1), the hypothalamic- 2,27 Kisspeptin, neurokinin B, and dynorphin are released by specialized including kisspeptin, neurokinin B, dynorphin, leptin, and ghrelin. 28 key regulator of the pulsatile secretion of gonadotropin releasing neurons, the KNDy neurons in the hypothalamus. Kisspeptin is a 29,30 B stimulates, and dynorphin inhibits the release of kisspeptin, which hormone (GnRH) from the hypothalamus. In addition, neurokinin implies that both coordinate a pulsatile release of kisspeptin. 31 Sub- sections. sequently, the activated HPG axis induces the pituitary gland to secrete luteinising hormone (LH) and follicle stimulating hormone (FSH). As a result, gametogenesis occurs, and the gonads will release sex hormones. Consequently, secondary sex characteristics develop including breast development in girls and an increased testicular vol- 2,26,32 is possibly due to differences in levels of body fat, hypothalamic-pitui- THE ONSET OF PUBERTY IN GIRLS ume in boys. The age at puberty onset varies greatly among individuals, which 19 35 menstruation), and pubic hair development. 33 genome-wide association studies have provided important new tary-adrenal (HPA) axis activity, and genetic background. Recent The average age of However, this age differs between cultures and ethnicities, and since 1980, age at menarche is girls at start of menarche is 12.4 years. 36 significantly decreasing. 36-39 F I G U R E 1 Hormonal regulation in the initiation of puberty in boys and girls. The secretion of kisspeptin, neurokinin B, and dynorphin from KNDy neurons initiate the release of gonadotropin releasing hormone (GnRH) from the hypothalamus. This activates the pituitary gland to produce and secrete luteinising hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate the gonads to produce estrogen and testosterone in girls and boys, respectively 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 3 of 10 T A B L E 1 Summary of included studies Authors Year Country Study Design Primary Outcome Sex Sample Size (n) Age (y) Data Collection Lian et al21 2019 China Cross-sectional Puberty starts earlier in Chinese Han girls with obesity compared with Chinese Han girls with normal weight. Girls 2996 9-19 2012 and 2013 Biro et al12 Lazzeri et al20 2018 USA 2018 Italy Longitudinal Cross-sectional Body mass index had a greater effect on age at menarche than did race and ethnicity. Girls 946 6-16 2004-2014 Li et al23 2018 China Longitudinal For both, boys and girls, a higher BMI (ie, overweight and obese) is associated with earlier onset of puberty Girls Girls Boys Girls 542 Deng et al22 Flom et al15 2017 China Cross-sectional Increased BMI is associated with early timing spermarche and menarche. Boys Girls Girls 1278258 9-15 2005-2012 He et al24 Holmgren et al17 2017 China 2017 Sweden Cross-sectional Longitudinal Onset of puberty is not related to obesity in boys. Boys Boys Girls Girls 782 7-17 972 929 5839 Kelly et al19 2017 UK 2016 Brazil 2016 USA Longitudinal prospective cohort Higher BMI in girls is associated with the onset of menstruation at an earlier age. 11 10-18 11-17 Barcellos Gemelli et al25 Cross-sectional Longitudinal Excess weight is associated with early age of menarche. Girls 727 2014 2003-2009 Glass et al16 Lee et al26 In girls, but not in boys, greater adiposity is associated with the earlier onset of puberty. Boys Girls 135 Cabrera et al27 Leonibus et al14 2014 USA 2013 Italy Cross-sectional Longitudinal Thelarche occurred earlier than recently reported, while age of menarche remained unchanged. Girls 610 3-17.9 2007 2005-2012 Currie et al13 2012 Europe, USA, Canada Cross-sectional Overweight/obesity during childhood predicts the early onset of puberty in girls. Girls 20410 11, 13, 15 2005-2006 2017 USA Prospective birth cohort Overweight/obese status at the age of 7 ye was associated with increased risk of early menarche 788 From birth to menarche occurred Pregnancies 1959-1966 2016 USA Cross-sectional Boys with overweight enter puberty earlier compared with boys with normal weight or obesity, while puberty starts later in boys with obesity compared with boys with normal weight and overweight. Boys 3872 6-16 2005-2010 Overweight during childhood shows a relation with the early onset of puberty in girls. 6535 4259 695 11 15 5.8-12.2 2009/2010 2013/2014 2014-2017 Higher BMI during childhood is associated with early puberty. 2008 and 2009 2000-2002 Obesity during childhood is related to the earlier onset of puberty. Boys Girls 84 123 71 (Continues) 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 4 of 10 NIEUWENHUIS ET AL. 3.1 | Fat storage For the initiation of puberty, the timing of stimulation and/or inhibi- tion of different hormones is important, and additionally, a certain amount and distribution of body fat is needed in order to start menar- che, which emphasizes the importance of body fat. From an evolution- ary point of view, body fat increases in mammalian females during puberty onset, and it highlights the need to guarantee a healthy preg- 40 women with anorexia nervosa. particularly body fat localized predominantly on the gluteofemoral fat depots, is profoundly associated with start of menarche, more than nancy, offspring, and maternal survival. fat, sex-hormones, and neuroendocrine alterations can evolve in men- strual dysfunction, for instance, in women with severe obesity or in 41-43 44-46 to gluteofemoral fat depots suggesting that leptin may convey infor- amount of total body fat. mation on body fat distribution to the hypothalamus during puberty. An improper level of body Importantly, body fat distribution, Blood leptin levels are strongly related 45 3.2 | HPG axis The HPG axis is activated by the release of kisspeptin resulting in the release of GnRH from the hypothalamus, and LH and FSH from the pituitary gland. In girls, FSH is involved in the development of the folli- cles in the ovaries, and it promotes the secretion of estrogen. LH stim- ulates the production of androgen hormones and induces ovulation 48 9,47 the release of kisspeptin and neurokinin B, and kisspeptin thereby (Figure 1). The secretion of estrogen has an inhibitory effect on inhibits the GnRH release from the hypothalamus. pattern of GnRH is important for the regulation of the menstrual cycle. This roughly 28-day-cycle comprises several phases, including the follicular phase and luteal phase. During the follicular phase, increasing levels of FSH stimulate the maturation of follicles and the production of estrogen from the ovaries. This in turn inhibits the release of FSH from the pituitary gland. A high level of estrogen will induce the production of LH by the pituitary gland, resulting in ovula- tion. The matured follicle secretes progesterone thereby inhibiting the release of GnRH. When the corpus luteum is demolished, there is less 48 3.3 | Adipokines According to results from studies reported in Table 1, girls with obe- sity enter puberty earlier compared with girls with normal higher leptin concentrations inhibit the intake of food and increases inhibition of GnRH. As a consequence, the cycle will start again. whole process, starting from the activated HPG axis, results in the development of the secondary sex characteristics in girls including 9,47 thelarche and menarche. 13,14,16-23,49-51 weight. these girls might be found in the secretion of adipokines. For instance, leptin is positively associated with the amount of body fat. Generally, energy expenditure. 9,52-54 An explanation for the early onset of puberty in The expression This TABLE 1 (Continued) Authors Year Country Study Design Primary Outcome Sample Sex Size (n) Age (y) Data Collection Herman-Giddens et al28 2012 USA Cross-sectional Observed mean ages of beginning genital and pubic hair growth and early testicular volumes were earlier than in past studies, depending on the characteristic and race/ethnicity. Boys 4131 6-16 2005-2010 Sorensen et al29 Aksglaede et al30 2010 2009 Denmark Denmark Cross-sectional/longitudinal Longitudinal Puberty onset at earlier ages was associated with an increased BMI in boys. Boys 1528 5.8-19.9 1991-1993/2006-2008 1930-1969 Juul et al31 Ribeiro et al32 2007 2006 Denmark Portugal Retrospective cohort Cross-sectional Higher BMI is associated with early voice break. 11-15 10-15 1990-1999 Kaplowitz et al18 Abbreviation: BMI, body mass USA Cross-sectional The early onset of puberty in Caucasian girls is likely related to an increased BMI. 5-12 1992-1993 2001 index. The higher BMI in boys and girls at 7 y of age, the earlier they enter puberty. Boys 21 612 Girls 135 223 Boys 463 Boys 382 Girls 437 Girls 10 750 Early sexual maturation in boys and girls is associated with overweight. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 5 of 10 Leptin may possibly play a role in adrenarche as its plasma level increases with higher levels of body fat and as it can modulate both girls. 33 ing adrenarche. In coherence, in children with obesity, the androgen These findings suggested that lower reproductive status was associated with higher total adiponectin concentrations and that a higher reproductive status was related to higher HMW adiponectin the HPA and HPG axes. These axes are functionally integrated dur- DHEAS was positively associated with leptin levels. Nevertheless, concentrations in girls. In addition, individuals with obesity often another study showed that enhanced adrenal androgen secretion in girls with premature adrenarche was not explained by leptin or BMI 55 ated with androgen levels in girls ; however, it was not related to levels. and IL-6. TNF-Îą alters, and IL-6 inhibits the expression of 56 8 In addition, the adipokine adiponectin was negatively associ- 57 differences of adiponectin seem to develop during the progression of 56 adiponectin (Figure 2). Thereby, a low level of total adiponectin and/or high levels of inflammatory cytokines in individuals with obe- sity can promote the onset of puberty. Many more adipokines are secreted by WAT including omentin, 52,65-67 9,36,62,68 adrenarche in girls with Prader-Willi syndrome. Interestingly, sex puberty. adrenarche; however, both are not required factors. Thus, leptin and adiponectin might be able to influence In gonadarche, leptin can stimulate the secretion of kisspeptin, and subsequently activation of the HPG axis, which eventually increases the expression of estrogen and androstenedione in the ova- 58 2,60 65-67 The expression of these ries (Figure 2). Ob gene in WAT, resulting in the synthesis and secretion of leptin. Thus, high levels of leptin promote onset of puberty in girls via secre- tion of kisspeptin, and estrogen stimulates leptin secretion addition- ally. Moreover, adiponectin can affect the HPG axis due to the expression of adiponectin receptors in the hypothalamus, pituitary In return, estrogen stimulates the expression of the 59 gland, and gonads. onset as it inhibits the secretion of kisspeptin and GnRH in the hypo- thalamus and the release of GH and LH in the pituitary gland, and 2,60-62 52,60 63 girls with central precocious puberty (CPP). Moreover, total adiponectin had negative correlations with progression of puberty in girls (defined by Tanner stages), whereas HMW adiponectin had FIGURE 2 Adipokinesaffectingthe initiation of puberty in girls. Leptin stimulates the release of kisspeptin in KNDy neurons, which activates the hypothalamus to produce gonadotropin releasing hormone (GnRH). In response to the release of GnRH, the pituitary gland secretes follicle stimulating hormone (FSH) and luteinising hormone (LH), which stimulates the ovaries to release estrogen resulting in the formation of secondary sex characteristics in girls. Estrogen stimulates the production of leptin. Adiponectin inhibits GnRH release resulting in reduced levels of GnRH and thereby a delayed onset of puberty. TNF- Îą and IL-6 inhibit the production of adiponectin and therefore stimulate the onset of puberty In detail, adiponectin is a regulator of puberty thereby inhibiting the onset of puberty (Figure 2). with obesity often have low levels of adiponectin. et al. showed that total adiponectin was significantly lower, whereas high molecular weight (HMW) adiponectin was significantly higher in ment. 55 63 develop a chronic low-grade inflammatory state, which can be indi- cated by a high level of circulating inflammatory cytokines like TNF-Îą 64 Individuals Sitticharoon positive associations with LH levels and the progression of puberty in 63 visfatin, resistin, and chemerin. and visfatin are expressed in the ovaries. adipokines in the ovaries suggests a role within the reproductive sys- tem; however, the exact biological processes have to be examined. Thus, specifically leptin, adiponectin, and inflammatory cytokines pro- duced by WAT could be permissive key players during an early onset of puberty in girls with obesity. As an exception, HMW adiponectin seems to have a stimulatory effect on peripheral repro- ductive function as HMW is not able to cross the blood brain 63 barrier. 4 | Markers that are used to assess puberty onset in boys are THE ONSET OF PUBERTY IN BOYS spermarche, voice break, testicular volume, and pubic hair develop- 35 spermarche develop in the early stages of puberty onset, voice In women, omentin, chemerin, While pubic hair development, larger testicular volume, and 69 testicular volume increases, which occurs at an average age of break usually appears in later stages of puberty. Generally, first 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 6 of 10 NIEUWENHUIS ET AL. 11.9 years, followed by the development of pubic hair at 12.2 years of average, and lastly, boys experience spermarche around an aver- 55 related with leptin levels. Thereby, leptin plausibly has a minor impact in adrenarche in boys. Since leptin receptors are found in the hypothalamus, pituitary gland, and testes, they might be involved in the onset of puberty by affecting the HPG axis during gonadarche. Leptin stimulates the release of kisspeptin and GnRH, and as a consequence, it accelerates the onset of puberty (Table 1, Figure 3). In contrast, adiponectin inhibits the secretion of GnRH, GH, LH, and FSH therewith delaying the onset of puberty. However, adiponectin levels are generally lower in men compared with women and even lower in men with obe- age age of 13.4 years. 