The upregulation of glial glutamate transporter-1 participates in the induction of brain ischemic tolerance in rats.

Glial glutamate transporter-1 (GLT-1) plays an essential role in removing glutamate from the extracellular space and maintaining the glutamate below neurotoxic level in the brain. To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP), the present study was undertaken to observe in vivo changes in the expression of GLT-1 and glial fibrillary acidic protein (GFAP) in the CA1 hippocampus during the induction of BIT, and the effect of dihydrokainate (DHK), an inhibitor of GLT-1, on the acquisition of BIT in rats. Immunohistochemistry for GFAP showed that the processes of astrocytes were prolonged after a CIP 2 days before the lethal ischemic insult, which could protect pyramidal neurons in the CA1 hippocampus against delayed neuronal death induced normally by lethal ischemic insult. The prolonged processes extended into the area between the pyramidal neurons and tightly surrounded them. These changes made the pyramidal layer look like a 'shape grid'. Simultaneously, the prolonged and extended processes showed a great deal of GLT-1. Western blotting analysis showed significant upregulation of GLT-1 expression after the CIP, especially when it was administered 2 days before the subsequent lethal ischemic insult. Neuropathological evaluation by thionin staining showed that DHK dose-dependently blocked the protective role of CIP against delayed neuronal death induced normally by lethal brain ischemia. It might be concluded that the surrounding of pyramidal neurons by astrocytes and upregulation of GLT-1 induced by CIP played an important role in the acquisition of the BIT induced by CIP.     

The CLDN5 locus may be involved in the vulnerability to schizophrenia.

The present study was designed to detect three single nucleotide polymorphisms (SNPs) located on 22q11 that was thought as being of particularly importance for genetic research into schizophrenia. We recruited a total of 176 Chinese family trios of Han descent, consisting of mothers, fathers and affected offspring with schizophrenia for the genetic analysis. The transmission disequilibrium test (TDT) showed that of three SNPs, rs10314 in the 3'-untranslated region of the CLDN5 locus was associated with schizophrenia (chi(2) = 4.75, P = 0.029). The other two SNPs, rs1548359 present in the CDC45L locus centromeric of rs10314 and rs739371 in the 5'-flanking region of the CLDN5 locus, did not show such an association. The global chi-square (chi(2)) test showed that the 3-SNP haplotype system was not associated with schizophrenia although the 1-df test for individual haplotypes showed that the rs1548359(C)-rs10314(G)-rs739371(C) haplotype was excessively non-transmitted (chi(2) = 5.32, P = 0.02). Because the claudin proteins are a major component for barrier-forming tight junctions that could play a crucial role in response to changing natural, physiological and pathological conditions, the CLDN5 association with schizophrenia may be an important clue leading to look into a meeting point of genetic and environmental factors.     

Parvalbumin 3 is an Abundant Ca2+ Buffer in Hair Cells

Ca2+ signaling serves distinct purposes in different parts of a hair cell. The Ca2+ concentration in stereocilia regulates adaptation and, through rapid transduction-channel reclosure, underlies amplification of mechanical signals. In presynaptic active zones, Ca2+ mediates the exocytotic release of afferent neurotransmitter. At efferent synapses, Ca2+ activates the K+ channels that dominate the inhibitory postsynaptic potential. A copious supply of diffusible protein buffer isolates the three signals by restricting the spread of free Ca2+ and limiting the duration of its action. Using cDNA subtraction and a gene expression assay based on in situ hybridization, we detected abundant expression of mRNAs encoding the Ca2+ buffer parvalbumin 3 in bullfrog saccular and chicken cochlear hair cells. We cloned cDNAs encoding this protein from the corresponding inner-ear libraries and raised antisera against recombinant bullfrog parvalbumin 3. Immunohistochemical labeling indicated that parvalbumin 3 is a prominent Ca2+-binding protein in the compact, cylindrical hair cells of the bullfrog's sacculus, and occurs as well in the narrow, peanut-shaped hair cells of that organ. Using quantitative Western blot analysis, we ascertained that the concentration of parvalbumin 3 in saccular hair cells is approximately 3 mM. Parvalbumin 3 is therefore a significant mobile Ca2+ buffer, and perhaps the dominant buffer, in many types of hair cell. Moreover, parvalbumin 3 provides an early marker for developing hair cells in the frog, chicken, and zebrafish.     

