NaCl胁迫对美国白蜡幼苗部分生理指标的影响

美国白蜡(Fraxinus americana Linn.)为木犀科(Oleaceae)白蜡树属(Fraxinus Linn.)落叶乔木,原产加拿大南部和美国,其干形通直、树形美观,是水土保持和庭院绿化的优良树种[1],具有较为突出的耐干旱和耐盐碱能力[2]。目前对美国白蜡耐盐能力的研究主要集中于引种试验和树种对比方面[2-4]。郝明灼等[5]的研究结果显示:在NaCl胁迫条件下美国白蜡叶肉细胞超微结构无明显损伤,显示出较强的耐盐能力。为进一步探讨美国白蜡耐盐的生理机制,作者以美国白     

血流感中的病原菌分布及耐药性分析

目的了解血流感染中的病原菌种类、分布及耐药性,为临床合理选用抗菌药物提供依据。方法按照无菌操作方法采集疑为血流感染患者的血液标本进行血培养,采用美国BD公司PHOENIX-100全自动细菌鉴定药敏系统进行细菌鉴定及药敏试验,并对结果进行统计分析。结果共检出1080株病原菌,其中革兰阴性杆菌630株（占58．3％）,革兰阳性球菌428株（占39．6％）,真菌22株（占2．1％）。药敏结果显示：革兰阳性球菌对万古霉素、利奈唑胺敏感率最高,对青霉素、红霉素、头孢菌素等耐药率较高。革兰阴性杆菌对碳青霉烯类、哌拉西林／他唑巴坦、头孢哌酮／舒巴坦敏感率较高,对青霉素类、头孢菌素类和喹诺酮类耐药率较高。结论引起血流感染的病原菌分布复杂,耐药率较高,临床应提高血培养送检率,根据药敏结果合理选用抗菌药物,以减少多重耐药菌的发生和传播。     

血清降钙素原在小儿早期中枢神经系统感染鉴别诊断中的价值

目的研究细菌性脑膜炎和病毒性脑炎患儿血清降钙素原（PCT）水平的变化,探讨其在小儿早期中枢神经系统感染鉴别诊断中的价值。方法采用双抗夹心免疫发光测量法,检测78例早期中枢神经系统感染患儿的血清及脑脊液降钙素原水平,分析它们之间的相关性;并和脑脊液白细胞数、血白细胞数、血清C反应蛋白相对比;PCT阳性细菌性脑膜炎患儿使用抗生素治疗后再测定血清PCT。结果33例急性细菌性脑膜炎患儿的血清降钙素原浓度为（18．46±9．18）ng／mL,45例急性病毒性脑炎的血清降钙素原水平轻度升高（0．58±0．31）ng／mL,P〈0．01,两者相比较差异有统计学意义。细菌性脑膜炎组患儿血清PCT在经过抗生素治疗后较入院时明显下降,两者比较差异有统计学意义（P〈0．05）。并且在细菌组急性期脑脊液PCT与血清PCT存在正相直线相关性。结论血清降钙素原检测在小儿早期中枢神经系统感染鉴别诊断中有重要应用价值。     

褶皱臂尾轮虫同胞物种复合类群分类的研究进展

褶皱臂尾轮虫包含复杂的同胞物种,对其分类研究经过了一个长期发展的过程。综述了轮虫分类手段的发展进程,介绍和分析了轮虫特别是褶皱臂尾轮虫同胞物种复合类群分类的研究进展。褶皱臂尾轮虫的L-型和S-型属于B.plicatilis和B.rotundiformis两个物种。这个复合类群中还包括更多的种类,如B.plicatilis sensu stricto、B.ibericus和B.rotundiformis,其中B.plicatilis sensu stricto属于L型,B.ibericus属于SM-型,B.rotundiformis属于SS-型。此类研究丰富了轮虫系统分类学,提高了水域生态调查的准确性。     