70 4.1 | Fat storage Many aspects of the reproductive physiology are energetically demanding,71 and therefore, an adequate energy level is necessary. In boys, a dynamic change in body composition occurs around the age of 10 to 13 years, in which they gain approximately 40% of sity. culating inflammatory cytokines. levels can stimulate the HPG axis and therewith an early onset of puberty in boys. Nevertheless, leptin can inhibit the production of tes- 72 mostly consisting of lean mass, which causes exhaustion of most of fat. Subsequently, a growth spurt follows in which they gain tissue 72 in boys, an adequate amount of body fat is important in the onset of their body fat. These alterations in amount of body fat indicate that 4.2 | Puberty in boys is initiated by the release of kisspeptin. As mentioned before, this activates the HPG axis, resulting in the release of GnRH from the hypothalamus, and consequently the release of LH and FSH 9,74 puberty. tosterone from the testes, to estrogen (Figure 3). of the development of secondary sex characteristics in boys. Additionally, leptin can affect fertility in men as it can modulate the nutritional support of spermatogenesis, and moreover, dysfunction of spermatogenesis is associated with an increased leptin level and 73 58 2,60-62 HPG axis from the pituitary gland (Figure 1). and LH stimulates the secretion of testosterone from the testes, which inhibits the release of kisspeptin from the KNDy neurons and 9,48 in men, the release of kisspeptin is more consistent, causing a con- 29,48 subsequently GnRH from the hypothalamus. receptors expressed on KNDy neurons. In humans, KNDy neurons Contrarily to women, LH-induced testosterone levels lead to the stant release of LH. development of secondary sex characteristics in boys. differences between sexes in kisspeptin release are related to a sex- specific and sex steroid-dependent kisspeptin system as estrogen and progesterone modulate kisspeptin activity through the sex-steroid 48 in the infundibular nucleus are involved in negative and positive sex- 48 tal exposure to sex steroids and result in sex-specific differences in steroid feedbacks. kisspeptin release. These sexual dimorphisms are induced by perina- 75,76 4.3 | Adipokines The association between obesity and puberty onset in boys is rather controversial compared with findings in girls. Most studies reported an early onset of puberty in boys associated with increased ate adipose tissue from actual breast tissue. stages are more difficult to assess than female stages as boys lack a more determined marker such as menarche. Thirdly, puberty onset can be indicated by the activation of the HPG axis, and the presence of these secondary sex characteristics is the result of hormonal 2 14,17,22,23,50,51,77,78 BMI, 20,49 all while others reported no associations at Current markers used 79 16,80 or a delayed onset of puberty (Table 1). The presence of excessive adipose tissue can be involved in puberty onset in boys as the secretion of adipokines can modulate both adrenarche and gonadarche. Leptin can affect adrenarche by modulating both the HPG and HPA axes,33 and moreover, androgen levels were positively 55 nal androgen secretion in boys with premature adrenarche was not associated with plasma leptin levels. Nevertheless, enhanced adre- 9 In more detail, 61,62 adiponectin, and individuals with obesity often have high levels of cir- Moreover, inflammatory cytokines, TNF-Îą, and IL-6, inhibit expression of the leptin receptor in the testis. FSH induces spermatogenesis, too. function and role still have to be examined. 64 High leptin and low adiponectin and fat tissue can convert testosterone Both processes might result in the delay 29,61,79 81,82 In men, other adipokines like chemerin are found in the gonads 65 Thus, particularly high leptin and low adiponectin levels stimulate the HPG axis and thereby accelerate the onset of puberty in boys. Additionally, leptin can dysregulate the development of secondary sex characteristics and spermatogenesis by affecting testosterone levels and nutritional sup- port of spermatogenesis. 5 | LIMITATIONS AND FUTURE RESEARCH DIRECTIONS Even though multiple epidemiological studies have shown the link between puberty onset and obesity, there are some important limita- tions. Firstly, determining both the onset and stage of puberty is rather difficult. For instance, assessing the stage of breast develop- ment in girls with obesity is complicated as clinicians should differenti- 2 changes in response to the activated HPG axis. to determine the onset of puberty refer to secondary sex characteris- tics, such as testicular volume in boys and breast development in girls. A more accurate measurement of puberty onset would be to combine secondary sex characteristics with plasma or serum hormone level measurements such as LH, FSH, adipokines, e.g. leptin. Thereby, differences in puberty measurements could explain variations in the age of puberty onset between boys and girls within different Thereby, resistin is expressed in the testes of rats, but its exact 83 Secondly, male pubertal 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 7 of 10 FIGURE 3 Adipokines affecting the initiation of puberty in boys. Leptin activates kisspeptin secretion in KNDy neurons, this activates the production of gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the pituitary gland to secrete follicle stimulating hormone (FSH) and luteinising hormone (LH), activating the production of testosterone from the testes allowing the development of secondary sex characteristics. Leptin also inhibits the production of testosterone, which may cause a delayed onset of puberty. Adiponectin inhibits GnRH release. Low levels of adiponectin, as a result of TNF-Îą and IL-6 expression, lead to a reduced inhibition of GnRH. In response to GnRH release, the pituitary gland will secrete FSH and LH, and the testes will produce testosterone resulting in the development of secondary sex characteristics in boys countries, and In addition, the inclusion of a of puberty. ferent time points is complicated, as subjects examined several decades ago presented pronounced differences concerning lifestyle patterns such as nutrition and exercise habits. Lastly, obesity or over- weight is often determined by BMI, a classification based on weight and height measurements. Additionally, it is important that all studies studies or across continents, ethnicities proper age range (8-16 years) is important when assessing the onset (Figure 4). 12-15,17,20-23,49,77-79,84,85 30,47 Furthermore, comparison between studies from dif- 86 Specifically in children, BMI is often dependent on age and growth use the same anthropometric standards and sex-specific cut-offs. 13,14,16-23,49-51,77-80 fat and would represent a more accurate measurement in its regard. Based on this review, several suggestions can be made for further research. Firstly, the roles of adipokines like resistin, chemerin, visfatin, and omentin in puberty onset, fertility, and sexual maturation should be examined in detail. Secondly, future research examining the onset of puberty should combine indicators of puberty onset (e.g. breast development or testicular volume) with plasma or serum hor- mone measurements such as LH, FSH, sex-steroids, adipokines (e.g. spurts. ment in case of growth spurts. distribution of body fat should be taken into account in determining puberty and obesity in children. For instance, the body adiposity index (BAI), which was introduced in 2011 by Bergman et al.,87 uses hip cir- cumference and height in order to estimate the percentage of body 87 Thereby, BMI is a less accurate measure- F I G U R E 4 87,88 Therefore, both percentage and Average age of puberty onset in Europe, China, and the United States according to several studies from Table 1. Age of puberty onset ranges from 8.47 to 13.33 years in girls and from 8.63 leptin), and body fat distribution (e.g. BAI,87 waist-hip ratio's and/or dual-energy X-ray absorptiometry (DXA)2). Additionally, defining con- sistent and general measurements of puberty in both boys and girls, combined with a proper age range (8-16 years), would facilitate the comparisons between different studies and their results. 12-15, 17, 20-23, 25-29, 31 to 13.7 years in boys. included if average age of markers used to assess puberty was not reported. Pink: girls. Blue: boys Studies (Table 1) were not 39, 56 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 8 of 10 NIEUWENHUIS ET AL. 6 | CONCLUSION In conclusion, epidemiological data regarding obesity and puberty onset in girls show similar outcomes as adiposity results in the early onset of puberty in girls. 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Ann Epidemiol. 2017;27(3):187-93.e2. 16. Glass NA, Torner JC, Letuchy EM, et al. The relationship between greater prepubertal adiposity, subsequent age of maturation, and bone strength during adolescence. Journal of bone and mineral research: the official journal of the American Society for Bone and Min- eral Research. 2016;31(7):1455-1465. 17. Holmgren A, Niklasson A, Nierop AF, et al. Pubertal height gain is inversely related to peak BMI in childhood. Pediatr Res. 2017;81(3): 448-454. 18. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, Herman- Giddens ME. Earlier onset of puberty in girls: relation to increased body mass index and race. Pediatrics. 2001;108(2):347-353. 19. Kelly Y, Zilanawala A, Sacker A, Hiatt R, Viner R. Early puberty in 11-year-old girls: Millennium Cohort Study findings. Arch Dis Child. 2017;102(3):232-237. 20. Lazzeri G, Tosti C, Pammolli A, et al. Overweight and lower age at menarche: evidence from the Italian HBSC cross-sectional survey. BMC Womens Health. 2018;18(1):168-174. thereby an early onset of obesity. leptin can inhibit the production of testosterone in boys and subse- quently inhibit the development of secondary sex characteristics affecting spermatogenesis. for other adipokines, like resistin and omentin, are present in the testes and ovaries suggesting a role in puberty or reproduction; 58, 71 however, their plausible function is still unknown. that adipokines may be key regulators in an early onset of puberty in both girls and boys with obesity, specifically by affecting the HPG axis during gonadarche. Future research should focus on assessing puberty onset by measuring consistent puberty markers and determine the percentage of body fat and its distribution and adipokines and hormone serum levels particularly involved in the HPG axis. CONFLICTS OF INTEREST The authors declare no conflict of interest. FUNDING INFORMATION This research was funded by Europees Fonds voor Regionale Ontwikkeling (EFRO), project BriteN 2016. ORCID Ilse A.C. Arnoldussen Amanda J. Kiliaan https://orcid.org/0000-0002-7395-5284 https://orcid.org/0000-0002-2158-6210 13, 14, 16-26, 29-32 Furthermore, several receptors Nevertheless, We conclude Search strategy We searched PubMed for articles published before Novem- ber 15th, 2019 using relevant keywords, including âonset of puberty and adiposity/obesityâ, âonset of pubertyâ, âchildren with obesityâ, âadipose tissueâ, âchildhood obesityâ, âadiposityâ, âobesityâ, âadipokine(s)â, âHPG axisâ, âadipokines ovary/ova- riesâ, or âadipokines testesâ, either alone or in combination. Selection criteria used were English language, longitudinal or cross-sectional studies assessing the onset of puberty, including menarche, thelarche, spermarche, or voice break, combined with high BMI or obesity/adiposity, and articles assessing or reviewing adipokines and its effects on the reproductive system. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 9 of 10 21. Lian Q, Mao Y, Luo S, et al. Puberty timing associated with obesity and central obesity in Chinese Han girls. BMC Pediatr. 2019; 19(1):1-7. 22. Deng Y, Liang J, Zong Y, et al. Timing of spermarche and menarche among urban students in Guangzhou, China: trends from 2005 to 2012 and association with Obesity. Sci Rep. 2018;8(1):263-270. 23. Li W, Liu Q. Association of prepubertal obesity with pubertal devel- opment in Chinese girls and boys: a longitudinal study. 2018;30: e23195. 24. Mendle J, Beltz AM, Carter R, Dorn LD. Understanding puberty and its measurement: ideas for research in a new generation. Journal of research on adolescence: the official journal of the Society for Research on Adolescence. 2019;29(1):82-95. 25. Pagani S, Meazza C, Gertosio C, Bozzola E, Bozzola M. Growth hor- mone receptor gene expression in puberty. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2015;47:581-584. 26. Abreu AP, Kaiser UB. Pubertal development and regulation. Lancet Diabetes Endocrinol. 2016;4(3):254-264. 27. Aguirre RS, Eugster EA. Central precocious puberty: from genetics to treatment. Best Pract Res Clin Endocrinol Metab. 2018;32(4): 343-354. 28. Sultan C, Gaspari L, Maimoun L, Kalfa N, Paris F. Disorders of puberty. Best Pract Res Clin Obstet Gynaecol. 2018;48:62-89. 29. Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH path- way in human reproductive health and disease. Hum Reprod Update. 2014;20(4):485-500. 30. Dahl SK, Amstalden M, Coolen L, Fitzgerald M, Lehman M. Dynorphin immunoreactive fibers contact GnRH neurons in the human hypothal- amus. Reprod Sci. 2009;16(8):781-787. 31. Navarro VM, Gottsch ML, Chavkin C, Okamura H, Clifton DK, Steiner RA. Regulation of gonadotropin-releasing hormone secretion by kisspeptin/dynorphin/neurokinin B neurons in the arcuate nucleus of the mouse. J Neurosci. 2009;29(38):11859-11866. 32. Zhai L, Liu J, Zhao J, et al. Association of obesity with onset of puberty and sex hormones in chinese girls: a 4-year longitudinal study. PLoS ONE. 2015;10(8):1-12, e0134656. 33. Cizza G, Dorn LD, Lotsikas A, Sereika S, Rotenstein D, Chrousos GP. Circulating plasma leptin and IGF-1 levels in girls with premature adrenarche: potential implications of a preliminary study. Horm Metab Res. 2001;33(3):138-143. 34. Cousminer DL, WidĂŠn E, Palmert MR. The genetics of pubertal timing in the general population: recent advances and evidence for sex-spec- ificity. Curr Opin Endocrinol Diabetes Obes. 2016;23(1):57-65. 35. Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child. 1969;44(235):291-303. 36. Lacroix AE, Whitten R. Physiology. Treasure Island (FL): Menarche. StatPearls. StatPearls Publishing; 2018. 37. McDowell MA, Brody DJ, Hughes JP. Has Age at Menarche Chan- ged? Results from the National Health and Nutrition Examination Sur- vey (NHANES) 1999â2004. J Adolesc Health. 