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Fetal origins hypothesis - Wikipedia

Data from experimental species suggest possible mechanisms for the origin of chronic disease early in life.

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Abstract The “fetal origins” hypothesis ..

Pathik D Wadhwa, Claudia Buss, Sonja Entringer, James M Swanson Developmental origins of health and disease: brief history of the approach and current focus on epigenetic mechanisms. Semin. Reprod. Med.: 2009, 27(5);358-68

The “Fetal Origins” Hypothesis: Challenges and Opportunities for ..

The exact source of the ERG b-wave is still under dispute. The major contribution comes from light-induced activity in ON-center bipolar cells. The extracellular currents that generate the b-wave either originate directly in these cells or reflect potassium-induced changes in the membrane potential of Müller cells enveloping them. Regardless of the exact mechanism, the b-wave is telling us about light-induced electrical activity in retinal cells post-synaptic to the photoreceptors. The b-wave is also affected by OFF-center bipolar cells and by light-induced activity in 3rd order retinal neurons (amacrine and ganglion cells). This contribution can be isolated in the laboratory by using specific drugs but in the clinical environment, the ERG b-wave of patients reflects all contributions summed together. In the future, more sophisticated analytical approaches may allow separation of the different contributions and allow identity of more exact sites of retinal diseases.

The fetal origins hypothesis—10 years on | The BMJ

Christina Kanaka-Gantenbein Fetal origins of adult diabetes. Ann. N. Y. Acad. Sci.: 2010, 1205;99-105

5. The Appearance of Homo Sapiens. The transition from the Homo erectus to the Homo sapiens species occurred so gradually that a number of remains were classified as "modern" erectus or "archaic" sapiens. This transition is believed to have taken place between 200.000 and 100.000 years ago. In those times, the earliest forms of sapiens (i.e. archaic Homo sapiens ) had already become extinct. The same is to be said for the Neanderthal men living in Europe and in the Middle East between 100,000 and 37,000 years ago who, however, left no descendants. Human remains dating from 90,000 years agofound in Palestine, descending from the African forms of archaic Homo sapiens have been officially recognized as evidence of the origins of the Homo sapiens sapiens species, i.e. present-day human beings. Numerous sapiens sapiens remains were uncovered in Europe dating from Upper Paleolithic, such as in Cro-Magnon, Chancelade, Combe Capelle, and so on. The Homo sapiens sapiens must have experienced an explosive development: from 35,000 years ago, it has settled in all the continents, including America and Australia. Sapiens culture is undoubtedly advanced, as shown by stone and bone industries, notably from Upper Paleolithic, in rock paintings, and funerary rituals. Evidence of the earliest burials, dating from 90,000 years ago, have been assembled after excavations in Skuhl and Qafzeh, Palestine. However, we know that Neanderthal men did bury their dead. Particular attention to the deceased is proven by the frequent presence of funerary belongings and the fetal position they were found in.

Documents set to be delivered to the House Subcommittee on HumanRights and Wellness appear to show that the original "seeds" usedto produce the Sabin [oral] vaccine could have been tainted with SV40; thatthe company that manufactured the vaccine, Wyeth Lederle, may have usedRhesus monkeys -- which are more likely to carry the disease -- rather thanthe African Green monkeys it says it used, according to company documents;and that the company may not have performed all of the screening tests required."

What is FETAL ORIGINS HYPOTHESIS

Simon C Langley-Evans, Sarah McMullen Developmental origins of adult disease. Med Princ Pract: 2010, 19(2);87-98

Fetal growth and long-term consequences in animal models of growth retardation. "Perturbations of the maternal environment involve an abnormal intrauterine milieu for the developing fetus. The altered fuel supply (depends on substrate availability, placental transport of nutrients and uteroplacental blood flow) from mother to fetus induces alterations in the development of the fetal endocrine pancreas and adaptations of the fetal metabolism to the altered intrauterine environment, resulting in intrauterine growth retardation. The alterations induced by maternal diabetes or maternal malnutrition (protein-calorie or protein deprivation) have consequences for the offspring, persisting into adulthood and into the next generation."

“The fetal origins hypothesis states that fetal undernutrition in middle to late gestation, which leads to disproportionate fetal growth, programmes later coronary heart disease.”

