Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update

Taurine appears to have multiple functions in the brain participating both in volume regulation and neurotransmission. In the latter context it may exert its actions by serving as an agonist at receptors of the GABAergic and glycinergic neurotransmitter systems. Its interaction with GABA_A and GABA_B receptors as well as with glycine receptors is reviewed and the physiological relevance of such interactions is evaluated. The question as to whether local extracellular concentrations of taurine are likely to reach the threshold level for the pertinent receptor populations cannot presently be answered satisfactorily. Hence more sophisticated analytical methods are warranted in order to obtain a definite answer to this important question. Special issue dedicated to Dr. Simo S. Oja     

胭脂花野生居群花粉形态多样性研究

胭脂花是分布于中国北部的报春花科报春花属花柱二型植物,为了阐明胭脂花花粉形态的多样性,对胭脂花分布范围内的7个野生居群的花粉形态进行了测定。结果表明,胭脂花花粉属N3P4C5型,极面观多为三角形,具三孔沟,少数为四边形,具4孔沟;短花柱植株的花粉粒较大(16.53×17.58μm),花粉粒外壁粗糙,表面纹饰多,网眼大;长花柱植株的花粉粒较小(12.95×13.72μm),花粉粒外壁较光滑,表面纹饰少,网眼小。不同居群间花粉粒在大小、网眼直径、外壁纹饰等方面存在显著差异,花粉形态变异系数在4.88%~35.48%之间;短花柱类型各居群的平均变异系数为16.18%,居群间差异较大,其中庞泉沟居群变异系数最大(24.05%),海坨山居群最小(10.13%);长花柱类型各居群的平均变异系数为14.89%,庞泉沟居群的变异系数最大(19.75%),五台山与海坨山居群最小(12.50%),长花柱类型的花粉性状比短花柱植株更为稳定。UPGMA聚类分析发现,7个居群聚为两大类,除庞泉沟居群外,其他居群聚为一组,地理距离相近的居群一般聚在一起。研究结果为胭脂花种质资源遗传多样性及育种研究提供了依据。     

石质文物微生物检测技术的研究进展

本论文针对国内外最新的石质文物微生物的检测技术进行了论述,主要包括核酸分析鉴定方法、细胞膜分析法、次级代谢产物分析法和传统培养法等。并综合比较各种方法的优势和不足,对石质文物的生物保护提出展望。石质文物微生物的无损或微损快速检测技术的建立,对于进一步清理石质文物的微生物污染,有效防治微生物对石质文物的腐蚀,保护我国宝贵的文化遗产具有重要的意义。     

一种动物实验监控系统的设计

本文主要设计动物生命体征参数（体温、呼吸率和脉搏率）的监控系统。硬件电路采用MSP430F5438芯片作为微控制器,体温、呼吸和脉搏生理参数的信号采集使用了相应的信号调理电路和处理电路,主要由电信号转换电路、放大滤波电路、AD转换电路、脉冲转换电路、LCD显示电路、加热垫和蜂鸣器驱动电路等组成。     

人口腔鳞癌组织中HIF—1a和NF—κB的表达及意义

目的：探讨缺氧诱导因子（HIF—1a）和核因子-κB（NF—κB）口腔鳞癌中的表达及相互关系,研究它们的表达与肿瘤临床病理指标的联系。方法：应用SP染色法检测HIF—1a和NF—κB在49例口腔鳞癌组织、10例正常口腔黏膜组织中的阳性率。结果在口腔鳞癌中HIF—1a和NF—κB的阳性表达率分别为80．0％和78．4％,其阳性率及表达等级均显著高于正常对照组（P〈0．05）,在中-低分化组和有淋巴结转移组中的表达显著高于高分化组和无淋巴结转移组（P〈0．05）。HIF—1a表达与NF—κB表达成等级正相关（r=0．45,P〈0．05）。结论：HIF-1a或NF—κB与口腔鳞癌生物学行为有密切关系,二者的联合检测,有助于口腔鳞癌恶性程度和生物学特性的判断。     

人口腔鳞癌组织中HIF-1a和NF-kB的表达及意义

目的:探讨缺氧诱导因子(HIF-1a)和核因子-KB(NF-KB)口腔鳞癌中的表达及相互关系,研究它们的表达与肿瘤临床病理指标的联系.方法:应用SP染色法检测HIF-1a和NF-KB在49例口腔鳞癌组织、10例正常口腔黏膜组织中的阳性率.结果在口腔鳞癌中HIF-1a和NF-KB的阳性表达率分别为80.0%和78.4%,其阳性率及表达等级均显著高于正常对照组(P<0.05),在中一低分化组和有淋巴结转移组中的表达显著高于高分化组和无淋巴结转移组(P<0.05).HIF-1a表达与NF-KB表达成等级正相关(r=0.45,P<0.05).结论:HIF-1a或NF-KB与口腔鳞癌生物学行为有密切关系,二者的联合检测,有助于口腔鳞癌恶性程度和生物学特性的判断.     