2007;40(3):227-231. 38. de Muinich Keizer SM, Mul D. Trends in pubertal development in Europe. Hum Reprod Update. 2001;7(3):287-291. 39. Talma H, SchĂśnbeck Y, van Dommelen P, Bakker B, van Buuren S, Hirasing RA. Trends in menarcheal age between 1955 and 2009 in the Netherlands. PLoS ONE. 2013;8:e60056-e60056. 40. Kaplan HS, Lancaster JB. An evolutionary and ecological analysis of human fertility, mating patterns, and parental investment. Off- spring: Human fertility behavior in biodemographic perspective. 2003;1: 170-223. 41. Mitan LA. Menstrual dysfunction in anorexia nervosa. J Pediatr Adolesc Gynecol. 2004;17(2):81-85. 42. Xu H, Li P-H, Barrow TM, et al. Obesity as an effect modifier of the association between menstrual abnormalities and hypertension in young adult women: Results from Project ELEFANT. PLoS ONE. 2018; 13(11):e0207929-e0207929. 43. Tauqeer Z, Gomez G, Stanford FC. Obesity in women: insights for the clinician. J Womens Health (Larchmt). 2018;27(4):444-457. 44. de Ridder CM, Thijssen JH, Bruning PF, Van den Brande JL, Zonderland ML, Erich WB. Body fat mass, body fat distribution, and pubertal development: a longitudinal study of physical and hormonal sexual maturation of girls. J Clin Endocrinol Metab. 1992;75(2): 442-446. 45. Lassek W, Gaulin S. Brief communication: menarche is related to fat distribution. Am J Phys Anthropol. 2007;133(4):1147-1151. 46. Loomba-Albrecht LA, Styne DM. Effect of puberty on body composi- tion. Curr Opin Endocrinol Diabetes Obes. 2009;16:10-15. 47. Simonneaux V, Bahougne T. A multi-oscillatory circadian system times female reproduction. Front Endocrinol. 2015;6:1-15. 48. Marques P, Skorupskaite K, George JT, Anderson RA. Physiology of GNRH and gonadotropin secretion. In: Feingold KR, Anawalt B, Boyce A, et al., eds. Endotext. Endotext.org: South Dartmouth (MA); 2000. 49. Barcellos Gemelli IF, Farias EDS, Souza OF. Age at menarche and its association with excess weight and body fat percentage in girls in the Southwestern Region of the Brazilian Amazon. J Pediatr Adolesc Gynecol. 2016;29(5):482-488. 50. Aksglaede L, Juul A, Olsen LW, Sorensen TI. Age at puberty and the emerging obesity epidemic. PLoS ONE. 2009;4:1-6, e8450. 51. Ribeiro J, Santos P, Duarte J, Mota J. Association between over- weight and early sexual maturation in Portuguese boys and girls. Ann Hum Biol. 2006;33(1):55-63. 52. Budak E, Fernandez Sanchez M, Bellver J, Cervero A, Simon C, Pellicer A. Interactions of the hormones leptin, ghrelin, adiponectin, resistin, and PYY3-36 with the reproductive system. Fertil Steril. 2006;85(6):1563-1581. 53. Castellano JM, Tena-Sempere M. Metabolic control of female puberty: potential therapeutic targets. Expert Opin Ther Targets. 2016; 20(10):1181-1193. 54. Venancio JC, Margatho LO, Rorato R, et al. Short-term high-fat diet increases leptin activation of CART neurons and advances puberty in female mice. Endocrinology. 2017;158(11):3929-3942. 55. l'Allemand D, Schmidt S, Rousson V, Brabant G, Gasser T, Gruters A. Associations between body mass, leptin, IGF-I and circulating adrenal androgens in children with obesity and premature adrenarche. Eur J Endocrinol. 2002;146(4):537-543. 56. BĂśttner A, Jr K, MĂźller G, et al. Gender Differences of adiponectin levels develop during the progression of puberty and are related to serum androgen levels. J Clin Endocrinol Metabol. 2004;89(8):4053- 4061. 57. Unanue N, Bazaes R, IĂąiguez G, Cortes F, Avila A, Mericq V. Adre- narche in Prader-Willi syndrome appears not related to insulin sensi- tivity and serum adiponectin. Horm Res. 2007;67(3):152-158. 58. Michalakis K, Mintziori G, Kaprara A, Tarlatzis BC, Goulis DG. The complex interaction between obesity, metabolic syndrome and repro- ductive axis: a narrative review. Metabolism: clinical and experimental. 2013;62(4):457-478. 59. Machinal-Quelin F, Dieudonne MN, Pecquery R, Leneveu MC, Giudicelli Y. Direct in vitro effects of androgens and estrogens on ob gene expression and leptin secretion in human adipose tissue. Endo- crine. 2002;18(2):179-184. 60. Dobrzyn K, Smolinska N, Kiezun M. Adiponectin: A new regulator of female reproductive system. Int J Endocrinol. 2018;2018:1-12, 7965071. 61. Martin LJ. Implications of adiponectin in linking metabolism to testic- ular function. Endocrine. 2014;46(1):16-28. 62. Mathew H, Castracane VD, Mantzoros C. Adipose tissue and repro- ductive health. Metabolism: clinical and experimental. 2018;86:18-32. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 10 of 10 NIEUWENHUIS ET AL. 63. Sitticharoon C, Sukharomana M, Likitmaskul S, Churintaraphan M, Maikaew P. 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Introduction to Free Fall A free-falling object is an object that is falling under the sole influence of gravity. Any object that is being acted upon only by the force of gravity is said to be in a state of free fall. There are two important motion characteristics that are true of free-falling objects: ⢠Free-falling objects do not encounter air resistance. ⢠All free-falling objects (on Earth) accelerate downwards at a rate of 9.8 m/s/s (often approximated as 10 m/s/s for back-of-the-envelope calculations) Because free-falling objects are accelerating downwards at a rate of 9.8 m/s/s, a ticker tape trace or dot diagram of its motion would depict an acceleration. The dot diagram at the right depicts the acceleration of a free-falling object. The position of the object at regular time intervals - say, every 0.1 second - is shown. The fact that the distance that the object travels every interval of time is increasing is a sure sign that the ball is speeding up as it falls downward. Recall from an earlier lesson, that if an object travels downward and speeds up, then its acceleration is downward. Free-fall acceleration is often witnessed in a physics classroom by means of an ever-popular strobe light demonstration. The room is darkened and a jug full of water is connected by a tube to a medicine dropper. The dropper drips water and the strobe illuminate the falling droplets at a regular rate - say once every 0.2 seconds. Instead of seeing a stream of water free-falling from the medicine dropper, several consecutive drops with increasing separation distance are seen. The pattern of drops resembles the dot diagram shown in the graphic at the right. The Acceleration of Gravity It was learned in the previous part of this lesson that a free-falling object is an object that is falling under the sole influence of gravity. A free-falling object has an acceleration of 9.8 m/s/s, downward (on Earth). This numerical value for the acceleration of a free-falling object is such an important value that it is given a special name. It is known as the acceleration of gravity - the acceleration for any object moving under the sole influence of gravity. A matter of fact, this quantity known as the acceleration of gravity is such an important quantity that physicists have a special symbol to denote it - the symbol g. The numerical value for the acceleration of gravity is most accurately known as 9.8 m/s2. There are slight variations in this numerical value (to the second decimal place) that are dependent primarily upon on altitude. We will occasionally use the approximated value of 10 m/s2 in order to reduce the complexity of the many mathematical tasks that we will perform with this number. By so doing, we will be able to better focus on the conceptual nature of physics without too much of a sacrifice in numerical accuracy. g = 9.8 m/s2, downward Look It Up! Even on the surface of the Earth, there are local variations in the value of the acceleration of gravity (g). These variations are due to latitude, altitude and the local geological structure of the region. Recall from an earlier lesson that acceleration is the rate at which an object changes its velocity. It is the ratio of velocity change to time between any two points in an object's path. To accelerate at 9.8 m/s2 means to change the velocity by 9.8 m/s each second. If the velocity and time for a free-falling object being dropped from a position of rest were tabulated, then one would note the following pattern. Time (s) Velocity (m/s) 0 0 1 - 9.8 2 - 19.6 3 - 29.4 4 - 39.2 5 - 49.0 . Observe that the velocity-time data above reveal that the object's velocity is changing by 9.8 m/s each consecutive second. That is, the free-falling object has an acceleration of approximately 9.8 m/s2. Another way to represent this acceleration of 9.8 m/s2 is to add numbers to our dot diagram that we saw earlier in this lesson. The velocity of the ball is seen to increase as depicted in the diagram at the right. (NOTE: The diagram is not drawn to scale - in two seconds, the object would drop considerably further than the distance from shoulder to toes.) Representing Free Fall by Graphs ⢠Early in Lesson 1 it was mentioned that there are a variety of means of describing the motion of objects. One such means of describing the motion of objects is through the use of graphs - position versus time and velocity vs. time graphs. In this part of Lesson 5, the motion of a free-falling motion will be represented using these two basic types of graphs. Representing Free Fall by Position-Time Graphs A position versus time graph for a free-falling object is shown below. Observe that the line on the graph curves. As learned earlier, a curved line on a position versus time graph signifies an accelerated motion. Since a free-falling object is undergoing an acceleration (g = 9.8 m/s/s), it would be expected that its position-time graph would be curved. A further look at the position-time graph reveals that the object starts with a small velocity (slow) and finishes with a large velocity (fast). Since the slope of any position vs. time graph is the velocity of the object (as learned in Lesson 3), the small initial slope indicates a small initial velocity and the large final slope indicates a large final velocity. Finally, the negative slope of the line indicates a negative (i.e., downward) velocity. Representing Free Fall by Velocity-Time Graphs A velocity versus time graph for a free-falling object is shown below. Observe that the line on the graph is a straight, diagonal line. As learned earlier, a diagonal line on a velocity versus time graph signifies an accelerated motion. Since a free-falling object is undergoing an acceleration (g = 9,8 m/s/s, downward), it would be expected that its velocity-time graph would be diagonal. A further look at the velocity-time graph reveals that the object starts with a zero velocity (as read from the graph) and finishes with a large, negative velocity; that is, the object is moving in the negative direction and speeding up. An object that is moving in the negative direction and speeding up is said to have a negative acceleration (if necessary, review the vector nature of acceleration). Since the slope of any velocity versus time graph is the acceleration of the object (as learned in Lesson 4), the constant, negative slope indicates a constant, negative acceleration. This analysis of the slope on the graph is consistent with the motion of a free-falling object - an object moving with a constant acceleration of 9.8 m/s/s in the downward direction. The Kinematic Equations The goal of this first unit has been to investigate the variety of means by which the motion of objects can be described. The variety of representations that we have investigated includes verbal representations, pictorial representations, numerical representations, and graphical representations (position-time graphs and velocity-time graphs). In Lesson 6, we will investigate the use of equations to describe and represent the motion of objects. These equations are known as kinematic equations. There are a variety of quantities associated with the motion of objects - displacement (and distance), velocity (and speed), acceleration, and time. Knowledge of each of these quantities provides descriptive information about an object's motion. For example, if a car is known to move with a constant velocity of 22.0 m/s, North for 12.0 seconds for a northward displacement of 264 meters, then the motion of the car is fully described. And if a second car is known to accelerate from a rest position with an eastward acceleration of 3.0 m/s2 for a time of 8.0 seconds, providing a final velocity of 24 m/s, East and an eastward displacement of 96 meters, then the motion of this car is fully described. These two statements provide a complete description of the motion of an object. However, such completeness is not always known. It is often the case that only a few parameters of an object's motion are known, while the rest are unknown. For example as you approach the stoplight, you might know that your car has a velocity of 22 m/s, East and is capable of a skidding acceleration of 8.0 m/s2, West. However you do not know the displacement that your car would experience if you were to slam on your brakes and skid to a stop; and you do not know the time required to skid to a stop. In such an instance as this, the unknown parameters can be determined using physics principles and mathematical equations (the kinematic equations). The BIG 4 The kinematic equations are a set of four equations that can be utilized to predict unknown information about an object's motion if other information is known. The equations can be utilized for any motion that can be described as being either a constant velocity motion (an acceleration of 0 m/s/s) or a constant acceleration motion. They can never be used over any time period during which the acceleration is changing. Each of the kinematic equations include four variables. If the values of three of the four variables are known, then the value of the fourth variable can be calculated. In this manner, the kinematic equations provide a useful means of predicting information about an object's motion if other information is known. For example, if the acceleration value and the initial and final velocity values of a skidding car is known, then the displacement of the car and the time can be predicted using the kinematic equations. Lesson 6 of this unit will focus upon the use of the kinematic equations to predict the numerical values of unknown quantities for an object's motion. The four kinematic equations that describe an object's motion are: There are a variety of symbols used in the above equations. Each symbol has its own specific meaning. The symbol d stands for the displacement of the object. The symbol t stands for the time for which the object moved. The symbol a stands for the acceleration of the object. And the symbol v stands for the velocity of the object; a subscript of i after the v (as in vi) indicates that the velocity value is the initial velocity value and a subscript of f (as in vf) indicates that the velocity value is the final velocity value. Each of these four equations appropriately describes the mathematical relationship between the parameters of an object's motion. As such, they can be used to predict unknown information about an object's motion if other information is known. In the next part of Lesson 6 we will investigate the process of doing this. Kinematic Equations and Problem-Solving The four kinematic equations that describe the mathematical relationship between the parameters that describe an object's motion were introduced in the previous part of Lesson 6. The four kinematic equations are: In the above equations, the symbol d stands for the displacement of the object. The symbol t stands for the time for which the object moved. The symbol a stand for the acceleration of the object. And the symbol v stands for the instantaneous velocity of the object; a subscript of i after the v (as in vi) indicates that the velocity value is the initial velocity value and a subscript of f (as in vf) indicates that the velocity value is the final velocity value. Problem-Solving Strategy In this part of Lesson 6 we will investigate the process of using the equations to determine unknown information about an object's motion. The process involves the use of a problem-solving strategy that will be used throughout the course. The strategy involves the following steps: 1. Construct an informative diagram of the physical situation. 