/////////////////This review has covered the broad impact of childhood abuse and other traumas on memory and the hippocampus. The hippocampus, a brain area involved in verbal declarative memory, is particularly sensitive to stress. Patients with combat and abuse-related PTSD were shown to have smaller hippocampal volume and deficits in hippocampal-based verbal declarative memory functions. Hippocampal dysfunction may underlie many symptoms of PTSD and may explain elevations in concentrations of CRF in PTSD. Another brain area affected by stress is the medial prefrontal cortex. Functional imaging studies show dysfunction in this area (as well as hippocampus) during provocation of PTSD symptoms and presentation of traumatic reminders. Medial prefrontal cortical inhibition of amygdala responsiveness is felt to underlie extinction to fear responding. Dysfunction of this area in abuse-related PTSD may lead to problems modulating emotion in PTSD.
//////////////////////////This study interrogated 68 genes. Although these genes were considered likely candidates for outcomes related to antidepressant treatment, there may be additional genes related to treatment-emergent suicidal ideation that were not studied here. For example, one previous study (34) found that markers in CREB1 were associated with treatment-emergent suicidal ideation in men. Moreover, the markers used did not cover the selected genes completely. Additional markers could detect additional association signals. Since markers were selected on the basis of low intermarker LD, haplotype tests would be expected to have poor power and thus were not performed. Still, this is the most comprehensive genetic study of treatment-emergent suicidal ideation conducted to date. More comprehensive studies will not likely emerge until after genome-wide association studies have been performed with this sample. As is true for most large studies, additional phenotypes have been and will continue to be tested over time in this sample. Our experiment-wide p value corrections, which are based on the hypotheses tested in this study, should be considered in this light.
Cryptic population stratification is always a risk in case-control genetic association studies. To address this, we showed that 1) there is no relationship between race and treatment-emergent suicidal ideation in this sample; 2) association p values were uniformly distributed within the largest (white) subset under the assumption of one population; and 3) there is no evidence of mismatch between participants with and without suicidal ideation within the white subset. Thus, these association results are not likely to be the result of population stratification.
Cryptic population stratification is always a risk in case-control genetic association studies. To address this, we showed that 1) there is no relationship between race and treatment-emergent suicidal ideation in this sample; 2) association p values were uniformly distributed within the largest (white) subset under the assumption of one population; and 3) there is no evidence of mismatch between participants with and without suicidal ideation within the white subset. Thus, these association results are not likely to be the result of population stratification.
/////////////////////////////PWS
PWS is considered a neurogenetic disorder, and it is probably the most common genetic syndrome characterized by life-threatening obesity. Like many multisystemic genetic disorders, the clinical manifestations are age-dependent, and the alert clinician must be aware of the various presentations.[66-69] During infancy, the most characteristic feature is hypotonia. Experienced mothers often report decreased fetal movement, and neonatal hypotonia may result in either respiratory or feeding problems, occasionally necessitating nasogastric feedings and frequently resulting in failure to thrive. Small hands and feet and almond-shaped eyes are often observed, but may be difficult to discern in the newborn, unless an index of suspicion already exists. In boys, micropenis and/or cryptorchidism may be observed.
