The effects of inflammatory cytokines on steroidogenic acute regulatory protein expression in macrophages

Objective: To investigate the expression of steroidogenic acute regulatory protein (StAR) in macrophages and the effects of inflammatory cytokines on StAR expression. Methods: The macrophages isolated from ApoE knockout mice and C57BL/6J mice and RAW264.7 cells (a cell line from mouse macrophage. ATCC Number: TIB-71^TM) were cultured in DMEM containing 10% fetal bovine serum. RAW264.7 cells were treated with different inflammatory cytokines (TNF-α, IFN-γ and TGF-β1) and 8-Br-cAMP, a cAMP analog. RT-PCR and Western blot analysis were applied to evaluate the effects of inflammatory cytokines on StAR expression. Results: RT-PCR and Western blot analysis demonstrated the expression of StAR in the macrophages isolated from ApoE knockout mice, C57BL/6J mice and RAW264.7 cells. Proinflammatory cytokines TNF-α and IFN-γ significantly decreased StAR mRNA and protein levels in RAW264.7 cells. The inhibition was dose- and time-dependent. In contrast, anti-inflammatory cytokine TGF-β1 increased StAR mRNA and protein levels. At 1:15 molecular ratio, TGF-β1 blocked the down-regulation of StAR expression mediated by TNF-α. cAMP also induced StAR expression in RAW264.7 cells. When the cells were co-treated with 8-Br-cAMP and TNF-α, 8-Br-cAMP failed to induce StAR expression. Conclusion: Our results provide interesting evidence that inflammatory cytokines regulate StAR expression in macrophages. Received 12 August 2006; returned for revision 28 September 2006; returned for final revision 28 May 2007; accepted by M. Katori 22 June 2007     

高压氧治疗重度颅脑损伤后临床、脑电地形图及预后的探讨

目的:探讨高压氧治疗重度颅脑损伤的疗效。方法:重度颅脑损伤患者35例为治疗组,20例为对照组,观察高压的氧治疗前后临床、脑电地形图的变化及预后。结果:治疗组临床(GCS)、脑电地形图及预后经高压氧治疗后均明显改善,而对照组改善不明显。结论:高压氧能够明显改善重度颅脑损伤患者的临床,脑电地形图及预后。     

Reproductive genetic counselling in non-mosaic 47,XXY patients: implications for preimplantation or prenatal diagnosis: Case report and review

With an incidence of approximately 1 in 500 male newborns, the 47,XXY genotype is one the most common sex chromosome anomalies. It is also the most frequent genetic cause of human infertility. Some non-mosaic 47,XXY patients have sperm production which allows infertility treatment to be offered by ICSI. Therefore, the risk of transmitting a chromosome anomaly to the next generation is an important problem in reproductive genetic counselling of these patients. Here, we report on a twin pregnancy where two karyotypically normal neonates 46,XX and 46,XY were born after the use of ICSI in assisted reproduction of a patient with a non-mosaic 47,XXY syndrome. To date, only 38 evolving pregnancies including the present cases, have been reported after ICSI using sperm from non-mosaic 47,XXY patients. Although these data are scarce, they suggest that the risk of chromosome anomaly in the offspring of these patients is low; hence, their reproductive genetic counselling can be reassuring, and management of the pregnancy can proceed with caution.     

243例健康人血红细胞悬浮液射频介电特性的研究

本文应用同轴传输线反射法建立的细胞悬浮液介电测量系统，测量了２４３例健康人（男１２０，女１２３名）血红细胞悬浮液在１～５００ＭＨｚ频率范围的介电常数和电导率。结果表明不同性别和不同血型之间的红细胞悬浮液的介电参数无显著差异。将１９～８０岁之间的受试者按１０岁年龄间隔分成六个组，探讨年龄差别对介电参数的影响；发现５０岁左右是人红细胞介电参数有显著差异的临界年龄，４９岁后三个高年龄组的介电参数显著地低于４９岁前的三个低年龄组的数值（Ｐ＜０．０５）。本文的结果证明年龄对人血红细胞的介电参数有明确的影响。     

肾脏的交感神经支配

采用大体解剖学方法和肾内注射HRP逆行标记神经元的方法,研究了猫肾脏的交感神经支配。发现了下述的待点。1.猫左、右侧腹腔神经节相互融合,呈半环状包绕在肠系膜上(前)动脉的起始处,于其融合部,各发出左、右肾支。肠系膜上神经节与右侧腹腔神经节融合。2.肾交感神经节后神经元,分别位于腹腔神轻节,同侧主动脉肾神经节和T_(12)～L~4节段的交感干神经节内,並具有局部定位分布的关系。3.肾交感神经节后纤维主要来自腹腔神经节(82.08％),其次是主动脉肾神经节(12.76％),交感干神经节最少(5.16％)。4.肾交感神经节后神经元,多呈圆形或椭圆形,交感干神经节中有少量呈梭形。5.支配肾周腹膜的交感神经节后神经元与肾交感神经节后神经元存在部位、数量和在各种神经节内分布形式均不相同。     

