角膜损伤后神经再生的实验研究

应用神经组织化学技术观察了兔角膜NA能神经及AchE阳性神经在角膜损伤后的再生,证实术后1月,两种神经均有再生轴突进入植片;术后3月可见交界区和植床内神经密度明显增加;同时,对术后两种神经再生的功能意义进行了讨论。     

Transient Brain Ischaemia Provokes Ca2+, PIP2 and Calpain Responses Prior to Delayed Neuronal Death in Monkeys

To clarify the mechanism of postischaemic delayed cornu Ammonis (CA)-1 neuronal death, we studied correlations among calpain activation and its subcellular localization, the immunoreactivity of phosphatidylinositol 4,5-bisphosphate (PIP₂) and Ca²⁺ mobilization in the monkey hippocampus by two independent experimental approaches: in vivo transient brain ischaemia and in vitro hypoxia-hypoglycaemia of hippocampal acute slices. The CA-1 sector undergoing 20 min of ischaemia in vivo showed microscopically a small number of neuronal deaths on day 1 and almost global neuronal loss on day 5 after ischaemia. Immediately after ischaemia, CA-1 neurons ultrastructurally showed vacuolation and/or disruption of the lysosomes. Western blotting using antibodies against inactivated or activated μ-calpain demonstrated μ-calpain activation specifically in the CA-1 sector immediately after ischaemia. This finding was confirmed in the perikarya of CA-1 neurons by immunohistochemistry. CA-1 neurons on day 1 showed sustained activation of μ-calpain, and increased immunostaining for inactivated and activated forms of μ- and m-calpains and for PIP₂. Activated μ-calpain and PIP₂ were found to be localized at the vacuolated lysosomal membrane or endoplasmic reticulum and mitochondrial membrane respectively, by immunoelectron microscopy. Calcium imaging data using hippocampal acute slices showed that hypoxia-hypoglycaemia in vitro provoked intense Ca²⁺ mobilization with increased PIP₂ immunostaining specifically in CA-1 neurons. These data suggest that transient brain ischaemia increases intracellular Ca²⁺ and PIP₂ breakdown, which will activate calpain proteolytic activity. Therefore, we suggest that activated calpain at the lysosomal membrane, with the possible release of biodegrading enzyme, will cause postischaemic CA-1 neuronal death.     

Influence of Osteoarthritis on Serum Marker Levels of Bone Formation and Resorption in Patients with Benign Prostatic Hypertrophy

Background :
The aim of this study was to investigate the influence of osteoarthritis of lumbar vertebrae on serum bone formation and resorption marker levels of patients with benign prostatic hypertrophy (BPH).
Methods :
Serum levels of carboxyterminal propeptide of type I procollagen (PICP), alkaline phosphatase (ALP), carboxyterminaltelopeptide of type I collagen (ICTP), and prostate-specific antigen (PSA) were examined in 40 patients with BPH, and the presence of osteoarthritis at the lumbar vertebrae of the patients was evaluated by plain x-ray-p.
Results :
Findings of osteoarthritis were observed in 23 of the 40 patients (58%), and 10 of the patients had severe osteoarthritis (involving at least 2 lumbar vertebral bodies). The serum levels of PICP, ALP, ICTP, and PSA of the patients without osteoarthritis findings were not different from those of the patients with osteoarthritis or severe osteoarthritis.
Conclusion :
The influence of osteoarthritis on serum bone formation and resorption marker levels of patients with BPH appears to be rather slight, if there is any influence at all.     

Vasodilator effects of C-type natriuretic peptide on cerebral arterioles in rats

The vasodilator effects of C-type natriuretic peptide (CNP) were investigated in isolated rat cerebral arterioles. CNP caused dose-dependent vasodilation, maximally by 10.0±2.2% at 10⁻⁶ M. The median effective concentration (EC₅₀) was 5.2×10⁻¹⁰ M. In contrast, atrial natriuretic peptide and B-type natriuretic peptide, other members of the natriuretic peptide family, produced little or no vasodilation. Pretreatment with methylene blue (10⁻⁴ M) abolished CNP-induced vasodilation, whereas pretreatment with N^G-monomethyl-

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-arginine or indomethacin did not inhibit vasodilation. Thus, CNP is suggested to cause significant vasodilation in cerebral arterioles via a cyclic guanosine monophosphate-dependent mechanism. © 1997 Elsevier Science B.V. All rights reserved.     

