Neurological manifestations in chronic mountain sickness: the burning feet-burning hands syndrome

OBJECTIVE: To characterise the clinical features and nerve biopsy findings in patients with chronic mountain sickness (CMS) living in the Peruvian Andes, with particular attention to the occurrence of the "burning feet-burning hands" syndrome. METHODS: Symptoms and signs were documented clinically in 10 patients with CMS and compared with those in five healthy subjects all living at 4338 metres altitude. Sural nerve biopsies were obtained from three patients with CMS.The nerve fibre population and endoneurial microvessels were analyzed morphometrically. RESULTS: All patients with CMS experienced burning and tingling paraesthesiae in the distal parts of their limbs. Similar but milder symptoms confined to the feet occurred in four of five controls. Three patients with CMS had a mild sensory neuropathy on examination, controls were clinically normal. Nerve biopsies showed a mild demyelinating neuropathy in all three with a reduction in the unmyelinated axon population in one. The endoneurial blood vessels showed a reduced thickness in the basal laminal zone compared with control values but were otherwise normal. CONCLUSIONS: Apart from well recognised symptoms and signs of CMS, the study has shown that such patients may also exhibit a mild sensory neuropathy. Its relation to the burning feet-burning hands syndrome, which was not confined to the patients but was also found in controls at altitude, is uncertain. The time course and pattern of the centrifugal resolution of the burning paraesthesiae complex on low altitude sojourn of high altitude natives raises the possibility that a mechanism involving altered axonal transport may be involved. The reduced thickness of the basal laminal zone of microvessels implies that adaptive structural changes to hypobaric hypoxia may also occur in peripheral nerve and are similar to those reported in other tissues of high altitude natives.     

Intracellular processing and toxicity of the truncated androgen receptor: nuclear congophilia-associated cell death

The pathogenesis of the selective motor neuron death in spinal bulbar muscular atrophy (SBMA) is not fully understood. Similar to observations with other mutant polyglutamine (poly Q) expanded proteins, truncated androgen receptor (AR) with expanded poly Q tract cause intracellular aggregates; however, the precise relationship between aggregates and disease pathogenesis is unresolved. In order to have a better understanding of the cellular processing and toxicity of the mutant AR, we focused on a short N-terminal portion of AR containing normal or expanded poly Q repeats, and have carried out biochemical, immunocytochemical, cytochemical and ultrastructural studies of BHK cells at different intervals after transfection. In cells expressing mutant truncated AR, using an anti-AR N-terminal antibody, we observed no immune staining in the nucleus and identified immune negative aggregates surrounded by immunopositive material in the cytoplasm. Congo red staining identified a component of aggregates with a beta-pleated secondary structure in both cytosol and nucleus, while electron microscopy revealed a fibrillary-granular material as the ultrastructural correlate. In addition, acid phosphatase staining and ubiquitin immunocytochemistry demonstrated that in transfected cells, both lysosomal and nonlysosomal degradation systems are actively involved in handling the mutant truncated AR. The temporal relationship of nuclear congophilia to a subsequent massive cell death suggests that entry of proteolytic cleavage products into the nucleus, perhaps the expanded poly Q stretch itself, may play an important role in cell toxicity.     

RP-HPLC进行甲氨蝶呤血药浓度监测时保留时间校准方法研究

目的 建立RP—HPLC进行MTX血药浓度监测时保留时间校准方法。方法应用容量因子与流动相比例的三次方多项式模型，建立MTX流动相比例与保留时间的函数，并通过此函数用保留时间求算流动相比例，与理论流动相比例比较，从而计算流动相应该补充组分的量，达到调整保留时间的目的。结果四种不同色谱条件下容量因子与流动相比例的三次方多项式模型拟合关系良好，R0均为1．000，保留时间经校准后RSD为0.9％(n=5)。结论本方法能准确校准因流动相比例引起变化的保留时间，适用于MTX血药浓度监测时保留时间的校准，方法新颖、有效、简单。     

干扰素α-1b治疗肾综合征出血热的临床疗效

目的 :观察干扰素α 1b对早期肾综合征出血热 (HFRS)的疗效。方法 :将诊断明确的早期HFRS 181例分成 2组。治疗组 94例 ,在液体综合疗法基础上给予干扰素α 1b ,10 0万U ,im ,qd ,疗程 3d ,少数重症患者适当增加剂量和疗程 ;对照组 87例仅采用液体综合疗法。结果 :治疗组用药后退热时间、低血压期、少尿期和多尿期持续时间 ,与对照组比较均明显缩短 (P <0 0 1)。治疗组未出现低血压期或少尿期 ,以及此 2期均未出现而直接进入多尿期的发生率较对照组明显升高 (P <0 0 1)。治疗组的并发症也较对照组减少。结论 :干扰素α 1b治疗早期HFRS临床疗效满意 ,不良反应少。     

