Consequences of Altered Prenatal Environment

Consequences of Altered Prenatal surroundDiscuss the express that an change antepartum environment (e.g. due to agnatic(p) provenderal status, stress or exposure to chemicals) has long-term consequences for procreative blend in of the consequence.The Developmental Origins of Health and Disease (DOHaD) hypothesis focuses on the idea that non-communicable diseases, such(prenominal) as coronary heart disease and diabetes, buzz off origins in foetal study. The embryo or foetus hindquarters be unresolved to trustworthy ch aloneenges during its tuition that permanently alter the physiological development of that organism and this croup show its effects postnatally later on in life (Moore 2017). A lot of focus has been directed towards metabolic dys unravel and problems with the cardiovascular system, only if more recently it has become app arnt that there ar to a fault lifelong effects of the prenatal environment on generative function of the outcome. Aspects of the pr enatal environment include motherlike mal provender, maternal stress, maternal alcoholic beverage consumption, and maternal smoking, amongst others, which can all influence the development of the foetus and its wellness come to the forecomes later on in life. However, there is a lack of evidence for universe, although offspring of mothers affected by the Dutch Famine have been followed up throughout their life to see the effects of the acute maternal undernutrition (de Rooij et al. 2016) (Painter et al. 2006), hence a lot of the experiments be performed on rodent, porcine and ovine models. objet dart there argon a number of differences between the mammalian models and humans, such as duration of gestation and sensitivity to the maternal environment, there are periods of exceptional vulnerability that are similar in both mammalian models and humans which allow us to map the effects of an altered prenatal environment from these creatures to humans (Zambrano et al. 2014).The inc idence of non-communicable diseases in adults significantly increases when maternal nutrition is compromised at vital periods of foetal development (Chavatte-Palmer et al. 2008). During the periconceptional period, it appears that the embryo has a microscope stage of developmental plasticity and it takes advantage of this when existence exposed to veritable challenges in the maternal environment. This means that it changes the way it develops and adapts to the surrounding environment, which has consequences for later life. This is illustrated by the epidemiological study of female person survivors of the Dutch Famine in World contend II, which has shown altered reproductive function of their female offspring who were conceived during the famine. The offspring were show to have irregular menstrual cycles, change magnitude risk of breast malignant neoplastic disease and a younger age at which they underwent menopause (Sloboda et al. 2011). There was no significant change in th e reproductive function in adults whose mothers were exposed to the famine during late stages of motherliness when compared to adults who were born before the famine (Painter et al. 2006), which suggests that the sentence around conception is very sensitive to the maternal environment. The study was conducted by authors who were fortunate to be able to collect the data that they did be eccentric, for obvious respectable reasons, a study like this could not be purposefully carried out on humans. As inhumane as the famine was, it has provided us with whatever useful data to ascertain what is happening in utero when maternal nutrition is compromised.Animal studies of maternal undernutrition have been conducted to add to the findings of the Dutch Famine epidemiology. In ewes, the female offspring had decreased rates of ovulation afterward experiencing prenatal undernutrition. regular(a) earlier, it was found that the foetal ovary at twenty-four hours 47 already had altered concen trations of oogonia and meiotic arrest in the ovary was delayed even longer than common on day 62 of foetal life (Sloboda et al. 2011). Growth curtail rats have shown staggered onset of signs of sexual maturation, for example first oestrus, mating and advancement of full fertility were separated in time rather than creation simultaneous (Sloboda et al. 2011). Moreover, pregnant ewes on a calorie restricted sustenance produced offspring who grew up to have reduced ovarian and granulosa cell proliferation and increase apoptosis in their ovaries. This could be due to a change in the hypothalamic-pituitary-gonadal axis activity or hormonal environment in the ovary which is set by the mothers nutritional status (Sloboda et al. 2011).Furthermore, maternal protein parturiency in rats delays seminiferous tubule lumen formation and increases apoptosis of germ cells during the neonatal period. Histological sections of the testes of male offspring show some tubules with no lumen at all a t even when they have a control diet after birth (Zambrano et al. 2014). Also, apoptosis in the testes of male neonates at postnatal day 14 is increased in those who have feature maternal protein restriction either during motherliness, during lactation, or during both (Zambrano et al. 2014). There have been some animal studies done using various mammalian models to produce data that we can apply to humans. So far, the data has been reproducible but it is still earliest days in this field of science so the longer these experiments are reproduced in different models, the better and more sure we can be when advising mothers of the risk their diet may have on the health and reproductive potential of their offspring.Although poverty and undernutrition remain global crises, it is clear that overfeeding and the obesity epidemic in the Western World come with severe implications on health of the population and future generations. Several studies in animal models have demonstrated that maternal overnutrition can affect the fertility of the offspring later on in life. For example, in pregnant sheep that are overfed, the offspring experience intrauterine growth restriction and are born crushed for their gestational age, but as well the females are born with ovarian retardation (Chavatte-Palmer et al. 2008). special studies have been done and have other, similar conclusions for female offspring fertility. A purloin study shows that mothers fed high fat diets during pregnancy produced female offspring with a 4-fold reduction in the number of primordial follicles in their ovaries (Cheong et al. 2014). This could be due to them having an early onset of puberty, similar to the female offspring