小剂量低LET辐射对人淋巴细胞SCE的影响

本文用磷酸盐Giemsa法观察了小剂量X射线照射对人离体外周血淋巴细胞SCE的影响。其结果照射组各剂量点均不明显地高于对照组,证实了SCE对电离辐射不敏感,说明染色体结构畸变和SCE的发生是彼此独立的两个不同事件。     

Does a common pathophysiological basis exist in the association of ulcerative colitis and Takayasu's aortitis? Report of a case.

A case of a young Japanese woman with long-standing ulcerative colitis complicated by preinfarction angina due to Takayasu's aortitis is presented. Successful emergency aorto-coronary bypass operation was performed. Whether the association of these two diseases can be explained by a common mechanism is discussed.     

热分析中系列相关反应的补偿效应研究

根据热分析谱图峰顶的数学特征与Ｃｏａｔｓ－Ｒｅｄｆｅｒｎ方程，推得在一定实验条件下，在系列相关反应中，若峰顶温度相接近，则各反应的表观活化能Ｅ与指前因子Ａ之间存在着有动力学意义的补偿效应，即ｌｎＡ＝ａＥ＋ｂ。并经系列含水硫酸盐脱水反应实验验证。     

高原康胶囊对大批快速进入高原者血浆醛固酮、血管紧张素II及水负荷的影响及意义

目的 :了解高原康胶囊对快速进入高原者血浆醛固酮 (Aldosterone ,ALD)、血管紧张素II(AngiotensinII ,AII)及水负荷的影响及意义。方法 :将 80名由平原快速进入高原的新兵随机分为实验组 4 0名 ,对照组 4 0名 ,实验组于平原登机前开始给予口服高原康胶囊 ,连服 3日 ,对照组给予安慰剂 ,两组均于进入高原的前 1天及进入高原的第 3天午给予水负荷实验 ,并对饮水前血浆ALD、AII及饮水后 15 0min内各时间段的尿量及两组进入高原后 7天内急性高原病 (Acutehighal titudediseaes ,AHAD)的发病率进行对照比较。结果 :对照组进入高原后与平原相比血浆ALD、AII显著升高 ,水负荷实验 6 1min～ 15 0min各时间段的尿量及相应时间的总尿量与平原时相应各时间段的尿量及相应时间的总尿量相比则显著减少 (P <0 0 5～ 0 0 0 1) ,而实验组则无显著变化 (P >0 0 5 ) ;进入高原后实验组与对照组相比水负荷实验 6 1min～ 90min的尿量及 12 0min、15 0min的尿总量则显著多于对照组 (P <0 0 5 ) ;血浆ALD、AII及AHAD发病率则显著低于对照组 (P <0 0 5～ 0 0 0 1)。结论 :高原康胶囊能显著降低快速进入高原者的血浆ALD、AII ,通过对水负荷调节的影响减少机体的钠水潴留 ,从而防止快速进入高原者AHAD的发生 ,可用于大批快     

细胞黏附分子(ICAM-1)在大鼠弥漫性脑损伤中的表达意义

目的探讨ICAM—1在大鼠弥漫性脑损伤中的表达及意义。方法采用Marmarou方法获得大鼠弥漫性脑损伤模型．实时定量RT—PCR、S—P免疫组化法分别测定ICAM—1蛋白和mRNA在外伤后不同时间点的表达变化．干湿重法测脑组织含水量．组织切片苏木精一伊红染色观测炎性细胞浸润情况。结果外伤组与假手术对照组比较，ICAM—1蛋白表达分别于伤后6h明显升高．72h达到高峰（P〈0.05），ICAM—ImRNA表达3h即明显升高，72h达最高峰，其后下降。7d时仍高于假手术对照组（P〈0．01）。伤后脑组织含水量较假手术对照组高，同时炎性细胞大量聚集。结论大鼠脑外伤诱导了ICAM—1的表达．ICAM—1通过介导炎性细胞的浸润可能参与了伤后脑水肿的形成过程．     

Extracellular signal regulated kinases 1/2 signal pathway and responses of astrocytes after diffuse brain injury

