H0+N2 collisions at low-kilo-electron-volt energies.
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Biomedical subjects
Publications and source records attributed to E Pollack.
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Epidermolysis bullosa simplex (EBS) is a group of epidermal blistering diseases almost invariably transmitted as a dominant trait, which has recently been shown to arise from mutations in keratins 14 and 5 (K14 and K5). We describe a family with recessive EBS in which the disease is tightly linked to the substitution of the highly conserved glutamic acid-144 to alanine in the first helical segment of the rod domain of keratin 14. In contrast, linkage with keratin 5 was excluded. The loss of an ionic interaction with keratin 5 is likely to affect K14-K5 heterodimer formation. Our data suggest that this mutation underlies EBS in our family, and that mutations in keratin genes may impair the mechanical integrity of basal keratinocytes in a recessive as well as dominant fashion.
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Intraperitoneal injections in rats of two different dosages of hypertonic solutions containing mannitol or glycerol caused complex and differential changes in brain amino acids. When plasma osmolalities were elevated to toxic levels of 397--432 mOsm/kg H2O, brain sodium was increased, whereas plasma sodium was decreased. Brain potassium was not affected. Brain water decreased significantly, concomitant with elevation of plasma osmolality. Both brain lactic acid and [125I]albumin space rose significantly. Brain amino acids (mostly aliphatic and basic amino acids) as well as Gaba and glycine (putative inhibitory neurotransmitters) increased after both mannitol and glycerol. Ammonia was stimulated by mannitol but was unaffected by glycerol. Plasma amino acids, which generally increased after mannitol, were decreased by glycerol. When the plasma osmolalities were elevated only to moderate levels (about 350 mOsm/kg H2O), only glycerol induced a significant increase in brain taurine, aspartic acid, alanine, leucine and lysine. Thus, with moderate hyperosmolality, glycerol has striking effects on brain amino acid metabolism that are not observed with mannitol.
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The effects of three pharmacological treatments, methylphenidate hydrochloride, thioridazine hydrochloride, a methylphenidate/thioridazine combination, and placebo were studied in outpatient hyperkinetic children rated hyperactive both in school and at home or clinic. Active treatment lasted 12 weeks; placebo lasted four weeks. Significant clinical improvement was obtained in a variety of settings--all treatments were superior to placebo on ratings filled out by parents, teachers, and clinic staff. Though initially the combination of methylphenidate and thioridazine tended to produce greater clinical improvement, it was not superior to methylphenidate alone after 12 weeks of treatment. Methylphenidate alone and the methylphenidate/thioridazine combination were more effective than thioridazine alone. The salient side effects with methylphenidate treatment were decrease in appetite, difficulty in falling asleep, and increased mood sensitivity. In contrast, thioridazine administration was associated with appetite increase and enuresis.
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