The Role of Protein Kinase C and Cyclic AMP in the Ammonia-Induced Shift of the Taurine Uptake/Efflux Balance Towards Efflux in C6 Cells

A previous study showed that treatment of C6 glioma cells with 10 mM ammonium chloride (ammonia) for 24 h decreases taurine uptake and evokes sodium-dependent taurine efflux, indicating reversal of the taurine transporter (TauT)-mediated transport as an underlying mechanism. Consistent with the involvement of TauT we now show that the ammonia-induced changes in Tau uptake and efflux are inhibited by the protein kinase C (PKC) activator phorbol 12,13-dibutyrate (PDBu). Ammonia treatment of C6 cells resulted in increased intracellular accumulation of cAMP. Incubation of the cells with dibutyryl cAMP (dbcAMP) mimicked the effects of ammonia on both taurine uptake and efflux. The effects of dbcAMP on taurine uptake and efflux were additive to the effects of ammonia. Collectively, the results suggest that the effects of ammonia on taurine uptake and efflux may be partly mediated by cAMP. Consistent with this mechanism, the adenyl cyclase inhibitor, miconazole reduced the stimulation of efflux by ammonia.     

Analysis of Glutamine Accumulation in Rat Brain Mitochondria in the Presence of a Glutamine Uptake Inhibitor,Histidine, Reveals Glutamine Pools With a Distinct Access to Deamidation

Rat cerebral nonsynaptic mitochondria were incubated in medium containing 2 mM glutamine (Gln) or 2 mM glutamate (Glu), in the presence of a Gln uptake inhibitor histidine (His) as well as other basic amino acids, lysine and arginine (Lys, Arg) not inhibiting Gln uptake. Subsequently, the mitochondrial contents of Glu and Gln were determined by HPLC. Incubation in the presence of Glu alone increased the Glu content from 3.5 to 15 nmol/mg protein, without affecting the Gln content. On the other hand, incubation with Gln increased the content of Gln from 1.5 to 12 nmol/mg, and that of Glu to 10 nmol/mg. As expected, addition of His did not alter the Glu and Gln content resulting from incubation with Glu. However, His significantly decreased to almost the preincubation level the content of Glu in mitochondria incubated with Gln, without affecting the content of Gln. No other amino acid had any effect on these parameters. The results point to the existence of distinct Gln pools, one of which is accessible to external Gln via a His-sensitive transporter and is accessible for deamidation in the mitochondria.Special issue dedicated to Dr. Lawrence F. Eng.     

Whole-exome sequencing identifies novel pathogenic mutations and putative phenotype-influencing variants in Polish limb-girdle muscular dystrophy patients

Background

Limb girdle muscular dystrophies (LGMD) are a group of heterogeneous hereditary myopathies with similar clinical symptoms. Disease onset and progression are highly variable, with an elusive genetic background, and around 50% cases lacking molecular diagnosis.

Methods

Whole exome sequencing (WES) was performed in 73 patients with clinically diagnosed LGMD. A filtering strategy aimed at identification of variants related to the disease included integrative analysis of WES data and human phenotype ontology (HPO) terms, analysis of genes expressed in muscle, analysis of the disease-associated interactome and copy number variants analysis.

Results

Genetic diagnosis was possible in 68.5% of cases. On average, 36.3 rare variants in genes associated with various muscle diseases per patient were found that could relate to the clinical phenotype. The putative causative mutations were mostly in LGMD-associated genes, but also in genes not included in the current LGMD classification (DMD, COL6A2, and COL6A3). In three patients, mutations in two genes were suggested as the joint cause of the disease (CAPN3+MYH7, COL6A3+CACNA1S, DYSF+MYH7). Moreover, a variety of phenotype-influencing variants were postulated, including in patients with an identified already known primary pathogenic mutation.

Conclusions

We hypothesize that LGMD could be better described as oligogenic disorders in which dominant clinical presentation can result from the combined effect of mutations in a set of genes. In this view, the inter- and intrafamilial variability could reflect a specific genetic background and the presence of sets of phenotype-influencing or co-causative mutations in genes that either interact with the known LGMD-associated genes or are a part of the same pathways or structures.