2. Identify and list the given information in variable form. 3. Identify and list the unknown information in variable form. 4. Identify and list the equation that will be used to determine unknown information from known information. 5. Substitute known values into the equation and use appropriate algebraic steps to solve for the unknown information. 6. Check your answer to ensure that it is reasonable and mathematically correct. The use of this problem-solving strategy in the solution of the following problem is modeled in Examples A and B below. Example Problem A . Ima Hurryin is approaching a stoplight moving with a velocity of +30.0 m/s. The light turns yellow, and Ima applies the brakes and skids to a stop. If Ima's acceleration is -8.00 m/s2, then determine the displacement of the car during the skidding process. (Note that the direction of the velocity and the acceleration vectors are denoted by a + and a - sign.) The solution to this problem begins by the construction of an informative diagram of the physical situation. This is shown below. The second step involves the identification and listing of known information in variable form. Note that the vf value can be inferred to be 0 m/s since Ima's car comes to a stop. The initial velocity (vi) of the car is +30.0 m/s since this is the velocity at the beginning of the motion (the skidding motion). And the acceleration (a) of the car is given as - 8.00 m/s2. (Always pay careful attention to the + and - signs for the given quantities.) The next step of the strategy involves the listing of the unknown (or desired) information in variable form. In this case, the problem requests information about the displacement of the car. So d is the unknown quantity. The results of the first three steps are shown in the table below. Diagram: Given: Find: vi = +30.0 m/s vf = 0 m/s a = - 8.00 m/s2 d = ?? The next step of the strategy involves identifying a kinematic equation that would allow you to determine the unknown quantity. There are four kinematic equations to choose from. In general, you will always choose the equation that contains the three known and the one unknown variable. In this specific case, the three known variables and the one unknown variable are vf, vi, a, and d. Thus, you will look for an equation that has these four variables listed in it. An inspection of the four equations above reveals that the equation on the top right contains all four variables. vf2 = vi2 + 2 ⢠a ⢠d Once the equation is identified and written down, the next step of the strategy involves substituting known values into the equation and using proper algebraic steps to solve for the unknown information. This step is shown below. (0 m/s)2 = (30.0 m/s)2 + 2 ⢠(-8.00 m/s2) ⢠d 0 m2/s2 = 900 m2/s2 + (-16.0 m/s2) ⢠d (16.0 m/s2) ⢠d = 900 m2/s2 - 0 m2/s2 (16.0 m/s2)*d = 900 m2/s2 d = (900 m2/s2)/ (16.0 m/s2) d = (900 m2/s2)/ (16.0 m/s2) d = 56.3 m The solution above reveals that the car will skid a distance of 56.3 meters. (Note that this value is rounded to the third digit.) The last step of the problem-solving strategy involves checking the answer to assure that it is both reasonable and accurate. The value seems reasonable enough. It takes a car a considerable distance to skid from 30.0 m/s (approximately 65 mi/hr) to a stop. The calculated distance is approximately one-half a football field, making this a very reasonable skidding distance. Checking for accuracy involves substituting the calculated value back into the equation for displacement and insuring that the left side of the equation is equal to the right side of the equation. Indeed it is! Example Problem B Ben Rushin is waiting at a stoplight. When it finally turns green, Ben accelerated from rest at a rate of a 6.00 m/s2 for a time of 4.10 seconds. Determine the displacement of Ben's car during this time period. Once more, the solution to this problem begins by the construction of an informative diagram of the physical situation. This is shown below. The second step of the strategy involves the identification and listing of known information in variable form. Note that the vi value can be inferred to be 0 m/s since Ben's car is initially at rest. The acceleration (a) of the car is 6.00 m/s2. And the time (t) is given as 4.10 s. The next step of the strategy involves the listing of the unknown (or desired) information in variable form. In this case, the problem requests information about the displacement of the car. So d is the unknown information. The results of the first three steps are shown in the table below. Diagram: Given: Find: vi = 0 m/s t = 4.10 s a = 6.00 m/s2 d = ?? The next step of the strategy involves identifying a kinematic equation that would allow you to determine the unknown quantity. There are four kinematic equations to choose from. Again, you will always search for an equation that contains the three known variables and the one unknown variable. In this specific case, the three known variables and the one unknown variable are t, vi, a, and d. An inspection of the four equations above reveals that the equation on the top left contains all four variables. d = vi ⢠t + ½ ⢠a ⢠t2 Once the equation is identified and written down, the next step of the strategy involves substituting known values into the equation and using proper algebraic steps to solve for the unknown information. This step is shown below. d = (0 m/s) ⢠(4.1 s) + ½ ⢠(6.00 m/s2) ⢠(4.10 s)2 d = (0 m) + ½ ⢠(6.00 m/s2) ⢠(16.81 s2) d = 0 m + 50.43 m d = 50.4 m The solution above reveals that the car will travel a distance of 50.4 meters. (Note that this value is rounded to the third digit.) The last step of the problem-solving strategy involves checking the answer to assure that it is both reasonable and accurate. The value seems reasonable enough. A car with an acceleration of 6.00 m/s/s will reach a speed of approximately 24 m/s (approximately 50 mi/hr) in 4.10 s. The distance over which such a car would be displaced during this time period would be approximately one-half a football field, making this a very reasonable distance. Checking for accuracy involves substituting the calculated value back into the equation for displacement and insuring that the left side of the equation is equal to the right side of the equation. Indeed, it is! The two example problems above illustrate how the kinematic equations can be combined with a simple problem-solving strategy to predict unknown motion parameters for a moving object. Provided that three motion parameters are known, any of the remaining values can be determined. In the next part of Lesson 6, we will see how this strategy can be applied to free fall situations. Or if interested, you can try some practice problems and check your answer against the given solutions. Kinematic Equations and Free Fall As mentioned in Lesson 5, a free-falling object is an object that is falling under the sole influence of gravity. That is to say that any object that is moving and being acted upon only be the force of gravity is said to be "in a state of free fall." Such an object will experience a downward acceleration of 9.8 m/s/s. Whether the object is falling downward or rising upward towards its peak, if it is under the sole influence of gravity, then its acceleration value is 9.8 m/s/s. Like any moving object, the motion of an object in free fall can be described by four kinematic equations. The kinematic equations that describe any object's motion are: The symbols in the above equation have a specific meaning: the symbol d stands for the displacement; the symbol t stands for the time; the symbol a stands for the acceleration of the object; the symbol vi stands for the initial velocity value; and the symbol vf stands for the final velocity. Applying Free Fall Concepts to Problem-Solving There are a few conceptual characteristics of free fall motion that will be of value when using the equations to analyze free fall motion. These concepts are described as follows: ⢠An object in free fall experiences an acceleration of -9.8 m/s/s. (The - sign indicates a downward acceleration.) Whether explicitly stated or not, the value of the acceleration in the kinematic equations is -9.8 m/s/s for any freely falling object. ⢠If an object is merely dropped (as opposed to being thrown) from an elevated height, then the initial velocity of the object is 0 m/s. ⢠If an object is projected upwards in a perfectly vertical direction, then it will slow down as it rises upward. The instant at which it reaches the peak of its trajectory, its velocity is 0 m/s. This value can be used as one of the motion parameters in the kinematic equations; for example, the final velocity (vf) after traveling to the peak would be assigned a value of 0 m/s. ⢠If an object is projected upwards in a perfectly vertical direction, then the velocity at which it is projected is equal in magnitude and opposite in sign to the velocity that it has when it returns to the same height. That is, a ball projected vertically with an upward velocity of +30 m/s will have a downward velocity of -30 m/s when it returns to the same height. These four principles and the four kinematic equations can be combined to solve problems involving the motion of free-falling objects. The two examples below illustrate application of free fall principles to kinematic problem-solving. In each example, the problem solving strategy that was introduced earlier in this lesson will be utilized. Example Problem A Luke Autbeloe drops a pile of roof shingles from the top of a roof located 8.52 meters above the ground. Determine the time required for the shingles to reach the ground. The solution to this problem begins by the construction of an informative diagram of the physical situation. This is shown below. The second step involves the identification and listing of known information in variable form. You might note that in the statement of the problem, there is only one piece of numerical information explicitly stated: 8.52 meters. The displacement (d) of the shingles is -8.52 m. (The - sign indicates that the displacement is downward). The remaining information must be extracted from the problem statement based upon your understanding of the above principles. For example, the vi value can be inferred to be 0 m/s since the shingles are dropped (released from rest; see note above). And the acceleration (a) of the shingles can be inferred to be -9.8 m/s2 since the shingles are free-falling (see note above). (Always pay careful attention to the + and - signs for the given quantities.) The next step of the solution involves the listing of the unknown (or desired) information in variable form. In this case, the problem requests information about the time of fall. So t is the unknown quantity. The results of the first three steps are shown in the table below. Diagram: Given: Find: vi = 0.0 m/s d = -8.52 m a = - 9.8 m/s2 t = ?? The next step involves identifying a kinematic equation that allows you to determine the unknown quantity. There are four kinematic equations to choose from. In general, you will always choose the equation that contains the three known and the one unknown variable. In this specific case, the three known variables and the one unknown variable are d, vi, a, and t. Thus, you will look for an equation that has these four variables listed in it. An inspection of the four equations above reveals that the equation on the top left contains all four variables. d = vi ⢠t + ½ ⢠a ⢠t2 Once the equation is identified and written down, the next step involves substituting known values into the equation and using proper algebraic steps to solve for the unknown information. This step is shown below. -8.52 m = (0 m/s) ⢠(t) + ½ ⢠(-9.8 m/s2) ⢠(t)2 -8.52 m = (0 m) *(t) + (-4.9 m/s2) ⢠(t)2 -8.52 m = (-4.9 m/s2) ⢠(t)2 (-8.52 m)/(-4.9 m/s2) = t2 1.739 s2 = t2 t = 1.32 s The solution above reveals that the shingles will fall for a time of 1.32 seconds before hitting the ground. (Note that this value is rounded to the third digit.) The last step of the problem-solving strategy involves checking the answer to assure that it is both reasonable and accurate. The value seems reasonable enough. The shingles are falling a distance of approximately 10 yards (1 meter is pretty close to 1 yard); it seems that an answer between 1 and 2 seconds would be highly reasonable. The calculated time easily falls within this range of reasonability. Checking for accuracy involves substituting the calculated