Poisoning by Datura leaves used as edible wild vegetables.

The causes of Datura intoxication include medication overdose, misuse of edible vegetables, deliberate abuse as a hallucinogen, homicidal or robbery and accidental intoxication from contaminated food. We report an incident of 14 people with Datura intoxication caused by ingesting wild Datura suaveolans for food. The incubation period was 15 to 30 min. The symptoms/signs were dizziness, dry mouth, flushed skin, palpitation, nausea, drowsiness, tachycardia, blurred vision, mydriasis, hyperthermia, disorientation, vomiting, agitation, delirium, urine retention, hypertension and coma. Three patients were hospitalized for 2-3 days. Thirteen persons received supportive fluid therapy. One patient did not receive medical therapy, he induced vomiting and drank a lot of water. Four patients presented with delirium/coma and 3 received physostigmine therapy with good response. One patient was intubated because of coma and respiratory depression. Three persons needed Foley catheterization for urine retention or coma status. One patient had a complication of urinary tract infection and antibiotic management. All patients recovered with no sequelae.     

Hepatic microsomal metabolism of N-nitrosodimethylamine to its methylating agent

Incubation of N-nitrosodi[¹⁴C]methylamine with calf thymus DNA and an isolated rat liver microsomal fraction resulted in a transfer of ¹⁴C-label from N-nitrosodi[¹⁴C]methylamine to biological macromolecules present in the in vitro assay system. This transfer of ¹⁴C-label from N-nitrosodi[¹⁴C]methylamine to biological macromolecules, believed to represent a methylation process, was dependent on the integrity and concentration of rat liver microsomes added to the in vitro assay system, as well as on the time of incubation. A requirement for NADPH was also observed. A study of the kinetics of this transfer of ¹⁴C-label from N-nitrosodi[¹⁴C]methylamine to biological macromolecules in vitro yielded values for the apparent K_m and V_max of 0.18 mm and 2.56 pmol methyl groups transferred per milligram of nucleic acid per milligram of microsomal protein per minute, respectively. The transfer reaction was inhibited by exposure of microsomes to carbon monoxide or pretreatment of animals with phenobarbital, 3-methylcholanthrene, or 2,3,7,8-tetrachlorodibenzo-p-dioxin. The capability of other rat liver subcellular fractions to mediate the reaction was examined.     

Microtubule-affinity regulating kinase (MARK) is tightly associated with neurofibrillary tangles in Alzheimer brain: a fluorescence resonance energy transfer study

Paired helical filaments, the main structural components of the neurofibrillary tangles in Alzheimer disease, consist of phosphorylated tau protein. Because the levels and degree of phosphorylation are significantly higher in paired helical filament (PHF)-derived tau than in normal adult tau, and because phosphorylation of tau severely disrupts microtubule stability, it is postulated that tau phosphorylation is an important step in PHF formation. The kinases and/or phosphatases that act in vivo to help induce such a pathological state of tau, however, are not yet known. In this study we implicate the non-proline directed kinase MARK in PHF-tau phosphorylation, by virtue of its close intermolecular association with the phosphorylated Ser262 epitope on PHF-tau as assessed by fluorescence resonance energy transfer. Moreover, because this tight enzyme-substrate association is observed in neurofibrillary tangles in Alzheimer tissue, we suggest that PHF-tau phosphorylation may occur to some extent on assembled PHF filaments.     

Amyotrophy in prion diseases

Amyotrophic lateral sclerosis was once thought to be caused by persistent viral infection, partly because some patients with transmissible Creutzfeldt-Jakob disease showed prominent amyotrophy. However, in the past 15 years there has been little interest in the amyotrophy in prion diseases, and the possible link to amyotrophic lateral sclerosis has been eschewed. We analyzed case reports of prion disease published after 1968 for evidence of amyotrophy. We defined amyotrophy as clinically evident fasciculation buttressed by electromyographic results in some cases. We sought evidence of motor neuron degeneration at autopsy. Prion disease was proved by transmissibility, immunohistochemistry demonstration of protease-resistant prion protein, or finding a mutation in the prion protein gene. Amyotrophy was noted in 27 patients: 13 with sporadic Creutzfeldt-Jakob disease, 2 with familial Creutzfeldt-Jakob disease, and 12 with Gerstmann-Str?ussler-Scheinker disease. Of the 27, 23 showed clinical fasciculation and 10 had electromyographic evidence of denervation. The spinal cord was examined in 8 patients: 6 showed loss of motor neurons, 1 showed vacuolation of motor neurons, and 1 reported no abnormalities. Another 23 patients had typical histopathological characteristics but lacked molecular or biochemical proof of prion disease. The total number of patients with amyotrophy and proven prion disease that we identified was 50. This case review supports the belief that amyotrophy is occasionally a prominent feature of Creutzfeldt-Jakob disease and underscores the importance of documenting lower motor neuron function and the crucial role of examining the spinal cord at autopsy in cases of prion disease.     

高原红细胞增多症16例围术期麻醉管理体会

16例高原红细胞增多症 (简称高红症 )病人 ,在围术期我们针对该类患者其血液成分 ,微循环 ,血液流变学等方面发生的一系列生理或 /和病理性改变。采取了血液稀释和自体输血等相应的对策 ,取得了较好的手术麻醉效果 ,大大降低了高红症病人手术麻醉的危险性