Recent studies established that mitochondrialdysfunction is involved in insulin resistance in general and fetalorigin of this state in particular.
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  • What does FETAL ORIGIN HYPOTHESIS mean

    07/02/2017 · In the epidemiological literature, the fetal origins hypothesis associated with David J

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    for future studies of the fetal origins of mental health ..

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Fetal origins hypothesis - Cucine Acciaio Inox Borlina

AB - Changes in fetal movement are associated with increased risk of stillbirth after 28 weeks of pregnancy. The majority of studies have focussed on maternal perception of reduced fetal movements, which is associated with stillbirth via placental dysfunction. Recent studies have also described an association between a single episode of excessive fetal movements and late stillbirth. We present a hypothesis that a sudden episode of excessive fetal activity indicates fetal compromise relating to underlying disturbance of the in utero environment, which if it persists can lead to fetal death. The origin of the excessive fetal movements is unknown; they may represent fetal seizures induced by asphyxia or infection, an attempt to release cord entanglement or a change in fetal behaviour (inducing signs of distress) in response to a noxious stimulus. It is also possible that an increase in maternal anxiety may lead to increased perception of fetal activity. Current evidence regarding excessive fetal movements is sparse; there is no clinical guidance regarding how reporting of this symptom might relate to a fetus at risk and which management might reduce the risk of subsequent stillbirth. This could be addressed by prospective observational studies of mothers presenting with excessive fetal movements which could both explore the underlying pathophysiology and determine which investigations could identify fetal compromise in this population. The presence of fetal seizures or umbilical cord entanglement could be evaluated at the time of presentation by cardiotocography and ultrasonography of the fetus and cord. Exposure to infection or noxious stimuli could be evaluated by maternal history and measurement of maternal blood for inflammatory markers or toxins. Maternal anxiety could be assessed by validated anxiety scores. Fetal outcome following excessive fetal movements can be recorded after birth. In addition, the presence of perinatal asphyxia can be assessed using Apgar scores, assessment of fetal acidaemia or measurement of stress-related factors in umbilical cord blood. The placenta and cord can be systematically examined for signs of hypoxia, infection or umbilical cord compression. Such studies would provide evidence regarding the underlying cause of excessive fetal movement and how this symptom might relate to in utero compromise and stillbirth. Ultimately, this approach will determine whether excessive fetal movements can be used alongside reduced fetal movements as a tool to reduce the perinatal mortality rate.

Women's Bioethics Blog: Fetal Origin of Disease Hypothesis

N2 - Changes in fetal movement are associated with increased risk of stillbirth after 28 weeks of pregnancy. The majority of studies have focussed on maternal perception of reduced fetal movements, which is associated with stillbirth via placental dysfunction. Recent studies have also described an association between a single episode of excessive fetal movements and late stillbirth. We present a hypothesis that a sudden episode of excessive fetal activity indicates fetal compromise relating to underlying disturbance of the in utero environment, which if it persists can lead to fetal death. The origin of the excessive fetal movements is unknown; they may represent fetal seizures induced by asphyxia or infection, an attempt to release cord entanglement or a change in fetal behaviour (inducing signs of distress) in response to a noxious stimulus. It is also possible that an increase in maternal anxiety may lead to increased perception of fetal activity. Current evidence regarding excessive fetal movements is sparse; there is no clinical guidance regarding how reporting of this symptom might relate to a fetus at risk and which management might reduce the risk of subsequent stillbirth. This could be addressed by prospective observational studies of mothers presenting with excessive fetal movements which could both explore the underlying pathophysiology and determine which investigations could identify fetal compromise in this population. The presence of fetal seizures or umbilical cord entanglement could be evaluated at the time of presentation by cardiotocography and ultrasonography of the fetus and cord. Exposure to infection or noxious stimuli could be evaluated by maternal history and measurement of maternal blood for inflammatory markers or toxins. Maternal anxiety could be assessed by validated anxiety scores. Fetal outcome following excessive fetal movements can be recorded after birth. In addition, the presence of perinatal asphyxia can be assessed using Apgar scores, assessment of fetal acidaemia or measurement of stress-related factors in umbilical cord blood. The placenta and cord can be systematically examined for signs of hypoxia, infection or umbilical cord compression. Such studies would provide evidence regarding the underlying cause of excessive fetal movement and how this symptom might relate to in utero compromise and stillbirth. Ultimately, this approach will determine whether excessive fetal movements can be used alongside reduced fetal movements as a tool to reduce the perinatal mortality rate.

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