value back into the equation for time and insuring that the left side of the equation is equal to the right side of the equation. Indeed it is! Example Problem B Rex Things throws his mother's crystal vase vertically upwards with an initial velocity of 26.2 m/s. Determine the height to which the vase will rise above its initial height. Once more, the solution to this problem begins by the construction of an informative diagram of the physical situation. This is shown below. The second step involves the identification and listing of known information in variable form. You might note that in the statement of the problem, there is only one piece of numerical information explicitly stated: 26.2 m/s. The initial velocity (vi) of the vase is +26.2 m/s. (The + sign indicates that the initial velocity is an upwards velocity). The remaining information must be extracted from the problem statement based upon your understanding of the above principles. Note that the vf value can be inferred to be 0 m/s since the final state of the vase is the peak of its trajectory (see note above). The acceleration (a) of the vase is -9.8 m/s2 (see note above). The next step involves the listing of the unknown (or desired) information in variable form. In this case, the problem requests information about the displacement of the vase (the height to which it rises above its starting height). So d is the unknown information. The results of the first three steps are shown in the table below. Diagram: Given: Find: vi = 26.2 m/s vf = 0 m/s a = -9.8 m/s2 d = ?? The next step involves identifying a kinematic equation that would allow you to determine the unknown quantity. There are four kinematic equations to choose from. Again, you will always search for an equation that contains the three known variables and the one unknown variable. In this specific case, the three known variables and the one unknown variable are vi, vf, a, and d. An inspection of the four equations above reveals that the equation on the top right contains all four variables. vf2 = vi2 + 2 ⢠a ⢠d Once the equation is identified and written down, the next step involves substituting known values into the equation and using proper algebraic steps to solve for the unknown information. This step is shown below. (0 m/s)2 = (26.2 m/s)2 + 2 â˘(-9.8m/s2) â˘d 0 m2/s2 = 686.44 m2/s2 + (-19.6 m/s2) â˘d (-19.6 m/s2) ⢠d = 0 m2/s2 -686.44 m2/s2 (-19.6 m/s2) ⢠d = -686.44 m2/s2 d = (-686.44 m2/s2)/ (-19.6 m/s2) d = 35.0 m The solution above reveals that the vase will travel upwards for a displacement of 35.0 meters before reaching its peak. (Note that this value is rounded to the third digit.) The last step of the problem-solving strategy involves checking the answer to assure that it is both reasonable and accurate. The value seems reasonable enough. The vase is thrown with a speed of approximately 50 mi/hr (merely approximate 1 m/s to be equivalent to 2 mi/hr). Such a throw will never make it further than one football field in height (approximately 100 m), yet will surely make it past the 10-yard line (approximately 10 meters). The calculated answer certainly falls within this range of reasonability. Checking for accuracy involves substituting the calculated value back into the equation for displacement and insuring that the left side of the equation is equal to the right side of the equation. Indeed, it is! Kinematic equations provide a useful means of determining the value of an unknown motion parameter if three motion parameters are known. In the case of a free-fall motion, the acceleration is often known. And in many cases, another motion parameter can be inferred through a solid knowledge of some basic kinematic principles.
MYTH The British helped the Jews displace the native Arab population of Palestine. FACT Herbert Samuel, a British Jew who served as the first High Commissioner of Palestine, placed restrictions on Jewish immigration âin the âinterests of the present populationâ and the âabsorptive capacityâ of the country.â1 The influx of Jewish settlers was said to force the Arab fellahin (native peasants) from their land. This was when less than a million people lived in an area that now supports more than nine million. The British limited the absorptive capacity of Palestine when, in 1921, Colonial Secretary Winston Churchill severed nearly four-fifths of Palestineâsome thirty-five thousand square milesâto create a new Arab entity, Transjordan. As a consolation prize for the Hejaz and Arabia (which are both now Saudi Arabia) going to the Saud family, Churchill rewarded Sharif Husseinâs son Abdullah for his contribution to the war against Turkey by installing him as Transjordanâs emir. The British went further and placed restrictions on Jewish land purchases in what remained of Palestine. By 1949, the British had allotted 87,500 acres of the 187,500 acres of cultivable land to Arabs and only 4,250 acres to Jews. This contradicted Article 6 of the Mandate which stated that âthe Administration of PalestineâŚshall encourage, in cooperation with the Jewish AgencyâŚclose settlement by Jews on the land, including State lands and waste lands not acquired for public purposes.â2 Ultimately, the British admitted that the argument about the countryâs absorptive capacity was specious. The Peel Commission said, âThe heavy immigration in the years 1933â36 would seem to show that the Jews have been able to enlarge the absorptive capacity of the country for Jews.â3 MYTH The British allowed Jews to flood Palestine while Arab immigration was tightly controlled. FACT The British response to Jewish immigration set a precedent of appeasing the Arabs, which was followed for the duration of the Mandate. The British restricted Jewish immigration while allowing Arabs to enter the country freely. Apparently, London did not feel that a flood of Arab immigrants would affect the countryâs âabsorptive capacity.â During World War I, the Jewish population in Palestine declined because of the war, famine, disease, and expulsion by the Turks. In 1915, approximately 83,000 Jews lived in Palestine among 590,000 Muslim and Christian Arabs. According to the 1922 census, the Jewish population was 83,000, while the Arabs numbered 643,000.4 Thus, the Arab population grew exponentially while that of the Jews stagnated. In the mid-1920s, Jewish immigration to Palestine increased primarily because of anti-Jewish economic legislation in Poland and Washingtonâs imposition of restrictive quotas.5 The record number of immigrants in 1935 (see table) was a response to the growing persecution of Jews in Nazi Germany. The British administration considered this number too large, however, so the Jewish Agency was informed that less than one-third of the quota it asked for would be approved in 1936.6 The British gave in further to Arab demands by announcing in the 1939 White Paper that an independent Arab state would be created within ten years and that Jewish immigration was to be limited to 75,000 for the next five years, after which it was to cease altogether. It also forbade land sales to Jews in 95% of the territory of Palestine. The Arabs, nevertheless, rejected the proposal. Jewish Immigration to Palestine7 1919 1,806 1931 4,075 1920 8,223 1932 12,533 1921 8,294 1933 37,337 1922 8,685 1934 45,267 1923 8,175 1935 66,472 1924 13,892 1936 29,595 1925 34,386 1937 10,629 1926 13,855 1938 14,675 1927 3,034 1939 31,195 1928 2,178 1940 10,643 1929 5,249 1941 4,592 1930 4,944 By contrast, throughout the Mandatory period, Arab immigration was unrestricted. In 1930, the Hope Simpson Commission, sent from London to investigate the 1929 Arab riots, said the British practice of ignoring the uncontrolled illegal Arab immigration from Egypt, Transjordan, and Syria had the effect of displacing the prospective Jewish immigrants.8 The British governor of the Sinai from 1922 to 1936 observed, âThis illegal immigration was not only going on from the Sinai, but also from Transjordan and Syria, and it is very difficult to make a case out for the misery of the Arabs if at the same time their compatriots from adjoining states could not be kept from going in to share that misery.â9 The Peel Commission reported in 1937 that the âshortfall of land isâŚdue less to the amount of land acquired by Jews than to the increase in the Arab population.â10 MYTH The British changed their policy to allow Holocaust survivors to settle in Palestine. FACT The gates of Palestine remained closed for the duration of the war, stranding hundreds of thousands of Jews in Europe, many of whom became victims of Hitlerâs âFinal Solution.â After the war, the British refused to allow the survivors of the Nazi nightmare to find sanctuary in Palestine. On June 6, 1946, President Truman urged the British government to relieve the suffering of the Jews confined to displaced persons camps in Europe by immediately accepting 100,000 Jewish immigrants. Britainâs foreign minister Ernest Bevin replied sarcastically that the United States wanted displaced Jews to immigrate to Palestine âbecause they did not want too many of them in New York.â11 Some Jews reached Palestine, many smuggled in on dilapidated ships organized by the Haganah. Between August 1945 and the establishment of the State of Israel in May 1948, sixty-five âillegalâ immigrant ships, carrying 69,878 people, arrived from European shores. In August 1946, however, the British began to intern those they caught in camps on Cyprus. Approximately 50,000 people were detained in the camps, and 28,000 remained imprisoned when Israel declared independence.12 MYTH As the Jewish population grew, the plight of the Palestinian Arabs worsened. FACT In July 1921, Hasan Shukri, the mayor of Haifa and president of the Muslim National Associations, sent a telegram to the British government in reaction to a delegation of Palestinians that went to London to try to stop the implementation of the Balfour Declaration. Shukri wrote: We are certain that without Jewish immigration and financial assistance there will be no future development of our country as may be judged from the fact that the towns inhabited in part by Jews such as Jerusalem, Jaffa, Haifa, and Tiberias are making steady progress while Nablus, Acre, and Nazareth where no Jews reside are steadily declining.13 The Jewish population increased by 470,000 between World War I and World War II, while the non-Jewish population rose by 588,000.14 The permanent Arab population increased by 120% between 1922 and 1947.15 This rapid growth of the Arab population was a result of several factors. One was immigration from neighboring statesâconstituting 37% of the total immigration to pre-state Israelâby Arabs who wanted to take advantage of the higher standard of living the Jews had made possible.16 The Arab population also grew because of the improved living conditions created by the Jews as they drained malarial swamps and brought improved sanitation and health care to the region. Thus, for example, the Muslim infant mortality rate fell from 201 per thousand in 1925 to 94 per thousand in 1945, and life expectancy rose from 37 years in 1926 to 49 in 1943.17 The Arab population increased the most in cities where large Jewish populations had created new economic opportunities. From 1922â1947, the non-Jewish population increased by 290% in Haifa, 131% in Jerusalem, and 158% in Jaffa. The growth in Arab towns was more modest: 42% in Nablus, 78% in Jenin, and 37% in Bethlehem.18 MYTH Jews stole Arab land. FACT Despite the growth in their population, the Arabs continued to assert they were being displaced. From the beginning of World War I, however, part of Palestineâs land was owned by absentee landlords who lived in Cairo, Damascus, and Beirut. About 80% of the Palestinian Arabs were debt-ridden peasants, semi-nomads, and Bedouins.19 Jews went out of their way to avoid purchasing land in areas where Arabs might be displaced. They sought land that was largely uncultivated, swampy, cheap, andâmost importantâwithout tenants. In 1920, Labor Zionist leader David Ben-Gurion expressed his concern about the Arab fellahin, whom he viewed as âthe most important asset of the native population.â He insisted that âunder no circumstances must we touch land belonging to fellahs or worked by them.â Instead, he advocated helping liberate them from their oppressors. âOnly if a fellah leaves his place of settlement,â Ben-Gurion added, âshould we offer to buy his land, at an appropriate price.â20 Jews only began to purchase cultivated land after buying all the uncultivated territory. Many Arabs were willing to sell because of the migration to coastal towns and because they needed money to invest in the citrus industry.21 When John Hope Simpson arrived in Palestine in May 1930, he observed, âThey [the Jews] paid high prices for the land and, in addition, they paid to certain of the occupants of those lands a considerable amount of money which they were not legally bound to pay.â22 In 1931, Lewis French conducted a survey of landlessness for the British government and offered new plots to any Arabs who had been âdispossessed.â British officials received more than 3,000 applications, of which 80% were ruled invalid by the governmentâs legal adviser because the applicants were not landless Arabs. This left only about 600 landless Arabs, 100 of whom accepted the government land offer.23 In April 1936, a new outbreak of Arab attacks on Jews was instigated by local Palestinian leaders who were later joined by Arab volunteers led by a Syrian guerrilla named Fawzi al-Qawuqji, the commander of the Arab Liberation Army. By November, when the British finally sent a new commission headed by Lord Peel to investigate, 89 Jews had been killed and more than 300 wounded.24 The Peel Commissionâs report found that Arab complaints about Jewish land acquisition were baseless. It pointed out that âmuch of the land now carrying orange groves was sand dunes or swamp and uncultivated when it was purchasedâŚThere was at the time of the earlier sales little evidence that the owners possessed either the resources or training needed to develop the land.â25 Moreover, the Commission found the shortage was âdue less to the amount of land acquired by Jews than to the increase in the Arab population.