烧伤血清刺激对大鼠肠上皮细胞结构和粘弹性的影响

目的　动态观察烧伤血清对体外肠上皮细胞 (IEC)骨架和细胞生物力学 (粘弹性 )的影响。　方法　培养大鼠肠上皮细胞株IEC 6 ,用烧伤血清刺激后 ,通过细胞骨架免疫组化、细胞ELISA法定量分析以及粘弹性测定技术 ,动态观察IEC致伤前后的变化。　结果　IEC在烧伤血清作用早期 ,骨架蛋白的表达即明显降低 ,微丝、微管蛋白阳性信号减弱 ,细胞粘弹性下降。　结论　细胞骨架的损伤可引起细胞脆性增加、粘弹性下降 ,导致细胞生物力学特性的改变。这种变化 ,可能直接参与烧伤后肠上皮细胞损伤的发生。     

Serotonergic projections from the midbrain periaqueductal gray and nucleus raphe dorsalis to the nucleus parafasccicularis of the thalamus

By a double-labeling method combining the retrograde tracing of horseradish peroxidase and the immunocytochemical technique, serotonin-like immunoreactive neurons in the midbrain periaqueductal gray (PAG) and nucleus raphe dorsalis (DR) of the rat were observed to send projection fibers to the nucleus parafascicularis of the thalamus bilaterally with an ipsilateral dominance. These serotonin-containing projecting neurons were observed mainly at the middle-caudal levels of the ventrolateral subdivision of the PAG and less at the middle-rostral levels of the DR.     

使用手性冠醚的高效毛细管电泳法研究伯胺类药物的手性分离

目的　采用HPCE法拆分伯胺类药物对映异构体。方法　缓冲液 2 0mmol/LTris 0 .1%H3 PO4(v/v)(pH 2 .0 6 ) +18 冠 6 四甲酸 (18C6H4) ;检测波长 2 10nm。结果　 8种伯胺类药物得以拆分。结论　缓冲液中添加手性冠醚的HPCE法能较好地拆分伯胺类药物。     

Segmental hyperintensity on T1-weighted MRI of the liver: Indication of segmental cholestasis

The purpose of this study was to determine the relationship between segmental hyperintensity of the liver on T1-weighted images and segmental cholestasis in patients with obstructive jaundice. T1-weighted and T2-weighted MR images were obtained of 73 patients with obstructive jaundice caused by various diseases. Fat-suppressed T1-weighted images were also obtained of 10 patients. Eleven patients with segmental intra-hepatic bile duct dilatation (cholestasis) showed segmental hyperintensity on T1-weighted images and/or fat-suppressed T1-weighted images and no signal intensity difference on T2-weighted images. Sixty-two patients with widespread intrahepatic bile duct dilatation showed no intensity difference on T1-weighted and T2-weighted images (P < .01). Segmental hyperintensity on T1-weighted images was correlated with intrahepatic cholestasis.     

Day-Night Variation of Urine Volume in Parkinson's Disease

Abstract: Studies on the circadian rhythm of urine excretion in healthy men have demonstrated that the maximal urine flow occurs in the early afternoon and the minimal around midnight. In this study, an abnormality in the variation of urine volume was found in parkinsonian patients. Urine samples were collected during daytime (9:00–21:00) and nighttime (21:00–9:00). Fifteen healthy control subjects were examined and found to excrete 60% during the daytime and 40% during the nighttime of the total urine volume. Sixteen parkinsonian patients excreted 43% during the daytime and 57% during the nighttime. In contrast to the control subjects, the parkinsonian patients excreted a smaller volume of their urine during the daytime than during the nighttime. This finding might be related to the degeneration of dopaminergic and/or nondopaminergic neurons in the brain which control urinary excretion.