Evaluation of a new sagittal classification system in adolescent idiopathic scoliosis

European Spine Journal - The purpose of the present study was to validate a new spinal sagittal classification. We retrospectively included 105 consecutive AIS patients who underwent posterior...     

Sites of action of sodium depletion on aldosterone biosynthesis in the dog

Secretion of cortisol, corticosterone, and aldosterone was measured in vivo in normal and sodium-depleted hypophysectomized dogs. Biogenesis of steroids was then measured in vitro with outer slices of the adrenals of the same dogs. In some studies, metyrapone or puromycin was added.In vivo, sodium depletion stimulated the production of cortisol, corticosterone, and aldosterone. In vitro, tissues from sodium-depleted animals released more aldosterone, but less corticosterone than those from sodium-replete controls.The results are interpreted to indicate that (a) biosynthesis of aldosterone is regulated at at least two sites in the biosynthetic pathway. The final conversion, that of corticosterone to aldosterone, is stimulated by sodium depletion. This effect persists for at least 3 hr while slices from sodium-depleted dogs are incubated in vitro. Stimulation at this site is thus relatively stable in vitro; its activation by sodium depletion is not inhibited by puromycin in the dog. Stimulation at this site can explain, at least in part, the increased effectiveness of adrenocorticotropin (ACTH) on aldosterone biogenesis during sodium depletion.(b) the earlier site at which sodium depletion stimulates the secretion of aldosterone is "above" the position of desoxycorticosterone in the pathway; it is probably at the conversion of cholesterol to pregnenolone. Stimulation at this site is quickly lost during incubation of adrenal slices. It is thus relatively unstable in vitro; its activation by sodium depletion is inhibited by puromycin in the dog.     

Patient-reported burden of intensified surveillance and surgery in high-risk individuals under pancreatic cancer surveillance

Familial Cancer - In high-risk individuals participating in a pancreatic cancer surveillance program, worrisome features warrant for intensified surveillance or, occasionally, surgery. Our...     

Die Traumatische Ätiologie und die Begutachtung der Symmetrischen Lipomatose

Ohne Zusammenfassung     

A placebo-controlled crossover study of oral clonidine in acute anorexia nervosa

The alpha 2-adrenergic agonist clonidine has been reported to increase feeding in several species. This study evaluated the effects of clonidine (500-700 micrograms/day), administered per os, to four treatment-resistant anorexia nervosa patients in a long-term placebo-controlled crossover trial. All patients increased their body weight significantly. Clonidine administration, however, did not influence the rate of weight gain, nor did clonidine affect hunger or satiety sensations. Similarly, 24-hour urinary 3-methoxy-4-hydroxyphenylglycol levels and levels of anxiety and depression were unchanged by clonidine. By contrast, clonidine showed significant hemodynamic effects; clonidine lowered systolic and diastolic blood pressure, reduced pulse rate, and produced sedation. Discontinuation of clonidine was associated with a small but significant weight loss compared to a small weight increase during the initiation of clonidine treatment. The results suggest that clonidine may not be indicated in the treatment of anorexia nervosa.     

Secondary biogenic amine deficiencies: genetic etiology,therapeutic interventions,and clinical effects

neurogenetics - Monoamine neurotransmitter disorders present predominantly with neurologic features, including dystonic or dyskinetic cerebral palsy and movement disorders. Genetic conditions that...