â The report concluded that the presence of Jews in Palestine, along with the work of the British administration, had resulted in higher wages, an improved standard of living, and ample employment opportunities.26 It is made quite clear to all, both by the map drawn up by the Simpson Commission and by another compiled by the Peel Commission, that the Arabs are as prodigal in selling their land as they are in useless wailing and weeping (emphasis in the original). âTransjordanâs king Abdullah27 Even at the height of the Arab revolt in 1938 (which began in April 1936 with the murder of two Jews by Arabs and the subsequent murder of two Arab workers by members of the Jewish underground28), the British high commissioner to Palestine believed the Arab landowners were complaining about sales to Jews to drive up prices for lands they wished to sell. Many Arab landowners had been so terrorized by Arab rebels they decided to leave Palestine and sell their property to the Jews.29 The Jews paid exorbitant prices to wealthy landowners for small tracts of arid land. âIn 1944, Jews paid between $1,000 and $1,100 per acre in Palestine, mostly for arid or semiarid land; in the same year, rich black soil in Iowa was selling for about $110 per acre.â30 By 1947, Jewish holdings in Palestine amounted to about 463,000 acres. Approximately 45,000 were acquired from the mandatory government, 30,000 were bought from various churches, and 387,500 were purchased from Arabs. Analyses of land purchases from 1880 to 1948 show that 73% of Jewish plots were purchased from large landowners, not poor fellahin.31 Many leaders of the Arab nationalist movement, including members of the Muslim Supreme Council, and the mayors of Gaza, Jerusalem, and s sold land to the Jews. Asâad el-Shuqeiri, a Muslim religious scholar and father of Palestine Liberation Organization chairman Ahmed Shuqeiri, took Jewish money for his land. Even King Abdullah leased land to the Jews.32 MYTH The British helped the Palestinians to live peacefully with the Jews. FACT In 1921, Haj Amin el-Husseini first began to organize fedayeen (âone who sacrifices himselfâ) to terrorize Jews. El-Husseini hoped to duplicate the success of Kemal AtatĂźrk in Turkey by driving the Jews out of Palestine just as Kemal had driven the invading Greeks from his country.33 Arab radicals gained influence because the British administration was unwilling to take effective action against them until they began a revolt against British rule. Colonel Richard Meinertzhagen, former head of British military intelligence in Cairo, and later chief political officer for Palestine and Syria, wrote in his diary that British officials âincline towards the exclusion of Zionism in Palestine.â The British encouraged the Palestinians to attack the Jews. According to Meinertzhagen, Col. Bertie Harry Waters-Taylor (financial adviser to the military administration in Palestine 1919â23) met with el-Husseini in 1920, a few days before Easter, and told him that âhe had a great opportunity at Easter to show the worldâŚthat Zionism was unpopular not only with the Palestine administration but in Whitehall.â He added that âif disturbances of sufficient violence occurred in Jerusalem at Easter, both General [Louis] Bols [chief administrator in Palestine, 1919â20] and General [Edmund] Allenby [commander of the Egyptian force, 1917â19, then high commissioner of Egypt] would advocate the abandonment of the Jewish Home. Waters-Taylor explained that freedom could only be attained through violence.â34 El-Husseini took the colonelâs advice and instigated a riot. The British withdrew their troops and the Jewish police from Jerusalem, allowing the Arab mob to attack Jews and loot their shops. Because of el-Husseiniâs overt role in instigating the pogrom, the British decided to arrest him. He escaped, however, and was sentenced to ten years in absentia. A year later, some British Arabists convinced High Commissioner Herbert Samuel to pardon el-Husseini and to appoint him Mufti (a cleric in charge of Jerusalemâs Islamic holy places). By contrast, Vladimir Jabotinsky and several followers, who had formed a Jewish defense organization during the unrest, were sentenced to 15 years. They were released a few months later.35 Samuel met with el-Husseini on April 11, 1921, and was assured âthat the influences of his family and himself would be devoted to tranquility.â Three weeks later, riots in Jaffa and elsewhere left forty-three Jews dead.36 El-Husseini consolidated his power and took control of all Muslim religious funds in Palestine. He used his authority to gain control over the mosques, the schools, and the courts. No Arab could reach an influential position without being loyal to the Mufti. His power was so absolute that âno Muslim in Palestine could be born or die without being beholden to Haj Amin.â37 The Muftiâs henchmen also ensured he would have no opposition by systematically killing Palestinians who discussed cooperation with the Jews from rival clans. As the spokesman for Palestinian Arabs, el-Husseini did not ask that Britain grant them independence. On the contrary, in a letter to Churchill in 1921, he demanded that Palestine be reunited with Syria and Transjordan.38 The Arabs found rioting an effective political tool because of the lax British response toward violence against Jews. In handling each riot, the British prevented Jews from protecting themselves but made little effort to prevent the Arabs from attacking them. After each outbreak, a British commission of inquiry would try to establish the cause of the violence. The conclusion was always the same: The Arabs feared being displaced by the Jews. To stop the rioting, the commissions would recommend that restrictions be placed on Jewish immigration. Thus, the Arabs learned they could always stop the influx of Jews by staging riots. This cycle began after a series of riots in May 1921. After failing to protect the Jewish community from Arab mobs, the British appointed the Haycraft Commission to investigate the cause of the violence. Although the panel concluded the Arabs had been the aggressors, it rationalized the cause of the attack: âThe fundamental cause of the riots was a feeling among the Arabs of discontent with, and hostility to, the Jews, due to political and economic causes, and connected with Jewish immigration, and with their conception of Zionist policy.â39 One consequence of the violence was the institution of a temporary ban on Jewish immigration. The Arab fear of being âdisplacedâ or âdominatedâ was an excuse for their attacks on Jewish settlers. Note, too, that these riots were not inspired by nationalistic fervorânationalists would have rebelled against their British overlordsâthey were motivated by economics, the radical Islamic views of the Mufti, and misunderstanding. In 1929, Arab provocateurs convinced the masses that the Jews had designs on the Temple Mount (a tactic still used today to incite violence). A Jewish religious observance at the Western Wall, which forms a part of the Temple Mount, served as a pretext for rioting by Arabs against Jews, which spilled out of Jerusalem into other villages and towns, including Safed and Hebron. Again, the British administration made no effort to prevent the violence, and, after it began, the British did nothing to protect the Jewish population. After six days of mayhem, the British finally brought troops in to quell the disturbance. By this time, most of Hebronâs Jews had fled or been killed. In all, 133 Jews were killed and 399 wounded in the pogroms.40 After the riots, the British ordered an investigation, resulting in the Passfield White Paper. It said the âimmigration, land purchase and settlement policies of the Zionist Organization were already or were likely to become, prejudicial to Arab interests. It understood the mandatory governmentâs obligation to the non-Jewish community to mean that Palestineâs resources must be primarily reserved for the growing Arab economy.â41 This meant it was necessary to restrict Jewish immigration and land purchases. MYTH The Mufti was not a Nazi collaborator. FACT In 1941, Haj Amin al-Husseini, the Mufti of Jerusalem, fled to Germany and met with Adolf Hitler, Heinrich Himmler, Joachim Von Ribbentrop, and other Nazi leaders. He wanted to persuade them to extend the Nazisâ anti-Jewish program to the Arab world. The Mufti sent Hitler fifteen drafts of declarations he wanted Germany and Italy to make concerning the Middle East. One called on the two countries to declare the illegality of the Jewish home in Palestine. He also asked the Axis powers to âaccord to Palestine and to other Arab countries the right to solve the problem of the Jewish elements in Palestine and other Arab countries in accordance with the interest of the Arabs, and by the same method that the question is now being settled in the Axis countries.â42 In November 1941, the Mufti met with Hitler, who told him the Jews were his foremost enemy. The Nazi dictator rebuffed the Muftiâs requests for a declaration in support of the Arabs, however, telling him the time was not right. The Mufti offered Hitler his âthanks for the sympathy which he had always shown for the Arab and especially Palestinian cause, and to which he had given clear expression in his public speeches.â He added, âThe Arabs were Germanyâs natural friends because they had the same enemies as had Germany, namelyâŚthe Jews.â Hitler told the Mufti he opposed the creation of a Jewish state and that Germanyâs objective was destroying the Jewish element in the Arab sphere.43 In 1945, Yugoslavia sought to indict the Mufti as a war criminal for his role in recruiting twenty thousand Muslim volunteers for the SS, who participated in the killing of Jews in Croatia and Hungary. He escaped French detention in 1946, however, and continued his fight against the Jews from Cairo and later Beirut where he died in 1974. MYTH The bombing of the King David Hotel was part of a deliberate terror campaign against civilians. FACT British troops seized the Jewish Agency compound on June 29, 1946, and confiscated large quantities of documents. At about the same time, more than 2,500 Jews from all over Palestine were arrested. A week later, news of a massacre of 40 Jews in a pogrom in Poland reminded the Jews of Palestine how Britainâs restrictive immigration policy had condemned thousands to death. In response to the British provocations, and a desire to demonstrate that the Jewsâ spirit could not be broken, the United Resistance Movement planned to bomb the King David Hotel, which housed the British military command and the Criminal Investigation Division in addition to hotel guests. The Haganah pulled out of the plot and left it up to the Irgun. Irgun leader Menachem Begin stressed his desire to avoid civilian casualties and the plan was to warn the British so they would evacuate the building before it was blown up. Three telephone calls were placed on July 22, 1946, one to the hotel, another to the French Consulate, and a third to the Palestine Post warning that explosives in the King David Hotel would soon be detonated. The call to the hotel was received and ignored. Begin quotes one British official who supposedly refused to evacuate the building, saying, âWe donât take orders from the Jews.â44 As a result, when the bombs exploded, the casualty toll was high: 91 killed and 45 injured. Among the casualties were 15 Jews. Few people in the main part of the hotel were injured.45 For decades, the British denied they had been warned. In 1979, however, a member of the British Parliament provided the testimony of a British officer who heard other officers in the King David Hotel bar joking about a Zionist threat to the headquarters. The officer who overheard the conversation immediately left the hotel and survived.46 In contrast to Arab attacks against Jews, which Arab leaders hailed as heroic actions, the Jewish National Council denounced the bombing of the King David.47 1 Aharon Cohen, Israel and the Arab World, (NY: Funk and Wagnalls, 1970), p. 172
10 years of experience designing engaging quizzes and interactive learning games for children aged 8-10 years old. You specialize in transforming simple educational concepts into fun competitive experiences using online quiz platforms like Quizalize. Objective: Design a complete interactive multiplication quiz for third-grade students (8â9 years old) on the Quizalize platform. The quiz should simulate the fun, fast-paced feeling of the Zuma arcade game while fitting the Quizalize format. The aim is to help students practice multiplication tables (1Ă1 to 12Ă12) in an exciting, motivating, and competitive environment. Instructions: Structure: Design at least 40 multiplication questions. Questions should appear in increasing difficulty: start from easy (e.g., 2Ă3, 4Ă2) and move to harder problems (e.g., 11Ă12, 9Ă8). Timing: Set a short time limit for each question (e.g., 10 seconds) to simulate the fast reaction needed in Zuma. Encourage fast thinking and rapid response under time pressure. Answer Choices: Use multiple-choice answers. Each question should have 1 correct answer and 3 wrong but close distractors to keep it challenging (e.g., for 7Ă6: options 42, 43, 36, 48). Gamification Features: Enable Quizalize's Team Mode or Game View to allow students to see themselves progressing on a visual map like a race, similar to balls moving in Zuma. Set points bonuses for speed and accuracy. Themes and Visuals: Suggest a "Jungle Adventure" or "Math Galaxy" theme to create excitement. Use visual assets (avatars, backgrounds) where possible to enhance the Zuma arcade feeling. Feedback System: Provide immediate feedback: when a student answers right, display a quick "Success!" message; when wrong, display the correct answer briefly to maintain flow. Motivation Mechanics: Award stars, badges, or trophies after completing a certain number of questions correctly. Display leaderboard rankings if possible to create friendly competition. Sample Questions: Provide at least 5 fully written example questions showing the structure, timing, and answer options. Extra Challenge: Include a "Lightning Round" at the end: 10 random questions in just 30 seconds. Important: Keep language child-friendly and motivational. Make sure no question looks too similar to the others to avoid boredom. Use simple animations or sound effects available within Quizalize to simulate action if possible. Take a deep breath and work on this problem step-by-step.
