Neuroprotective effects of electroacupuncture on hypoxic-ischemic encephalopathy in newborn rats are associated with increased expression of GDNF-RET and protein kinase B / 中国结合医学杂志

<p><b>OBJECTIVE</b>To explore the neuroprotective effects of electroacupuncture (EA) on hypoxic-ischemic encephalopathy (HIE) and to further investigate the role of glial cell line-derived neurotrophic factor (GDNF) family receptor member RET (rearranged during transfection) and its key downstream phosphatidylinositol 3 kinase (PI-3K)/protein kinase B (Akt) pathway in the process.</p><p><b>METHODS</b>A total of 220 seven-day-old SD rats (of either sex, from 22 broods) were randomly divided into two groups, one (30 rats) for sham-surgery group and the other (190 rats) for HIE model group. The HIE model was established using the left common carotid artery ligation method in combination with hypoxic treatment. The successfully established rats were randomly divided into five groups, including control model group, EA group, sham-EA group, antagonist group and antagonist plus electroacupuncture group, with 35 rats in each group. Baihui (GV 20), Dazhui (GV 14), Quchi (LI 11) and Yongquan (KI 1) acupoints were chosen for acupuncture. EA was performed at Baihui and Quchi for 10 min once a day for continuous 1, 3, 7 and 21 days, respectively. The rats were then killed after the operation and injured cerebral cortex was taken for the measurement of neurologic damage by hematoxylin-eosin (HE) staining and the degenerative changes of cortical ultrastructure by transmission electron microscopy. RET mRNA level and Akt protein level were detected by real-time reverse-transcription polymerase chain reaction (RT-PCR) and western blot analysis, respectively.</p><p><b>RESULTS</b>EA could ameliorate neurologic damage of the first somatic sensory area (S1Tr) and alleviate the degenerative changes of ultrastructure of cortical neurons in rats subjected to HIE. And the longer acupuncture treatment lasted, the better its therapeutic effect would be. This was accompanied by gradually increased expression of GDNF family receptor RET at the mRNA level and its downstream signaling Akt at the protein level in the ischemic cortex.</p><p><b>CONCLUSION</b>EA has neuroprotective effects on HIE and could be a potential therapeutic strategy for HIE in the neonate. Activation of RET/Akt signaling pathway might be involved in this process.</p>

Molecular-biological identification of pathogens which caused an outbreak of viral encephalitis in Jinan area / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To investigate the etiology of the outbreak of viral encephalitis in Jinan area in 2003.</p><p><b>METHODS</b>Virus-specific nucleic acid fragments were amplified by random PCR and RT-PCR using specific primers to enterovirus. After sequencing, the gene sequence was handled by the program BLAST for homologous analysis and the software Clustal W 1.82 for multiple sequence alignment to identify the etiology and its genotype.</p><p><b>RESULTS</b>Five strains were isolated from clinical specimens. A gene fragment for one strain was acquired using random PCR, which was highly homologous to enterovirus. Then, the 5' non-translated region and partial VP1 region were amplified and sequenced. The five isolated strains were all identified as Coxsackievirus B5, and what was more, they were most homologous to the strain isolated during the outbreak of aseptic meningitis and encephalitis in Zhejiang province from 2002 to 2004.</p><p><b>CONCLUSION</b>Coxsackievirus B5 is closely associated with the outbreak of viral encephalitis in Jinan area in 2003. It is an important etiology but other viruses may also played a role which remains to be clarified.</p>

Preliminary analyses for influence of mutant PrPs with different number of octapeptide / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>The present study was conducted to understand the effects of PrP in different octapeptide repeats on proliferation of HeLa cells.</p><p><b>METHODS AND RESULTS</b>Mutant PrPs with octapeptide repeat insertion were transiently expressed in HeLa cells and their results of MTT assay showed stronger cytotoxic effect on the proliferation of cells than wild-type PrP. Annexin V/PI assay also demonstrated that the expression of mutant PrPs was much easier to induce apoptosis than wild-type in HeLa cells. The percentage of both early and late stage apoptosis in mutant groups were significantly higher than that of wild type.</p><p><b>CONCLUSION</b>These data suggest that the expression of mutant PrPs associated with familial CJD is much easier to induce apoptosis in cultured cells than expression of wild type PrP.</p>