of mothers who had calorie restricted diets. Similarly, the female offspring in this age group alike had fewer (1.4-fold decrease in number) antral follicles developing into Graafian follicles in their ovaries (Cheong et al. 2014). However, the cohort sizes in this study were unfortunately quite small (10-15 mice per group) and it is unclear whether or not the groups were exposed to different nutritional challenges at the same time to chequer that the process was standardised. The results could be improved by repeating them with another cohort of mice and perhaps repeating the study in different species of mice to eliminate species-specific adaptations to maternal nutrition. If the same results are able to be replicated across other mouse species, then it is more plausible that these results might also be seen in humans.Some oestrogenic compounds have been observed to have effects on ovary development in later life of neonatal rodents that were exposed to the compounds prenatally. Two examples are activin and oestrogen derivatives (Woodruff and Walker 2008). Female rats exposed prenatally to oestradiol benzoate had delayed follicle and interstitial development by day 14 of age. By day 21, many of the larger follicles in the ovary were delayed in devel opment at the preantral and small antral follicular stage. This suggests that oestrogens inhibit follicular development (Ikeda et al. 2001). As the rats mature, the inhibited development could delay the onset of sexual maturity in the females and puberty wouldnt give until later.It is known that steroidogenic grammatical constituent 1 (SF1-) controls development of the ovary (Hanley et al. 2000), so grimace levels of genes that SF-1 regulates were examine in ovaries handle with oestradiol benzoate (Ikeda et al. 2001). It was found that ovarian tissue treated with oestradiol benzoate had downregulated SF-1 as well as genes including StAR and P450SCC, which have their expression controlled under SF-1 activity. This downregulation was present from postnatal day 6-21 and was relative to control ovary. some other genes were found to not change with oestradiol benzoate treatment and some had increased expression after treatment. This results indicate that oestrogen derivatives can i nfluence different genes related to SF-1 to be upregulated or downregulated during development of the ovary (Ikeda et al. 2001).Maternal stress during pregnancy is another important factor affecting development and function of the offsprings reproductive system. Corticosteroids are an important class of steroid hormone involved in the stress response and over exposure to these hormones can elicit changes in the developing reproductive system of the foetus. Administration of dexamethasone during pregnancy in rats is associated with various outcomes, such as delayed onset of puberty in both offspring sexes, less(prenominal) follicles in the ovaries of female pups, and lower kindred testosterone levels in male pups (Zambrano et al. 2014). Other corticosteroids, such as betamethasone, have shown afflicted sperm quality and fertility in male pups (Zambrano et al. 2014). These findings indicate that maternal stress should be kept to a minimum during pregnancy in order to maximise the rep roductive potential of her offspring. Although a certain academic degree of maternal stress is to be expected during pregnancy, chronic exposure to certain stress hormones can be detrimental to the developing foetus. Having said this, it is unclear what concentrations of these corticosteroids were administered to the pregnant rats, therefore it is difficult to determine what levels of these in the mother could cause developmental restrictions in the foetus. These results arguably are difficult to translate into humans when thinking about impact of human maternal stress on our offspring. Furthermore, human stress is difficult to control, unlike diet or smoking, so it is unfair to attribute blame to the mother for the relative fertility of her offspring when she perhaps cannot control the changes in her uterine environment if shes become accent during pregnancy.Evidence in the literature supporting this hypothesis is vast and then not all evidence has been covered. Even though the evidence provided is broadly speaking from animal models, the results can be translated to humans as well, since there are similarities in physiology and metabolism across all mammalian species. The animal models do have their limitations, such as being more or less sensitive to certain stimuli than humans and having different behavioural adaptations, but they also come baring less ethical issues with their exposure to laboratory experiments. That being said, it should also be considered that these animal models have been exposed to extremes of malnutrition and specific nutrient deficiencies, so when interpreting the results to advise pregnant women they should be presented to show that a balance of nutrition is fundamental to maintain a healthy pregnancy and ultimately healthy offspring with normal reproductive function.ReferencesCHAVATTE-PALMER, P. et al., 2008. Nutrition maternelle incidence sur la fertilit de la descendance et importance de la priode priconceptionelle pour le long terme. Gyncologie Obsttrique Fertilit, 36(9), 920-929CHEONG, Y. et al., 2014. Diet-induced maternal obesity alters ovarian geomorphology and gene expression in the adult mouse offspring. Fertility and Sterility, 102(3), 899-907HANLEY, N.A. et al., 2000. Steroidogenic factor 1 (SF-1) is essential for ovarian development and function. Molecular and Cellular Endocrinology, 163(1-2), 27-32IKEDA, Y. et al., 2001. neonatal estrogen exposure inhibits steroidogenesis in the developing rat ovary. Developmental Dynamics, 221(4), 443-453MOORE, S.E., 2017. Early-Life nutritionary Programming of Health and Disease in The Gambia. Annals of Nutrition metabolismPAINTER, R.C. et al., 2006. Early onset of coronary artery disease after prenatal exposure to the Dutch famine. The American Journal of Clinical Nutrition, 84(2), 322-327DE ROOIJ, S.R. et al., 2016. Prenatal Undernutrition and involuntary Function in Adulthood. Psychosomatic Medicine, 78(9), 991-997SLOBODA, D.M., M. HICKEY and R. HART, 2011. Reproduction in females the place of the early life environment. Human Reproduction Update, 17(2), 210-227WOODRUFF, T.K. and C.L. WALKER, 2008. fetal and Early postpartum Environmental Exposures and Reproductive Health Effects in the Female. Fertility and sterility, 89(2 Suppl), e47-e51ZAMBRANO, E. et al., 2014. Fetal programming of sexual development and reproductive function. Molecular and Cellular Endocrinology, 382(1), 538-549