Make mcq quiz with 4 option in which one is correct -'10 Basis of Material Science ⢠.....;;;";;;"~~;;,,;;,,,,;.;.,,;;,,,;,,;.;,.,------------ 6. Temporary materials: Some materials are meant to be placed in the oral cavity for a short period of time for different reasons. ⢠Temporary crowns: While a permanent crown is prepared in the dental laboratory, the patient must wait for few days before it can be fabricated and cemented into place. Does patient experience any problems during this time period? If the tooth is vital (the pulp is alive), the patient is likely to experience pain and sensitivity while eating and drinking, also it looks unesthetic. What can be done to solve this problem? A temporary crown is placed before the patient leaves the clinic. It is constructed and luted in the same appointment in which the crown preparation is done. Temporary crowns are not very strong or esthetic but they serve adequately till the permanent crown is ready to be cemented. ⢠Temporary restorations: Sometimes it is difficult to decide immediately the best line of treatment for a particular tooth. The exact condition of the pulp may not be obvious to the dentist from the patient's symptoms. A dentist removes all or part of the decay and then places a temporary restoration to have time to observe the behaviour of the pulp or to give the pilip time to heal before deciding the further treatment required. Classification based on Location of Fabrication 4,9 Materials can be classified based on the location of fabrication into: ⢠Direct restorative materials. ⢠Indirect restorative materials Direct restorative materials: They include those materials which are used to restore cavity preparations directly in the oral cavity (Box 1.5). Box 1.5: Examples of direct restorative materials Amalgam, composites, glass ionomer and other materials, which set by chemical reactions in the mouth. Indirect restorative materials: It includes those restorations which must be fabricated outside the mouth, indirectly on a cast/ model/ die, because their processing condition would harm oral tissues. Materials used in the construction of such prosthesis are called indirect restorative materials (Box 1.6). Box 1.6: Examples of indirect restorative materials Gold inlays, crowns of metal, ceramic and polymers, which are processed at elevated temperatures. Some indirect composite restorations can be processed under specific wavelength of light, e.g. Ceramage. Classification based on Longevity of Use 1. Permanent restorations: These restorations are not planned to be replaced for a particular time period. Though they are referred to as permanent, actually they are not, e.g. fillings, crowns, bridges and dentures do not last forever (Fig. 1.5). 2. Temporary restorations: These restorations are planned to be replaced in a short period of time, such as few days to weeks. For ~ Permanent C/) c c -.2 0 c- :;::; Cll co Interim ~ Q; 0 .8ll::1iJ C/) o~ Cll a:: c:=:J Temporary Time period Fig. 1.5: Diagram depicting the time period of use of a restoration. (Arrow in permanent restoration depicts that such restorations are not planned to be replaced for a long period of time.) Introducton to Dental Materials Dental materials Box 1.7: Characteristics of metals 1. High thermal and electrical conductivity 2. Ductility (pure metals are very soft and they can be bent without breaking) 3. Opacity (they do not transmit light) 4. Luster (they have a surface that strongly reflects light and appears bright and shiny) 5. They tend to dissolve to some extent in water or other aqueous solutions, producing cations. 6. All metals are white (actually gray) except for gold, which is yellow, and copper, which is reddish. 7. All metals are solid at room temperature except mercury, which is liquid at room temperature and is used with silver alloys as amalgam. 8. All metals have high melting temperatures because of high strength of the metallic bond that holds the atoms together. 3. Polymers 4. Composites Composites are mixtures of two or more of the first three classes in which the different components remain distinct from one another in the final structure. A common example is composite resin. Fig. 1.7a: Three-dimensional structure of iron (metal) Metals Metals are the oldest of the three classes of materials that have been used as dental materials. Metals are characterized by metallic bonds (Box 1.7) which will be discussed in the next chapter. Metals solidify with their atoms in a regular or crystalline arrangement (see Chapter 2), often in the form of a cube (Fig. 1.7a). example, temporary fillings done in a tooth during root canal treatment, which have to be replaced within 2-4 days during subsequent visits. They are used to protect the tooth and provide function till the final restoration is done. 3. Interim restoration: At times, dental treatment requires "long-term" definite temporary restorations or "interim" restorations. For examle, a 7-year-old child, met with trauma and fractured one of his central incisors. A large composite build- up may serve his immediate requirement until the root formation is completed and a permanent crown is placed. 5 Classification based on the Chemical Nature of the Material These are the atoms that make up a material and the way they are bonded together determine the properties of that materiaLS Weak bonds make for weak materials and vice versa (Table 1.4). Materials can be classified into different categories based on their primary atomic bonds (Fig. 1.6): 1. Metals 2. Ceramics Fig. 1.6: Classification of dental materials based on chemical nature 12 Basis of Material Science Box 1.9: Benefits of ceramics in dentistry 1. Many ceramic oxides are used as pigmenting agents. These oxides produce good range of colors. Due to this characteristic, we are able to match almost any tooth color with good esthetic results. 2. They are inert, i.e. not chemically reactive. This quality provides ceramics with good bio- compatibility. 3. Ceramic materials are translucent, like natural teeth. This translucency gives the ceramic crown a more natural appearance than any other dental material. Fig. 1.7b: Internal arrangement of tetrahedral structure of ceramic (silica) four large oxygen atoms surround smaller silicon atom Ceramics A ceramic is a compound formed by the union of a metallic and a non-metallic element (Box 1.8). Most of these materials are oxides, formed by the union of oxygen with metals such as silicon, aluminum, calcium and magnesium (Fig.1.7b). Ceramics may be simple or complex. Examples of simple ceramics are alumina and silica. Examples of complex ceramics are feldspar (potassium aluminum silicate) and kaolin (hydrated aluminum silicate). Ceramics may be crystalline or non- crystalline (i.e. amorphous). Porcelain is a specific type of ceramic used extensively in dentistry (Box 1.9). Box 1.8: Characteristics of ceramics 1. High melting points. 2. Brittleness, which means they cannot be bent or deformed (no sliding) to any extent without actually cracking and breaking. 3. They are poor conductor of heat and electricity. 4. They are chemically inert. 5. They have excellent esthetic result in terms of matching natural teeth. Fig. 1.8: Stucture of synthetic polymer Polymers They are the latest addition (early to mid- 1900s) to dental materials. Most of the polymers are nowadays synthesized by humans. Polymers are giant, long-chain organic molecules (Fig. 1.8). Polymers are characterized by covalent bonds within each molecule, giving them tremendous strength in a single direction. Try to break a nylon rope by pulling it! They are poor conductors of heat and electri- city. Most polymers have a structure containing thousands of carbon atoms linked together like beads on a string. Others, such as silicone polymers are formed with silicon-oxygen bonds. Introducton to Dental Materials Table 1.4: Characteristics of different materials 13 Characteristics Bond Properties Crystal structure Metals Metallic bonding High strength and hardness, high electrical and thermal conductivity BCC, FCC, or HCP unit cells Ceramics Ionic or covalent bonding, or both High hardness and stiffness, electrically insulating, refractory, and chemically inert Crystalline or amorphous Polymers Covalent bonding Low sensitivity, high electrical resistivity, and low thermal conductivity, strength and stiffness vary widely Amorphous and crystalline Composites Composites are combinations of any of the basic ceramic, metallic and polymeric materials (Box 1.10). Each material that makes up composites is called a phase. Their properties tend to be somewhere between those of their basic constituents and are used to enhance their performance, longevity and handling chracterstics. Box 1.10: Types of composites in dentistry 1. Ceramic - metallic composite: Tungsten carbide bur. 2. Metal - polymer composite: Die materials in dental laboratory. 3. Ceramic - polymer composite: Enamel, dentin, bone and restorative composites. A composite is a kind of "combination" of materials, which compliment each other. The properties lacking in one material are compensated by those of the other material. For example, restorative composite has two phases, namely resin and fillers. Teeth and bones are examples of natural composites. Enamel is a composite of hydroxyapatite (which is a ceramic material) and protein (which is a polymer). EVALUATION OF DENTAL MATERIALS Most manufacturers of dental materials maintain a quality assurance programme (As per international standard like ADA specifications) and materials are thoroughly tested before being released into the market for dental practitioner (Fig. 1.9). Laboratory Evaluations Most ADA/ ANSI specifications involve laboratory tests. The tests performed as per these specifications are useful but they all are performed in vitro, (carried out in the laboratory away from the clinical conditions) which have a lot of limitations in clinical practice.lO Clinical Notes 1. For example, most of the direct restorative materials are tested for their compressive strength but ultimately the material is subjected to a combination of compressive, tensile and shear stresses, which may decide the final success or failure of the material under masticatory load. 2. Similarly upper dentures mostly fracture along the midline because of bending. Hence a bending or transverse strength ~B-a-s-is-o-f-M-a-t-e-ria-I-S~c-ie-n-c-e-------------- ---------. test is far more meaningful for denture base materials than a compression test. Clinical Trials The majority of new materials are subjected to extensive clinical trials normally in co-operation with a dental college or hospital departments prior to their release. CONCLUSION As the number of available materials is going up, it is important that the dentist remains more aware about new products so that their judgement about the selection of material remains successful. Materials which have not been thoroughly evaluated should be avoided, specially with clinical dentistry falling under Consumer Protection Act (CPA). I Research and development I iI Manufacturer/analysis Ideal requirements for clinical use: Thermal, optical, mechanical, chemical, biological Available materials and their properties are evaluated Launch of new I product Choice and selection of material by the dentist Critical assessment based on clinical performance I I H feedback to I
Title (Slide 0): "Digging Deeper: The Truth About Tillage" Subtitle: How turning the soil affects plants, microbes, and the planet Slide 1: What Is Tillage? Tilling the soil means digging, turning, and loosening it using tools or machines. It's a common farming practice to prepare the land before planting. Slide 2: Why Do Farmers Till? Tillage is usually done before planting to: ⢠Soften and aerate the soil ⢠Mix in nutrients ⢠Remove weeds ⢠Bury crop residues for decomposition and fertility Slide 3: Tools Used for Tillage Farmers use tools like: ⢠Ploughs: Cut deep into the soil ⢠Harrows: Break up clumps and smooth the surface Slide 4: Ploughs vs. Harrows ⢠Ploughs: Used first, go deep, lift and flip soil ⢠Harrows: Used after ploughs, work on the surface to break clumps and level the soil Slide 5: Types of Tillage Systems From most to least soil disturbance: ⢠Conventional Tillage: Deep ploughing ⢠Minimum Tillage: Light disturbance ⢠Conservation Tillage: Only disturb seed zone, keep residues on top ⢠Zero Tillage (No-Till): Plant directly into undisturbed soil Slide 6: Problem 1 â Soil Erosion Tillage removes protective cover, exposing soil to wind and rain. Result: topsoilâthe most fertile layerâis easily washed or blown away. Slide 7: Problem 2 â Disruption of Soil Life Soil is a living ecosystem! ⢠Worms, fungi, and bacteria help aerate soil and release nutrients ⢠Tillage destroys their habitat, reducing fertility and soil health Slide 8: Problem 3 â Loss of Soil Structure Healthy soil has pores for air, water, and roots. Tillage breaks the sponge-like structure, and soil compacts over timeâlike flattening it into a pancake. Hard soil = poor plant growth. Slide 9: Problem 4 â Decreased Organic Matter Microbes "eat" organic matter through aerobic respiration (using Oâ and releasing COâ). Tillage adds oxygen, microbes speed up, and burn through the soilâs âpantryâ of organic matterâleaving it empty and poor. Slide 10: Problem 5 â Greenhouse Gas Emissions Faster decomposition = more COâ released. Tillage boosts microbial activity, which increases carbon dioxide emissionsâcontributing to climate change. â
Conclusion (Slide 11): đą Tillage: A Double-Edged Tool Tillage can help prepare the soil and control weedsâbut it comes at a cost. Over time, repeated tilling can strip away organic matter, destroy soil life, and release greenhouse gases. It's like spending all your savings for quick resultsâand being left with nothing for the future. The smarter path? Use reduced or no-till methods that protect soil health, keep carbon in the ground, and support long-term farming success.