小包装全氟丙烷气体动力学实验研究

为检验塑料小包装全氟丙烷气体（C3F8）在不同包装和储存方法时浓度变化，将装有5～7mlC3F8的聚氯乙烯小袋，根据不同储藏温度和外包装方法随机分成四组：（1）22℃聚乙烯外包装，（2）36℃聚乙烯外包装，（3）22℃铝箔真空外包装，（4）-29℃聚乙烯外包装；每一组C3F8小袋气体存放一定时间后，应用气相色谱分析方法进行浓度测量。结果：第3组C3F8浓度最高和稳定，第2组浓度随放置时间降低最明显，第4组是临床应用气体的储藏和包装方法，其30天样本浓度和第3组相等，但放置一年时浓度降低。结果显示：塑料小包装C3F8予以铝箔真空外包装是一种可行的方法，利于C3F8运输和普及；聚乙烯外包装的C3F8，应放在-29℃保存，时间不超过一年。     

Principles for managing penetrating craniocerebral injuries caused by firearm missiles

Penetrating craniocerebral firearm injuries remain one of the most lethal causes of all trauma and are common both in war or peace time. Data were reviewed for 4140 severely head-injured patients (Glasgow Coma Scale (GCS) scores 3-8) treated at Xi-Jing Hospital between 1973 and 1993; 51 of these patients had acute penetrating craniocerebral injuries caused by firearm missiles. These patients consisted of 46 males (90.2%) and 5 females (9.8%) ranging in age from 3 months to 48 years (median 22.4 years). The lesion types included 2 tangential wounds, 37 tubular wounds and 12 through-and-through wounds. All cases were urgent with the patients in severe and unstable states. After emergency treatment and operation, 5 cases died (9.8%). Follow up studies at three months showed that 23 cases (45.1%) had made a good recovery. Moderate disability, severe disability and vegetative states in this series were 29.4%, 13.7% and 2.0% respectively. Long term follow up studies indicated that 32 were able to resume their occupation. The principles for managing penetrating craniocerebral firearm injuries and suggestions for operation are discussed.     

紫外分光光度法测定SOD活性的应用及其意义

本文对SOD的紫外分光光度法测定进行了实用性研究。结果表明,本文方法具有用血量少,重现性好,快速、灵敏,试剂廉价等优点。西宁地区与平原地区人群的比较测定显示,前者SOD活性明显高于后者(P<0.01)。     

The effect of individual HLA-A and -B mismatches on the generation of cytotoxic T lymphocyte precursors

In order to study the correlation between HLA mismatches and the cytotoxic T lymphocyte precursor frequency, we used a limiting dilution analysis to determine the CTLp frequencies against individual mismatched HLA-A and -B alloantigens in 21 patients waiting for a renal transplant. Altogether, thirty-three mismatched HLA-A antigens and 55 HLA-B antigens were tested. The CTLp frequencies against mismatches of HLA-B locus antigens were found to be significantly higher than those against HLA-A antigens (P less than 0.002). This may explain why matching for HLA-B antigens is more important for a good renal allograft survival than matching for HLA-A antigens.     

Effects of an anti-interleuktn-6 (IL-6) murine monoclonal antibody in a patient with acute monoblastic leukemia

Because IL-6 has been involved in the pathogenesis of acute monoblastic leukemia, we investigated thein vitro anti-proliferative effect and thein vivo anti-tumoral effect of an anti-IL-6 murine monoclonal antibody (mAb) in a patient with MSB type acute leukemia. In the current study, we clearly show the IL-6 dependence of monoblastic cell viability and proliferationin vitro in short-term cultures of malignant cells and the clinical activity of the anti-IL-6 murine mAb. The complete neutralization of IL-6in vivo was associated with a transient but complete disappearance of malignant monoblastic cells in the peripheral blood, with improvement or even normalization of several other biological parameters of disease activity, No immunization against the anti-IL-6 murine mAb was observed.