Association between attention deficit hyperactivity disorder and the DXS7 locus

Attention deficit hyperactivity disorder (ADHD) is a prevalent disorder in children. The etiology of this disease is not clear. Genetics studies have suggested the involvement of the dopamine DRD-4 receptor gene and dopamine transporter gene (DAT1). Clinical studies have shown that monoamine oxidase-B (MAO-B) inhibitors are effective in the treatment of ADHD. These findings suggest that monoamine oxidase (MAO) genes might be involved in the origin of ADHD. In the present work, the DXS7 locus of chromosome X, which is closely linked to MAO genes, was selected as a marker to study the possible association between ADHD and MAO genes in the Chinese population. Haplotype-based haplotype relative risk (HHRR) and the transmission disequilibrium test (TDT) methods were employed to analyze the association and the linkage disequilibrium, respectively. Significant association (X(2) = 15.86; 1 df; P < 0.001) and linkage (X(2) = 14.88; 1 df; P < 0.001) were detected between the 157-bp allele of the DXS7 locus and the DSM-III-R-diagnosed ADHD (N = 72) in trios composed of father, mother, and affected offspring. The data suggested that ADHD was associated and in linkage with DXS7 locus.     

Postischaemic changes in protein synthesis in the rat brain: effects of hypothermia

Protein synthesis, measured as [¹⁴C]-leucine incorporation into proteins, was studied in the normothermic rat brain following 15 min of transient cerebral ischaemia and 1 h, 24 h and 48 h of recirculation, and in the hypothermic (33°C) brain following 1 h and 48 h of recirculation. Ischaemia was induced by bilateral common carotid occlusion combined with hypotension. Following normothermic ischaemia, incorporation of [¹⁴C]-leucine was depressed by 40–80% at 1 h of recirculation in all brain regions studied. At 48 h postischaemia, incorporation returned to normal or above normal levels in the inner layers of neocortex, the CA3 region, the striatum and the dentate gyrus, while in the outer layers of neocortex and in the hippocampal CA1 region the incorporation was persistently decreased by 26% and 40% respectively. At 24 and 48 h postischaemia, protein synthesis in the CA1 region and the striatum could be attributed to proliferating microglia. Intra-ischaemic hypothermia ameliorated the persistent depression of protein synthesis in the CA1 region at 48 h postischaemia, and a two-fold increase compared to the normothermic group was observed both in the CA1 region and the striatum. In the cortex, eucaryotic initiation factor 2 activity transiently decreased at 30 min postischaemia. In animals subjected to intra-ischaemic hypothermia, the eucaryotic initiation factor 2 activity was reduced by 50% of control at 30 min of recirculation compared with 77% in normothermic animals. We conclude that the postischaemic depression of protein synthesis is in part caused by a decrease in eucaryotic initiation factor 2 activity. The early postischaemic depression may reflect a reaction of the tissue to stress, while the late persistent depression, which is normalised by intra-ischaemic hypothermia, may be related to the mechanism of cell death.     

Mineralization behaviour of collagen type I immobilized on different substrates

Collagen type I as a robust fibre protein and main component of the extracellular matrix of most tissues is increasingly utilized for surface engineering of biomaterials using different immobilization methods. In the present work we studied the mineralization behaviour of fibrillar collagen type I in simulated body fluid as a measure for conformational changes caused by adsorptive immobilization or immobilization by partial incorporation into the anodic oxide layer on c.p.-titanium using microscopic and vibration spectroscopic methods. Adsorptive immobilization on highly oriented pyrolytic graphite (HOPG) and c.p.-titanium without collagen were used as references. In the initial phase (1-24 h) the kinetics of formation and the morphology of calcium phosphate phases (CPP) are strongly influenced both by the substrate and the immobilization method. Compared to HOPG both types of immobilization on titanium increasingly inhibit the formation of CPP. For longer times (30 d) these initial differences disappear-mineralization product on titanium, irrespective of the presence of collagen, is a mixture of amorphous calcium phosphate and octacalcium phosphate. Contrary to this the mineralization of HOPG substrates results in hydroxy apatite. This is discussed with respect to the conditions during the immobilization as well as the resulting interactions between substrate and immobilized collagen. It is shown that the mineralization process exhibits a high sensitivity with respect to conformational changes caused by these interactions. Possible cell biological relevance of these conformational changes is discussed.     

Bacterial superantigen-treated intestinal epithelial cells upregulate heat shock proteins 25 and 72 and are resistant to oxidant cytotoxicity

While the pathological events evoked by infection are commonly described, effective host responses to bacteria and their products should primarily be protective. Heat shock protein (Hsp) expression is upregulated by many stimuli and serves to maintain intracellular protein integrity. The ability of the prototypic superantigen, Staphylococcus aureus enterotoxin B (SEB) to induce Hsps was investigated with BALB/c mice and by in vitro addition to the murine small intestinal epithelial cell line MSIE. SEB-treated (5 or 100 microg intraperitoneally) mice revealed increased Hsp25 and Hsp72, but not Hsc73, in jejunal lymphocytes and epithelial cells. A similar Hsp response to SEB occurred in MSIE cells and was preceded by activation of the ERK1/2 and p38 mitogen-activated protein kinases but not the SAPK/JNK pathway; pharmacological inhibition of ERK1/2, but not p38, significantly reduced SEB-induced Hsps. Moreover, SEB-treated MSIE cells were protected against oxidant-induced cytotoxicity (measured by 51Cr release) and F-actin depolymerization. Thus, SEB exposure results in a rapid induction of the Hsp25 and Hsp72 in intestinal epithelial cells, both directly and through lymphocyte activation, and we suggest that this event is important in protecting the gut from damage by Staphylococcus infection or in the reparatory process and may be a generalized response to lumen-derived bacterial toxins.