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Fetal Alchohol Syndrome
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What Is Fetal Alcohol Syndrome? 1) When a pregnant person drinks alcohol, some of that alcohol easily passes across the placenta to the fetus. 2) People with this condition may have problems with their vision, hearing, memory, attention span, and abilities to learn and communicate. 3) You can prevent fetal alcohol syndrome by avoiding alcohol during pregnancy.
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PowerPoint presentation regarding many facets of Fetal Alcohol Spectrum Disorder. Feel free to share this with anyone who would benefit from this information. Some of the information is quite shocking. Included parenting and teaching strategies for those responsible for caring for a child with FASD.
Fetal Alcohol Syndrome Presentation
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sonicmercury
Slide show of the information research regarding fetal alcohol syndrome and the role of early childhood educators.
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jenny1tafe
What Is Fetal Alcohol Syndrome? 1) When a pregnant person drinks alcohol, some of that alcohol easily passes across the placenta to the fetus. 2) People with this condition may have problems with their vision, hearing, memory, attention span, and abilities to learn and communicate. 3) You can prevent fetal alcohol syndrome by avoiding alcohol during pregnancy.
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kajani1991
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snashley
PowerPoint presentation regarding many facets of Fetal Alcohol Spectrum Disorder. Feel free to share this with anyone who would benefit from this information. Some of the information is quite shocking. Included parenting and teaching strategies for those responsible for caring for a child with FASD.
Fetal Alcohol Syndrome Presentation
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Slide show of the information research regarding fetal alcohol syndrome and the role of early childhood educators.
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This presentation explains how alcohol affects your baby/fetus and what you can do to help yourself
How alcohol affects your baby
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FETAL ALCOHOL SYNDROME (FAS)
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abhilasha chaudhary
FETAL ALCOHOL SYNDROME (FAS) is the leading known cause of mental retardation and birth defects in the world. Fetal alcohol syndrome is a pattern of physical, behavioral and cognitive abnormalities seen in individuals exposed to alcohol in uterus. Because alcohol is a known teratogen and the damage done to a fetus by alcohol exposure is permanent, public education about the dangers of prenatal alcohol exposure has been extensive. Many of the features of the fetal alcohol syndrome are secondary to the effect of alcohol on brain development. These include microcephaly, short palpebral fissures, the long smooth philtrum and thin vermilion of the upper lip, joint anomalies, altered palmar crease pattern, and mental retardation. Animal studies as well as a limited amount of human data also show that maternal genotype is a key player : Advances in the development of novel antioxidant therapies as an approach for fetal alcohol syndrome prevention. Peptides NAPVSIPQ (NAP) and SALLRSIPA (SAL), related to activity-dependent neuroprotective protein (ADNP), prevent alcohol-induced damage in a mouse model of FAS. In a recent study, the thyroxin reversed the deficit both in the level of their genes and their social behaviour, research is going on how the prenatal thyroid hormone supplementation reverses the behavioural deficits in the fetal alcohol spectrum disorder model. Another study used a priori approach to assess molecular phenotype in the cranial neural folds (head fold) of early mouse embryos soon after maternal alcohol treatment. FAS can be modulated pharmacologically with PK11195, a potent ligand with specific binding to the mitochondrial peripheral-type benzodiazepine receptor recognition site. PK11195 has been shown to protect early mouse embryos from eye and brain defects induced with diverse teratogens and to protect adult tissues from some inflammatory lesions. Microarray transcript profiling of the embryonic head fold at 3.0 hr after alcohol exposure or PK11195 counter-exposure enabled prioritization of candidate pathways that integrate the genomic response with genetic susceptibility of the system. These findings are consistent with the growing view that developmental exposure to alcohol alters common signalling pathways linking receptor activation to cytoskeletal reorganization. The programmatic shift in cell motility and metabolic capacity further implies cell signals and responses that are integrated by the mitochondrial recognition site for PK11195. CONCLUSIONS: Until the advent of effective prevention measures, it will remain necessary to seek ways to treat the life-long neurobehavioral consequences of prenatal alcohol exposure. Nevertheless, alcohol is a widely accepted and legal social drug, and many pregnant mothers continue to drink it while pregnant. Whereas, FAS is totally preventable by avoiding alco