Hypotonia typically persists into infancy and early childhood, when, typically, it is accompanied by global developmental delay. Hyperphagia and progressive obesity usually become apparent by age 4-6 years. Growth failure may manifest at any age, but is usually relatively subtle. Often it is the presence of short stature in the face of exogenous obesity that triggers a suspicion of PWS. Short stature may be exacerbated by efforts at caloric restriction or, during adolescence, by hypothalamic hypogonadism. Various reports of mean adult height in PWS show a range of 155-162 cm in men and 148-150 cm in women.[70-72]
PWS is the consequence of paternal imprinting of a gene located on chromosome 15q11-q13. In the majority of cases, this is the result of deletion of a segment of the long arm of the paternally derived chromosome 15. Other cases may arise from maternal disomy of 15q, imprinting mutations of the paternal chromosome, or balanced translocations.[73-76]
Given the high degree of variability of growth patterns in PWS, it is not entirely surprising that the etiology of growth failure is not entirely clear.[69,77] Poor feeding in the neonatal period and resulting failure to thrive are certainly contributory factors, as are efforts at caloric restriction and hypogonadal hypogonadism. Although some studies have demonstrated low basal and stimulated GH levels and low serum IGF-1 concentrations for age, these are not consistent findings.[78-81] The interpretation of GH stimulation tests in the face of exogenous obesity is challenging, but, nevertheless, it is true that many children with PWS do fail conventional GH testing and meet the accepted criteria for GH deficiency.[78-80] In the study by Tauber,[77] which looked at PWS patients who had been treated with hGH, the mean serum IGF-1 SDS was -1.6, with a range of -2.9 to + 0.1 SD. Because PWS is now an indication approved by the US Food and Drug Administration for GH treatment, demonstration of GH deficiency is not mandatory for therapy.
PWS is considered a neurogenetic disorder, and it is probably the most common genetic syndrome characterized by life-threatening obesity. Like many multisystemic genetic disorders, the clinical manifestations are age-dependent, and the alert clinician must be aware of the various presentations.[66-69] During infancy, the most characteristic feature is hypotonia. Experienced mothers often report decreased fetal movement, and neonatal hypotonia may result in either respiratory or feeding problems, occasionally necessitating nasogastric feedings and frequently resulting in failure to thrive. Small hands and feet and almond-shaped eyes are often observed, but may be difficult to discern in the newborn, unless an index of suspicion already exists. In boys, micropenis and/or cryptorchidism may be observed.
Hypotonia typically persists into infancy and early childhood, when, typically, it is accompanied by global developmental delay. Hyperphagia and progressive obesity usually become apparent by age 4-6 years. Growth failure may manifest at any age, but is usually relatively subtle. Often it is the presence of short stature in the face of exogenous obesity that triggers a suspicion of PWS. Short stature may be exacerbated by efforts at caloric restriction or, during adolescence, by hypothalamic hypogonadism. Various reports of mean adult height in PWS show a range of 155-162 cm in men and 148-150 cm in women.[70-72]
PWS is the consequence of paternal imprinting of a gene located on chromosome 15q11-q13. In the majority of cases, this is the result of deletion of a segment of the long arm of the paternally derived chromosome 15. Other cases may arise from maternal disomy of 15q, imprinting mutations of the paternal chromosome, or balanced translocations.[73-76]
Given the high degree of variability of growth patterns in PWS, it is not entirely surprising that the etiology of growth failure is not entirely clear.[69,77] Poor feeding in the neonatal period and resulting failure to thrive are certainly contributory factors, as are efforts at caloric restriction and hypogonadal hypogonadism. Although some studies have demonstrated low basal and stimulated GH levels and low serum IGF-1 concentrations for age, these are not consistent findings.[78-81] The interpretation of GH stimulation tests in the face of exogenous obesity is challenging, but, nevertheless, it is true that many children with PWS do fail conventional GH testing and meet the accepted criteria for GH deficiency.[78-80] In the study by Tauber,[77] which looked at PWS patients who had been treated with hGH, the mean serum IGF-1 SDS was -1.6, with a range of -2.9 to + 0.1 SD. Because PWS is now an indication approved by the US Food and Drug Administration for GH treatment, demonstration of GH deficiency is not mandatory for therapy.
MOBP=PRADER WILLI-GH RX
///////////////Rasta, or the Rastafari movement, is a religion that accepts Haile Selassie I, the former Emperor of Ethiopia, as God incarnate, whom they call Jah
///////////////////IT IS LEGAL TO DISCRIMINATE ABT A WORKER WHO WORKS AT EMPLOYERS HOME
//////////NEMBUTAL NINE GRAMS
//////////////////BIOLOGY IS A PRODUCT OF THE UNIVERSE AND WILL NOT OUTLIVE IT
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