The Watts Riots Essay -- American History Race Riots

Imagine being born in a place where populate dont mix with angiotensin converting enzyme another(prenominal) and keep to their own kind. Imagine not being adequate to(p) to walk into a store because it is white owned. How would it feel if you were black, lived in a city that was run by a white government, where poverty, unemployment and lack of procreation were all in all problems of everyday life? If everyone were treated equally, indeed it would not be a problem. But for inner city African Americans that isnt the case. As humans, in that location is only so much we can take when it comes to segregation onward we act unwrap. There is only so much hate a person can take before letting it be known, once a person is pushed over that threshold there is no attribute back. Overwhelming hate and anger with revenge takes hold and all thoughts of consequences rushes out of a persons body. The only thought remaining is violence, which is where rioting comes into play. All it takes argon a few people to start protesting and yelling then the side by side(p) thing you know you have a group of people then a rabble. People are like sheep. When a person sees another person doing it, then they are more inclined to join in. soul then throws a rock, then a bottle, and then all of a sudden here comes an array of Molctov Cocktails and guns. You then have a mob of people with built up tension and anger, ready to crush and extirpate whatever stands in their way of their demonstration.Central Los Angeles, California was blown international by one of those demonstrations. It was the worst urban riot since the 1943 disturbance in Detroit (Bradley 896). According to reports, the Los Angeles riot all started on the evening of August 11, 1965 ii white California Highway Patrol Officers pursued a interweave automobile for six bl... ...nt Bush sent one thousand lawmen and quad thousand soldiers to Southern California to try and contain the problem. Astonis hingly, the most darling call for peace and calm came from Rodney King himself Can we all get out along? Can we stop making it horrible for the older people and the kids? Rioting is just not right. Its not going to change anything. Well all get our justice (Duffy 23).Works CitedDaniel, Clifton. Chronicle of the Twentieth Century. Mount Kisco, N.Y Chronicle, 1987.Dodson, Angela. twenty dollar bill Five Years After Kerner. The Quill April 1993pg.16-21.Duffy, Brain. Days of Rage. U.S New and terra firma Report May 11, 1992pg.20-27.Magill, Frank. Great Events From History. Englewood Cliffs, New Jersey, 1975. Watts Riots. Encyclopedia of Civil Rights in America. 1998ed. Watts Riots. Encyclopedia of Multiculturism. 1994ed.

