Analysis on origin and evolution of mumps]

There was a preliminary recognition on mumps during the Qin-Han to Sui-Tang dynasty, laying a foundation for the scholastic development on this topic in later generations. The title of this disease was identified in Song-Jin-Yuan dynasty with gradual deepening on its principle-method-formula-medication system, a great progress of recognition as compared with the previous ages. In the Ming-Qing dynasty, the recognition became even more systematic, with certain breakthrough in the system of principle-method-formula-medication. In modern age, the experiences were inherited and developed to integrate to modern biomedicine, so that the theory and clinical practice become even more perfect.     

慢性丙型肝炎患者α干扰素和α干扰素受体1的检测

目的建立检测外周血单个核细胞α干扰素受体1(IFNAR1)及检测诱导表达α干扰素(IFN-α)的方法,评价慢性丙型肝炎患者外周血单个核细胞(PBMC)细胞免疫功能与α干扰素治疗的关系。方法Poly IC体外刺激正常对照组和慢性丙型肝炎病毒(HCV)感染组患者PBMC,利用病毒保护试验研究干扰素治疗前后患者PBMC表达的干扰素抗病毒生物学活性差异;IFN-α治疗前后,RT-PCR检测慢性丙型肝炎患者不同干扰素应答组患者PBMC IFNAR1表达的变化。结果对照组PBMC分泌的干扰素活性显著高于慢性丙型肝炎患者应答组患者(P<0.001);干扰素应答组患者PBMC分泌的干扰素活性随治疗时间延长而增加,治疗1个月后显著高于无应答组患者PBMC分泌的干扰素活性(P<0.01),后者始终处于低下水平;IFN-α治疗期间干扰素应答组患者PBMC IFNAR1水平从治疗前的高表达而逐渐减少,正常对照和干扰素无应答组患者PBMC IFNAR1的表达始终较低。结论慢性HCV感染患者的细胞免疫功能受损,不能正常表达IFN-α,但应答组患者经干扰素治疗后IFN-α表达能力逐渐恢复;干扰素无应答组患者PBMC IFNAR1表达受到严重抑制;慢性丙型肝炎患者PBMCIFN-α活性检测及IFNAR1检测结果也许可以作为干扰素治疗预后的判断指标。     

Early uptake of 99mTc-C2A in the acute phase of myocardial infarction as a prognostic indicator for follow-up cardiac dysfunction

OBJECTIVE: The C2A domain of Synaptotagmin I is a molecular probe for the specific imaging of cell death. Here we test the hypothesis that the uptake of 99mTc-C2A in the acute phase of an infarction is associated with cardiac dysfunction in follow-ups. METHODS: The left coronary artery was occluded in Sprague-Dawley rats for 0, 10, 20, and 30 min. 99mTc-C2A was injected intravenously at 2 h of reperfusion. Anterior planar images were acquired with one million counts on a gamma camera 3 h after injection. 99mTc-C2A uptake was calculated as the total counts in the left ventricle region minus blood pool signal. The in-vivo signal detected was correlated with wall motion score index at 1 and 3 weeks follow-ups measured by echocardiography. RESULTS: 99mTc-C2A uptake was higher with increased ischemic time (2244+/-852, 4054+/-1223, and 6178+/-1451 for 10, 20, and 30 min ischemia, analysis of variance P<0.001). A significant correlation was found between 99mTc-C2A uptake and wall motion score index at 1 week (R=0.800, P=0.0006) and 3 weeks (R=0.810, P=0.0008). CONCLUSION: In this ischemia/reperfusion model, 99mTc-C2A uptake in the acute phase was associated with functional abnormality at 1 and 3 weeks. This demonstrates the potential diagnostic and prognostic value of 99mTc-C2A as a novel imaging agent.     

第2代(温控)射频消融子宫内膜切除术

目的探讨第2代（温度控制）射频消融子宫内膜切除术的疗效、安全性和可行性。方法2004年9月-2006年2月由上海市4家医院联合开展一项多中心、前瞻性研究,完成功能性子宫出血温控射频消融子宫内膜切除术81例。在超声监护下,射频治疗以温度控制模式输出功率50 W、温度设定85℃,按照两侧宫角、宫底、宫体、下段部位顺序射频消融子宫内膜。每个治疗点治疗时间为4 min。结果81例术后随访4-17个月。术后6个月随访70例,其中闭经48.6%（34/70）,点滴状月经41.4%（29/70）,少量月经10%（7/70）,总有效率为100%（70/70）。术后12个月随访67例,其中闭经56.7%（38/67）,点滴状月经29.9%（20/67例）,少量月经9.0%（6/67）,正常月经量3.0%（2/67）,月经量过多1.5%（1/67）,总有效率98.5%（66/67）。结论温控射频消融子宫内膜切除术不仅使患者的异常子宫出血在保留子宫的情况下得到有效的治疗,同时具有操作方便、治疗时间短、并发症少、术后恢复快等特点。     