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FETAL ALCOHOL SYNDROME (FAS) is the leading known cause of mental retardation and birth defects in the world. Fetal alcohol syndrome is a pattern of physical, behavioral and cognitive abnormalities seen in individuals exposed to alcohol in uterus. Because alcohol is a known teratogen and the damage done to a fetus by alcohol exposure is permanent, public education about the dangers of prenatal alcohol exposure has been extensive. Many of the features of the fetal alcohol syndrome are secondary to the effect of alcohol on brain development. These include microcephaly, short palpebral fissures, the long smooth philtrum and thin vermilion of the upper lip, joint anomalies, altered palmar crease pattern, and mental retardation. Animal studies as well as a limited amount of human data also show that maternal genotype is a key player : Advances in the development of novel antioxidant therapies as an approach for fetal alcohol syndrome prevention. Peptides NAPVSIPQ (NAP) and SALLRSIPA (SAL), related to activity-dependent neuroprotective protein (ADNP), prevent alcohol-induced damage in a mouse model of FAS. In a recent study, the thyroxin reversed the deficit both in the level of their genes and their social behaviour, research is going on how the prenatal thyroid hormone supplementation reverses the behavioural deficits in the fetal alcohol spectrum disorder model. Another study used a priori approach to assess molecular phenotype in the cranial neural folds (head fold) of early mouse embryos soon after maternal alcohol treatment. FAS can be modulated pharmacologically with PK11195, a potent ligand with specific binding to the mitochondrial peripheral-type benzodiazepine receptor recognition site. PK11195 has been shown to protect early mouse embryos from eye and brain defects induced with diverse teratogens and to protect adult tissues from some inflammatory lesions. Microarray transcript profiling of the embryonic head fold at 3.0 hr after alcohol exposure or PK11195 counter-exposure enabled prioritization of candidate pathways that integrate the genomic response with genetic susceptibility of the system. These findings are consistent with the growing view that developmental exposure to alcohol alters common signalling pathways linking receptor activation to cytoskeletal reorganization. The programmatic shift in cell motility and metabolic capacity further implies cell signals and responses that are integrated by the mitochondrial recognition site for PK11195. CONCLUSIONS: Until the advent of effective prevention measures, it will remain necessary to seek ways to treat the life-long neurobehavioral consequences of prenatal alcohol exposure. Nevertheless, alcohol is a widely accepted and legal social drug, and many pregnant mothers continue to drink it while pregnant. Whereas, FAS is totally preventable by avoiding alco
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In this captivating lecture, Dr. Faiza, an esteemed Assistant Professor of Physiology, embarks on a comprehensive journey into the multifaceted realm of local blood flow regulation. With meticulous detail and clarity, she unravels the intricate mechanisms that govern the dynamic balance between tissue perfusion and vascular resistance, shedding light on both acute and chronic aspects of blood flow control. Beginning with an exploration of acute influences, Dr. Faiza elucidates how physiological factors such as metabolic demand, myogenic responses, and autoregulatory mechanisms orchestrate rapid adjustments in local blood flow. Students gain insight into the vasodilator theory, which elucidates the role of metabolic byproducts and vasoactive metabolites in promoting vasodilation, alongside the oxygen demand theory, which underscores the interplay between tissue oxygenation and nutrient demand. Delving deeper, the lecture delves into the fascinating realm of humoral control, where hormones and vasoactive substances wield significant influence over vascular tone. Dr. Faiza navigates through the intricacies of endothelial-derived factors like nitric oxide (NO) and histamine, alongside hormonal regulators such as angiotensin II and vasopressin. Through vivid explanations and illustrative examples, she unveils the intricate dance of vasodilation and vasoconstriction orchestrated by these biochemical messengers. Moreover, the lecture extends its gaze to the extrinsic control of blood flow, where sympathetic innervation exerts a profound impact on vascular dynamics. Dr. Faiza elucidates the role of sympathetic tone in modulating vascular resistance, highlighting its implications in diverse physiological and pathological scenarios. From skin perfusion to coronary circulation, students gain a nuanced understanding of how neural inputs shape local blood flow patterns. Enriched with clinical insights and contemporary research findings, this lecture equips students with a holistic understanding of blood flow regulation. By exploring concepts like active and reactive hyperemia, vascular remodeling, and collateral circulation, Dr. Faiza fosters a deeper appreciation for the adaptive responses of the cardiovascular system to changing physiological demands and pathological insults.
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MedicoseAcademics
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Electrocardiogram (ECG) physiological basis .pdf
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Foetal Alcohol Syndrome
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Foetal Alcohol Syndrome
By Andrew & Maria Stage IV 2009
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