Low Birthweight Piglets Essay -- Food, Pork Industry

entreLow fork up weight piglets have high mortality and short(p) emergence postnatally. The pork industry has strategies to increase the piglets birth weight. Maternal growth hormone sermon with developmental timing and dose difference change magnitude foetal growth in pigs 1-4. As GH cannot cross the placenta 5, the increase in fetal growth must due to changes in parental(p) metabolism and/or placental development and function. Placental weight was increased with maternal GH treatment 4. However, none of the above studies has demonstrated the effect of maternal GH treatment on placental structural development and function in pigs therefore, this is the pass that will be addressed in this study. Birth WeightDe considerationinants of fetal growth and birth weight in pigsBirth weight is influenced by several factors during pregnancy, such as parity, maternal nutrition, uterine capacity and pack size. Pigs have two parity groups, sows and gilts. Sows are pigs which have given birth at least 3 times before, and gilts, are pigs that had never been pregnant. The outset birth weight of the progeny from gilts might be due to startle pregnancy. As gilts are growing when they pregnant, so mother and foetus were competing for limit nitrogenous substrates to meet their needs, and leads to low birth weight in fetus *gatford 2009 & Schoknecht 1993.Piglets from dam which has restriction in food intake or particularised nutrients during gestation have reduced in birth weight. The progeny of gilts ply with protein-deficient diet (0.5% protein) in early (d 1 to d44) or late (d 82 to term) during gestation have demoralize birth weight compared to the control (with 13% protein in diet) whereas protein deficient diet throughout pregnancy caused the progeny weigh... ...reased maternal tippytoe meat percentage *rehfeldt 2001. The backfat depth of pGH treated dams in *gatford 2010 was lower than the controls at farrowing and weaning *. This suggested that GH treatme nt can stimulate lean growth and inhibiting adipose tissue growth in pigs. The gestation length of sows, but not gilts was being shortened by long term GH treatment.Maternal GH treatment would also affect the concentration of maternal circulate metabolites and hormones. There was an increased in amino acids nitrogen and decreased in free fatty acids in maternal circulation by a 2 or 4 mg GH dose treatments from d 25 to d 51(gatford, 2000). Maternal plasma urea concentration was decreased by 28% by GH treatment with a dose 15ug/kg from days 25 to 50 *gatford 2009. There was a similar finding in other study with maternal GH treatment in underfed gilts *gatford 2000.

Grandparents House Essay -- Descriptive Writing Examples

Grandpargonnts House The car ride to my grandparents house depended to take half(a) a day even though it was only a twenty-minute press to Cedaredge. Although the prat road over Redlands Mesa was a twisty struggle road, it drug on like a boring documentary. When the car finally retarding forceed into the driveway of the long, white house with a neatly kept grand lawn, I knew it was going to be a gigantic day of fun, relaxation, and great food. As I walked just about to the back door, my eyes took in the yellowish pink of the grass swaying in the wind and the weathered barn off to the left wing of the pasture. Inside the barn I could see all sorts of different betting odds and ends hanging from the walls. When I opened the door to my grandparents old house, a sweet, cen jauntetal smell of cooking food filled my nostrils and made my empty hurt growl. The aroma in the air was always a tease to my erect and made me think my stomach was starting to eat away at itself.The no rmal activity of everyday life sends my family in a carbon different directions. My mom and dad both go to work, and my sisters and I go to school. After school, there are practices that all of us kids attend, and when we reach home, we eat, do homework and go to bed. There is no clip to sit ware and play a game as a family or to full hang out together and talk about how the day went. Weekends and holidays are a time that we get to go to my grandparents house as a family and have a day of fun visiting with family that I dont get to see very often.Their old house was to the west of the small township of Cedaredge, so there was not that many houses around it. When we went to my grandparents house, we would ride our bikes around the neighborhood. My sisters and I would race on our bikes to see who ... ...d watch. Usually we were still performing on the Nintendo when it was time to leave, so it was a struggle to get everybody to assay right away.After my whole family was piled i nto the car, which as my sisters and I got bigger was a harder and harder task, we would wave goodbye to my grandparents and any other relatives that had come for the day. As we would pull out of the driveway, I would think back on the day and escort that I had to go back to the hustle and bustle of my everyday life. The trip home was not as long as the way over, just I could never wait until the next time we could go back to my grandparents house in Cedaredge, for a relaxing day of spending time with my family and forgetting about our hectic life for at least a brusque while. Now, with both my sisters in college, the day when we go to my grandparents house does not seem to come often enough.