Commas Directions: Correct the sentences by adding commas where needed. 1. After the sound of the bell we realized it was a false alarm. 2. Mr. Yoshino the head of the department resigned yesterday. 3. The gentleman with the black umbrella who is an ambassador to the United States said hello to us as we were entering the hotel. 4. Even though we won the game the players unfortunately did not play their best. 5. Heather walked quickly up to the door and knocked hoping that someone would answer. Authorâs Purpose 6. An author writes a story about a boy who saves his town from a flood by using his quick thinking. The author includes exciting descriptions of the boy's bravery. What is the authorâs most likely purpose for writing this story? A. To inform readers about the dangers of floods B. To entertain readers with a heroic tale C. To explain how to prevent floods D. To persuade readers to prepare for emergencies 7. Which of the following is an example of an author writing to persuade? A. A science textbook chapter explaining the water cycle B. A commercial encouraging people to adopt shelter pets C. A short story about a girl who finds a magical necklace D. A recipe for making chocolate chip cookies 8. Read the following sentence: "Studies show that students who read for 20 minutes a day score higher on tests. Reading is one of the best habits you can develop for success in school and life." What is the authorâs purpose in this passage? A. To entertain readers with a fun story B. To persuade readers to read more often C. To inform readers about how books are written D. To explain how to find books to read 9. An author writes a how-to guide titled 10 Easy Steps to Plant a Garden. What is the authorâs primary purpose? A. To persuade readers to grow their own vegetables B. To inform readers how to plant a garden C. To entertain readers with funny garden tips 10. Read the excerpt: "Long ago, in a village surrounded by mountains, the people discovered a secret about their water well. Every full moon, the well water turned to gold for just one night. But no one knew why. This mystery brought travelers from far and wide, hoping to uncover the truth." What is the authorâs purpose in this excerpt? A. To persuade readers to visit the village B. To inform readers about a historical event C. To entertain readers with a mysterious tale D. To explain the science behind the water Main Idea When I stepped out into the bright sunlight from the darkness of the movie house, I had only two things on my mind: Paul Newman and a ride home. I was wishing I looked like Paul Newman--- he looks tough and I don't--- but I guess my own looks aren't so bad. I have light-brown, almost-red hair and greenish-gray eyes. I wish they were more gray because I hate most guys that have green eyes, but I have to be content with what I have. My hair is longer than a lot of boys wear theirs, squared off in back and long at the front and sides, but I am a greaser and most of my neighborhood rarely bothers to get a haircut. Besides, I look better with long hair. 11. What is the main idea? The narrator likes movies. The narrator wishes he was Paul Newman. The narrator is content with his appearance. The narrator looks better with long hair. 12. The narrator believes. . . looks are important. he should get a haircut. green eyes are bad. that he has red hair. Once there were four girls who shared a pair of pants. The girls were all different sizes and shapes, and yet the pants fit each of them. You may think this is a suburban myth. But I know it's true, because I am one of them, one of the sisters of the Traveling Pants. We discovered their magic last summer, purely by accident. The four of us were splitting up for the first time in our lives. Carmen had gotten them from a secondhand place without even bothering to try them on. She was going to throw them away, but by chance, Tibby spotted them. First Tibby tried them; then me, Lena; then Bridget; then Carmen. By the time Carmen pulled them on, we knew something extraordinary was happening. If the same pants fit and I mean really fit the four of us, they aren't ordinary. They don't belong completely to the world of things you can see and touch. My sister, Effie, claims I don't believe in magic, and maybe I didn't then. But after the first summer of the Traveling Pants, I do. 13. What is the main idea? Four friends were connected through a special pair of pants. A pair of pants called the Traveling Pants. Carmen finding a pair of pants from a second-hand shop. The girls believing in magic. 14. The narrator included that the pants fit all of them to emphasize how the girls become friends. the girls are different sizes. why the pants are special. where the pants came from. If you are interested in stories with happy endings, you would be better off reading some other book. In this book, not only is there no happy ending, there is no happy beginning and very few happy things in the middle. This is because not very many happy things happened in the lives of the three Baudelaire youngsters. Violet, Klaus, and Sunny Baudelaire were intelligent children, and they were charming, and resourceful, and had pleasant facial features, but they were extremely unlucky, and most everything that happened to them was rife with misfortune, misery, and despair. I'm sorry to tell you this, but that is how the story goes. 15. What is the main idea? description about the story to come. A warning about the story and its sad content. A declaration about the Baudelaire family. A beginning for the end of the story. 16. The narrator believes the reader does not like sad stories. likes stories with happy endings. canât enjoy the story. will find the story unhappy. 17. Read the following sentence: Of course you can exaggerate your story, but what you say must be based on truth. Which word means the same as exaggerate? repeat reveal overstate increase 18. What is the meaning of the word inaugurated, used in the following sentence: Less than two months after Abraham Lincoln was inaugurated President in 1861, he encountered one of the most difficult tasks ever experienced by a United States leader: civil war. elected by a vote brought into office identified by name viewed as an authority 19. What does the phrase âpractice your presentation so much that you could do it in your sleepâ suggest in the following sentence: The best advice is to practice your presentation so much that you could do it in your sleep. get plenty of sleep the night before giving a presentation give their presentations in front of a small audience first take advice from their teachers on how to write a presentation memorize their presentations before they give them 20. Read the following sentence: The Phoenix Mars Lander is a NASA spacecraft that landed on the Red Planet in May 2009 to study the history of water and potential for life on the planet. What is another word for potential? existence situation possibility qualification
Animal Rights and Diet Success Criteria I can explain key terms which describe the type of diets people have I can explain the advantages and disadvantages of different types of diet Animal Rights and Diet Match up the terms with the meaning Term Meaning Omnivore - eats fish but no other type of meat Vegetarian - eats most types of meat and vegetables Pescetarian - doesnât eat any products that come from animals Vegan - doesnât eat meat but will eat dairy products like milk Place the different diets on a spectrum All meat No animal products at all Vegetarian Vegan Omnivore Pescetarian Omnivore Omnivore Most people in the UK are omnivores Match the countries with the amount of meat eaten per person per year Country Meat per person per year India 9.9 kg USA 4.4 kg Bangladesh 120 kg UK 111.5kg Nepal 84.2 kg Australia 4 kg Numeracy How much meat is consumed in the UK per year? (Amount of meat eaten X the UK population) 2. How much meat is consumed in Bangladesh per year? (Amount of meat eaten X the Bangladesh population) Country Meat per person per year USA 120 kg Australia 111.5kg UK 84.2 kg Nepal 9.9 kg India 4.4 kg Bangladesh 4 kg UK â 64 million Bangladesh â 165 million http://www.telegraph.co.uk/travel/maps-and-graphics/world-according-to-meat-consumption/ 7 Why do people eat meat? Discuss Tradition (their family has always done it) Culture (celebrations) Taste Convenience Nutrients such as B12, protein and iron Consumption of meat is rising across developing countries because higher incomes generally mean more meat eating. Pescetarian "Yeah, I'm a vegetarian." "But that looks like fish you're eating." "Oh yeah, I eat fish.â An estimated 5% - 6% of people in the UK are pescetarians. How many people is this? Approx. 3.6 million Calculation â 66,000,000 /100 x 5.5 = 3,630,000 9 Which group is cuter? Animals Fish 10 People often donât feel as much love for fish as they do for fluffy, cute mammals. The may think fish donât feel pain. They may be fussy. They think fish isnât meat. Not farmed as much as mammals; can be wild. To get nutrients they wouldnât get from just vegetables and grains. (Omega 3 is in plants but in higher concentrations in oily fish) Why are people pescetarians? https://www.vegsoc.org/sslpage.aspx?pid=753 http://articles.mercola.com/omega-3.aspx Fish â In a perfect world, fish can provide you all the omega-3s you need. Unfortunately, the vast majority of the fish supply is now heavily tainted with industrial toxins and pollutants, such as heavy metals which include mercury, lead, arsenic, and cadmium, PCBs, and radioactive poisons. These toxins make eating fish no longer recommended. 11 Vegetarianism Vegetarians will not eat any meat or product that comes from the slaughter of animals e.g. gelatine. About 3% of the UK population are vegetarian. How many people is this? 1.9 million 12 Why are people vegetarian? They donât like the idea that animals are killed so they can eat Health reasons Donât like meat Brought up vegetarian Environmental reasons Religious reasons (e.g. some Buddhist, Hindus) Watch the following clip twice. The second time, write down the fact which surprises you the most. https://www.youtube.com/watch?v=VW6wfpHFdaI The World Health Organization has classified processed meats â including ham, salami, sausages and hot dogs â as a Group 1 carcinogen (same as smoking/alcohol) which means that there is strong evidence that processed meats cause cancer. Red meat, such as beef, lamb and pork has been classified as a 'probable' cause of cancer. 13 Veganism Not just a diet Around 1% of the population of UK are vegans. A vegan is described by the Vegan Society as âa philosophy and way of living which seeks to excludeâas far as is possible and practicableâall forms of exploitation of, and cruelty to, animals for food, clothing or any other purpose; and by extension, promotes the development and use of animal-free alternatives for the benefit of humans, animals and the environment. In dietary terms it denotes the practice of dispensing with all products derived wholly or partly from animalsâ Why are people vegan? Why are people vegan? James Aspey: https://www.youtube.com/watch?v=a22XxXP3nU8 Warning: some of the content in this video clip may upset some viewers from 7:14 â 8:11 https://www.youtube.com/watch?v=BtqXeym7H8A Why are people vegan? âDonât want bad karmaâ Feel healthier Reduce chances of diseases. Example heart disease. Donât want to exploit animals Believe in animal rights Sustainability Environment Create a Table of Pros & Cons of Veganism Pros â Cons - Create a Table of Pros & Cons of Veganism Pros Cons No animals have died for you to eat Some people think it is healthier Help the environment Fewer antibiotics/chemicals that are given to some animals Makes you feel good No vitamin B12 so have to supplement Harder to find food at shops or restaurants May be harder to get enough iron May be more expensive to get substitute meats Judged by family and friends Could put farmers out of business Group Work Source 1 Summarise it in your jotter Explain what the source is/what it says What does it suggest? What is your opinion? Feedback to rest of class https://www.youtube.com/watch?v=SYyjel5VuHg Farmerâs Poem