Isoflurane Preconditioning Improves Long-term Neurologic Outcome after Hypoxic-Ischemic Brain Injury in Neonatal Rats

Background: Preconditioning the brain with relatively safe drugs seems to be a viable option to reduce ischemic brain injury. The authors and others have shown that the volatile anesthetic isoflurane can precondition the brain against ischemia. Here, the authors determine whether isoflurane preconditioning improves long-term neurologic outcome after brain ischemia.

Methods: Six-day-old rats were exposed to 1.5% isoflurane for 30 min at 24 h before the brain hypoxia-ischemia that was induced by left common carotid arterial ligation and then exposure to 8% oxygen for 2 h. The neuropathology, motor coordination, and learning and memory functions were assayed 1 month after the brain ischemia. Western analysis was performed to quantify the expression of the heat shock protein 70, Bcl-2, and survivin 24 h after isoflurane exposure.

Results: The mortality was 45% after brain hypoxia-ischemia. Isoflurane preconditioning did not affect this mortality. However, isoflurane preconditioning attenuated ischemia-induced loss of neurons and brain tissues, such as cerebral cortex and hippocampus in the survivors. Isoflurane also improved the motor coordination of rats at 1 month after ischemia. The learning and memory functions as measured by performance of Y-maze and social recognition tasks in the survivors were not affected by the brain hypoxia-ischemia or isoflurane preconditioning. The expression of Bcl-2, a well-known antiapoptotic protein, in the hippocampus is increased after isoflurane exposure. This increase was reduced by the inhibitors of inducible nitric oxide synthase. Inducible nitric oxide synthase inhibition also abolished isoflurane preconditioning-induced neuroprotection.     

Histamine and tryptase modulate asthmatic airway smooth muscle GM-CSF and RANTES release.

Degranulating mast cells are increased in the airway smooth muscle (ASM) of asthmatics, where they may influence ASM function. The aim of the present study was to determine whether histamine and tryptase modulate ASM cell granulocyte-macrophage colony-stimulating factor (GM-CSF) and RANTES (regulated on activation, normal T-cell expressed and secreted) release and also to examine which receptors are involved in this release. Confluent, quiescent ASM cells from asthmatic and nonasthmatic donors were treated with histamine (1 microM-100 microM) with and without histamine receptor antagonist pre-treatment, or the protease-activated receptor (PAR)-2 agonists tryptase (0.5-5 nM) and SLIGKV (100 and 400 microM). The cells were then stimulated with interleukin (IL)-1beta and/or tumour necrosis factor (TNF)-alpha (10 ng.mL(-1)) or left unstimulated for 24 h. Release of GM-CSF and RANTES was determined by ELISA and prostaglandin (PG)E(2) measured by enzyme immunoassay. Neither histamine nor tryptase induced ASM GM-CSF or RANTES secretion. However, histamine increased IL-1beta-induced GM-CSF release and markedly reduced TNF-alpha-induced RANTES release by both asthmatic and nonasthmatic cells to a similar extent, but did not modulate PGE(2) release. All changes involved activation of the histamine H1 receptor as they were partially or fully blocked by chlorpheniramine, but not ranitidine. Tryptase, via its proteolytic activity, also potentiated GM-CSF, but not RANTES, release from asthmatic and nonasthmatic ASM cells induced by both cytokines. PAR-2 involvement in the tryptase potentiation was unlikely because SLIGKV had no effect. In conclusion, mast cells, through histamine and tryptase, may locally modulate airway smooth muscle-induced inflammation in asthma.     

不同针刺深度对前列腺增生症大鼠重量指数的影响及形态学观察

目的与方法 采用深刺和浅刺对丙酸睾酮所致前列增生症（BPH）大鼠模型进行干预，研究其作用殊同。结果 针刺组前列腺，膀胱指数明显小于模型组；形态学观察，针刺组较模型组增生明显减轻，腺上皮呈单层柱状，腺体数目明显减少，间质充血，钙化明显减轻，结缔组织无增生，腺腔内分泌物减少。深刺组好于浅刺组。结论 深刺对实验性BPH大鼠的干预作用好于浅刺方法。