降纤酶低分子肝素治疗短暂性脑缺血发作的研究

目的 观察降纤酶与低分子肝素治疗短暂性脑缺血发作的效果及副作用。方法 选择本院神经内科住院患者36例应用降纤酶10U加入加入250ml生理盐水中静脉滴注，隔日1次，共3次；低分子肝素0．5ml脐旁皮下注射，12h 1次，连用7—10d,同时常规给予复方丹参滴注，口服尼莫地平，维生素E，维生素C，停用低分了肝素后给予肠溶阿斯匹林75mg，每日1次口服。结果 治疗开始后TLA发作相继减少，停止发作时间分别为1d内9例，3d内15例，5d内12例。随访6个月—1年，1例2个月后复发，重新应用上药治愈。结论 降纤酶与低分子肝素治疗TLA安全有效、无明显副作用、不易复发。     

低分子肝素阿魏酸钠治疗不稳定型心绞痛

目的 了解低分子肝素与阿魏酸钠联合应用治疗不稳定型心绞痛的疗效，提高不稳定型心绞痛治疗效果。方法 选用本院治疗的120例病人，治疗组60例．对照组60例，对照组以静脉滴注二硝酸异山梨酯为主。治疗在对照组治疗基础上，采用低分子肝素5000U皮下注射，每日2次，连续7d，阿魏酸钠0．3加入5％葡萄糖液中缓慢滴注，1日1次，连用14d为一疗程。两组对比了心绞痛控制，心绞痛缓解和消失时间及心电图变化及治疗前后纤维蛋白原血浆比黏度等情况。结果 治疗组在心绞痛控制，心绞痛缓解和消失时间及心电图变化及血液比黏度，纤维蛋白原等情况，明显优于对照组。结论 低分子肝素联合阿魏酸钠治疗不稳定型心绞痛疗效显著。     

三七皂苷Rg1对失血性休克大鼠肠上皮细胞线粒体损伤保护作用的研究

 目的观察大鼠失血性休克后肠上皮细胞线粒体编码基因细胞色素氧化酶(COXⅠ，COXⅡ，COXⅢ)mRNA的表达变化，并探讨三七皂苷Rg1(Rg₁)对其保护作用的分子机制，为休克的防治提供实验依据。方法采用失血性休克模型，分离肠上皮细胞后进行RNA的提取，应用RT-PCR检测大鼠失血性休克后及用Rg₁治疗后COXⅠ，COXⅡ，COXⅢ mRNA的表达变化情况。结果大鼠失血性休克1h，COXⅠ，COXⅡ基因表达开始增强，2h表达最强，以后随着休克时间延长，表达又逐渐减弱，失血性休克晚期5 h表达显著低于正常对照鼠(P＜0.01)；Rg1(5 mg·kg^-1)治疗后，可使COXⅠ，COXⅡ mRNA表达显著增强(P＜0.01)。结论失血性休克可引起大鼠肠上皮细胞线粒体编码基因COXⅠ，COXⅡ mRNA的明显改变，Rg1可提高其表达,对失血性休克肠上皮细胞线粒体损伤有明显的保护作用。     

黄龙汤对动物肠运动的影响

目的：探讨黄龙汤对实验动物肠运动的作用。方法：采用肠管运动在体实验法测定排便时间及频度和肠推进运动．肠管运动的离体实验法测定动物不同肠段运动情况。结果：黄龙汤能使动物排便时间增快，次数增加，便稀且不成形。能明显促进动物在体肠推进运动。能增加动物离体回肠蠕动作用，对离体十二指肠及结肠则显示明显的抑制作用．且这种作用能被Ach短暂拮抗。结论：黄龙汤对实验动物有明显的泻下作用。可能是由于黄龙汤有促进动物肠肌运动的结果。对十二指肠及结肠显示的这种抑制作用表明本方在致泻的同时，可能有解痉止痛作用。     

姬松茸中挥发性风味物质的GC-MS分析

利用顶空GC-MS技术对姬松茸新鲜子实体和固体发酵的菌丝体挥发性风味物质进行了分析。在子实体中检测出7种主要的挥发性风味物质，其中以苯甲醛和苯甲醇为主，相对含量分别达到43．20％和28．98％；在菌丝体中检测出16种主要的挥发性风味物质，其中苯甲醛相对含量最高，达38．50％。苯甲醛和苯甲醇是姬松茸中的主要风味物质。     

风湿病发热的中医论治

从急性发作期、撤减激素反跳期、慢性活动期三期来探讨中医论治风湿病发热。急性发作期发热按卫、气、营、血辨证，治以疏风清热、清气分热、清营透气、凉血清营、清热解毒；撤减激素反跳期发热按气虚、脾肾阳虚辨证，治以益气养阴、清热温散、清营温通；慢性活动期按阴虚、血瘀辨证，治以滋阴清热，清热散瘀。