大同市103例高龄老人营养情况及心理状况调查

本文对103名高龄老人进行营养情况调查、心理状况调查和体测量,结果表明:高龄老人体质指数大于26者很少,只要老龄人的各种营养素达到供给量标准,心理状态乐观满意,且不吸烟不酗酒者,则可长命百岁。     

口服Sumatriptan治疗偏头痛的临床评价

本文报告口服Sumatriptan 100mg对偏头痛急性发作119例次的治疗结果。治疗后4h内显效91例次(76.5％),好转16例次(13.4％),无效12例次(10.1％),总有效率为89.9％。对偏头痛伴随症状恶心、呕吐和畏光、畏声的缓解率分别为94.2％、96％和94.3％。     

CD4+ T-epitope repertoire on the human acetylcholine receptor alpha subunit in severe myasthenia gravis: a study with synthetic peptides.

The alpha subunit of the nicotinic acetylcholine receptor (AChR) seems crucial in the pathogenesis of the autoimmune paralysis myasthenia gravis (MG) because it contains both the epitopes that dominate the antibody response against the AChR and those recognized by CD4+ AChR-specific T helper (Th) cells. To define the repertoire of anti-AChR Th cells, we investigated the response of unselected blood CD4+ cells or total lymphocytes, or both, from 22 MG patients to 20-residue overlapping synthetic peptides, screening the complete sequence of human-muscle AChR alpha subunit. Several epitopes were identified. Only the most severely affected patients recognized alpha subunit epitopes, and they were mainly young women. Detection of in vitro AChR-specific CD4+ response was facilitated by removal of the CD8+ cells because in two patients a clear response to several alpha subunit peptide sequences could be detected when CD(8+)-depleted cells were used, while their total peripheral blood mononuclear cell population did not respond to any alpha subunit peptide. Although each patient had a unique pattern of peptide recognition, four immunodominant regions recognized by long-term AChR-specific CD4+ T-cell lines, or flanking peptide sequences, were recognized most frequently (residues 48-67, 101-137, 293-337, and 308-437).     

Healing of 56 segmental femoral shaft fractures after locked nailing: Poor results of dynamization

We treated 56 consecutive acute segmental femoral shaft fractures with closed static locked nailing. 12 nails were dynamized after 6 (5-10) months due to slow fracture healing and 5 united after another 5 (3-8) months. The other 7 required cancellous bone grafting and all healed uneventfully 6 (5-8) months after grafting. Since dynamization did not promote healing in most of our cases we suggest early cancellous bone grafting in cases of delayed union.     

A Study on Extension－Flexion Dynamic Lumbar Spine Radiographsin Patients with Lumbar Intervertebral Disc Herniation

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Differential effects of luminol,nickel, and arsenite on the rejoining of ultraviolet light and alkylation-induced DNA breaks

When Chinese hamster ovary cells were treated with ultraviolet (UV) light or methyl methanesulfonate (MMS), a large number of DNA strand breaks could be detected by alkaline elution. These strand breaks gradually disappeared if the treated cells were allowed to recover in a drug-free medium. The presence of nickel or arsenite during the recovery incubation retarded the disappearance of UV-induced strand breaks, whereas the disappearance of MMS-induced strand breaks was retarded by the presence of arsenite or of luminol, a new inhibitor for poly(ADP-ribose) synthetase. Luminol, however, had no apparent effect on the repair of UV-induced DNA strand breaks, and nickel had no effect on the repair of MMS-induced DNA strand breaks. When UV- or MMS-treated cells were incubated in cytosine arabinofuranoside (AraC) plus hydroxyurea (HU), a large amount of low molecular weight DNA was detected by alkaline sucrose sedimentation. The molecular weight of these DNAs increased if the cells were further incubated in a drug-free medium. This rejoining of breaks in cells pretreated with UV plus AraC and HU was inhibited by nickel and by arsenite, but not by luminol. The rejoining of breaks in cells pretreated with MMS plus AraC and HU was inhibited by luminol and by arsenite, but not by nickel. These results suggest that different enzymes may be used in DNA resynthesis and/or ligation during the repairing of UV- and MMS-induced DNA strand breaks, and that nickel, luminol, and arsenite may have differential inhibitory effects on these enzymes. © 1994 Wiley-Liss, Inc.     

Efficacy of anticholinergic and beta-adrenergic agonist treatment of maximal cholinergic bronchospasm in tracheally intubated rabbits.

Cholinergically induced bronchoconstriction is thought to be a major cause of bronchospasm during anesthesia. We used tracheally intubated rabbits (4-mm endotracheal tube) stimulated with methacholine to assess the efficacy of beta-adrenergic agonist and anticholinergic treatment in reversing the increases in respiratory system resistance. Four groups were compared: (a) inhaled metaproterenol, 20 puffs via metered dose inhaler (0.65 mg/puff); (b) inhaled ipratropium bromide, 20 puffs from a metered dose inhaler (18 micrograms/puff); (c) 2 mg of intravenous atropine; and (d) no treatment after methacholine challenge as a control group. Methacholine increased respiratory system resistance from 0.041 +/- 0.001 (mean +/- SEM) to 0.098 +/- 0.006 cm H2O.mL-1.s-1 (P < 0.001). Whereas beta-adrenergic agonist treatment was ineffective in ameliorating bronchoconstriction, inhaled ipratropium bromide and atropine were highly effective, causing an 86%-88% reversal in the methacholine-induced increase in respiratory system resistance. Both these agents were also effective in improving dynamic compliance. We conclude that inhaled ipratropium bromide is effective in treating cholinergic bronchospasm even when administered via a small endotracheal tube and that the beta-adrenergic agonist metaproterenol is ineffective in rabbits in the face of maximal cholinergic stimulation.     

Effect of ethanol on ascorbate release in the nucleus accumbens and striatum of freely moving rats.

An in vivo voltammetry technique was used to monitor the extracellular ascorbate (AA) concentration in the nucleus accumbens and striatum of unanesthetized, freely moving rats. A single injection of ethanol, 1.0 g/kg intraperitoneally (IP), induced a significant increase in extracellular AA concentration in both the nucleus accumbens and striatum. This effect was dose dependent within a dose range from 0.5-2.0 g/kg. 4-Methylpyrazole (50 mg/kg, IP), which inhibits alcoholdehydrogenase, could not prevent the increase in AA concentration, evoked by ethanol. Furthermore, systemic administration of acetaldehyde (20 mg/kg, IP), the main metabolite of ethanol, did not have any effect on the level of AA in the nucleus accumbens or striatum. These results show that ethanol can alter the brain extracellular AA levels and that this effect seems to be attributed to ethanol itself and not to acetaldehyde. Consequently, these results indicate that a role for AA in the action of ethanol in the brain should be considered.