BACKGROUND: The treatment of diffuse brain injury during an acute period is focused on relieving degrees of secondary brain injury. Generation and development of pathological changes of secondary brain injury depend on signal conduction, so down-regulating over response of astrocyte through interfering a key link of signal conduction pathway may bring a new thinking for the treatment of diffuse brain injury. OBJECTIVE: To observe the effect of over activity of extracellular signal regulated kinases 1/2 (ERK1/2) signal pathway on the response of astrocyte during an acute period of diffuse brain injury. DESIGN: Completely randomized grouping and controlled animal study. SETTINGS: Department of Neurosurgery, the Third Affiliated Hospital, Nanchang University; Department of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: A total of 158 healthy male SD rats, of 11 weeks old, weighing 320–370 g, were provided by Experimental Animal Faulty, Tongji Medical College, Huazhong University of Science and Technology. Rabbit-anti-phosphorylated ERK1/2 (pERK1/2) polyclonal antibody was provided by R&D Company; rabbit-anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, SP immunohistochemical kit and horseradish peroxidase (HRP)-labeled goat-anti-rabbit IgG by Santa Cruz Company; specific inhibitor U0126 of ERK1/2 signal pathway by Alexis Company. METHODS: The experiment was carried out in the Laboratory of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from September 2004 to March 2006. ① Detection of pERK1/2 expression: A total of 110 rats were randomly divided into sham operation group (n =5), model group (n =35), high-dosage U0126 group (n =35) and low-dosage U0126 group (n =35). Rats in the sham operation group were only treated with incision of epicranium and fixation of backup plate, but not hit. Rats in the model group were used to establish diffuse brain injury models based on Marmarou free falling body without drug intervention. Rats in the high- and low-dosage U0126 groups were injected into caudal vein with 0.1 and 0.05 mg/kg U0126, respectively, and then, rats were hit to establish injured models. Every 5 rats were collected from model, high- and low-dosage U0126 groups at 5, 30 minutes, 3, 12, 24, 72 hours and 7 days after diffuse brain injury to detect pERK1/2 expression in cortex of parietal lobe based on Western blot technique. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Another 48 rats were randomly divided into sham operation group (n =3), model group (n =15), high-dosage U0126 group (n =15) and low-dosage U0126 group (n =15). The intervention and administration were dealt as the same as those mentioned above. Every 3 rats were collected from model, high- and low-dosage U0126 groups at 30 minutes, 3, 12, 24 and 72 hours after model establishment to observe the distribution of pERK1/2 and postive GFAP cells in brain tissue which was cut from coronal section at Bregma –4.8 mm layer with immunohistochemical staining. MAIN OUTCOME MEASURES: pERK1/2 expression in cortex of parietal lobe and distribution of pERK1/2 and positive GFAP cells in brain tissues. RESULTS: ① pERK1/2 expression: After diffuse brain injury, pERK1/2 expression in cortex of parietal lobe was rapidly increased in the model group, reached at peak at 5 minutes and then decreased gradually. But the expression was still in a high level until the 72nd hour and fallen to the basic level on the 7th day. pERK1/2 level was lower in high- and low-dosage U0126 groups than that in model group at various time points (P < 0.01); meanwhile, pERK1/2 level was lower in high-dosage U0126 group than that in low-dosage U0126 group. The results showed that there was a certain dosage dependence on pERK1/2 expression. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Positive expression of pERK1/2 lasted in brain tissue from 30 minutes to 72 hours after diffuse brain injury (P < 0.05). In addition, from 30 minutes to 3 hours, brown-yellow stained cells were mainly distributed in plasma, but rarely in nucleus. A lot of positive cells had tree-like apophysis, which was similar to neurons. With the time passing by, more and more nuclei manifested positive stains; moreover, nuclei mainly manifested positive staining until 24 hours after diffuse brain injury. Immune-positive pERK1/2 cells were widely distributed in brain tissue, especially mainly in binding site between deep cortex and cerebral white matter, and then in hippocampus. In addition, ependymal cell and vascular endothelial cells of choroids plexus also manifested strongly positive staining. As compared with model group, positive cells were decreased gradually in high- and low-dosage U0126 groups. However, number of positive cells was less in high-dosage U0126 group than that in low-dosage U0126 group. CONCLUSION: Diffuse brain injury strongly induces the activity of ERK1/2 signal pathway and response of astrocyte; in addition, U0126 can inhibit response of glial cells during an acute period, and the effect manifests dosage dependence.