Rip3 knockdown rescues photoreceptor cell death in blind pde6c zebrafish

Achromatopsia is a progressive autosomal recessive retinal disease characterized by early loss of cone photoreceptors and later rod photoreceptor loss. In most cases, mutations have been identified in CNGA3, CNGB3, GNAT2, PDE6C or PDE6H genes. Owing to this genetic heterogeneity, mutation-independent therapeutic schemes aimed at preventing cone cell death are very attractive treatment strategies. In pde6c^w59 mutant zebrafish, cone photoreceptors expressed high levels of receptor-interacting protein kinase 1 (RIP1) and receptor-interacting protein kinase 3 (RIP3) kinases, key regulators of necroptotic cell death. In contrast, rod photoreceptor cells were alternatively immunopositive for caspase-3 indicating activation of caspase-dependent apoptosis in these cells. Morpholino gene knockdown of rip3 in pde6c^w59 embryos rescued the dying cone photoreceptors by inhibiting the formation of reactive oxygen species and by inhibiting second-order neuron remodelling in the inner retina. In rip3 morphant larvae, visual function was restored in the cones by upregulation of the rod phosphodiesterase genes (pde6a and pde6b), compensating for the lack of cone pde6c suggesting that cones are able to adapt to their local environment. Furthermore, we demonstrated through pharmacological inhibition of RIP1 and RIP3 activity that cone cell death was also delayed. Collectively, these results demonstrate that the underlying mechanism of cone cell death in the pde6c^w59 mutant retina is through necroptosis, whereas rod photoreceptor bystander death occurs through a caspase-dependent mechanism. This suggests that targeting the RIP kinase signalling pathway could be an effective therapeutic intervention in retinal degeneration patients. As bystander cell death is an important feature of many retinal diseases, combinatorial approaches targeting different cell death pathways may evolve as an important general principle in treatment.     

Ubiquitination of Inositol-requiring Enzyme 1 (IRE1) by the E3 Ligase CHIP Mediates the IRE1/TRAF2/JNK Pathway

Deciphering the inositol-requiring enzyme 1 (IRE1) signaling pathway is fundamentally important for understanding the unfolded protein response (UPR). The ubiquitination of proteins residing on the endoplasmic reticulum (ER) membrane has been reported to be involved in the UPR, although the mechanism has yet to be fully elucidated. Using immunoprecipitation and mass spectrometry, IRE1 was identified as a substrate of the E3 ligase CHIP (carboxyl terminus of HSC70-interacting protein) in HEK293 cells under geldanamycin-induced ER stress. Two residues of IRE1, Lys⁵⁴⁵ and Lys⁸²⁸, were targeted for Lys⁶³-linked ubiquitination. Moreover, in CHIP knockdown cells, IRE1 phosphorylation and the IRE1-TRAF2 interaction were nearly abolished under ER stress, which may be due to lacking ubiquitination of IRE1 on Lys⁵⁴⁵ and Lys⁸²⁸, respectively. The cellular responses were evaluated, and the data indicated that CHIP-regulated IRE1/TRAF2/JNK signaling antagonized the senescence process. Therefore, our findings suggest that CHIP-mediated ubiquitination of IRE1 contributes to the dynamic regulation of the UPR.     

Tyr-301 Phosphorylation Inhibits Pyruvate Dehydrogenase by Blocking Substrate Binding and Promotes the Warburg Effect

The mitochondrial pyruvate dehydrogenase complex (PDC) plays a crucial role in regulation of glucose homoeostasis in mammalian cells. PDC flux depends on catalytic activity of the most important enzyme component pyruvate dehydrogenase (PDH). PDH kinase inactivates PDC by phosphorylating PDH at specific serine residues, including Ser-293, whereas dephosphorylation of PDH by PDH phosphatase restores PDC activity. The current understanding suggests that Ser-293 phosphorylation of PDH impedes active site accessibility to its substrate pyruvate. Here, we report that phosphorylation of a tyrosine residue Tyr-301 also inhibits PDH α 1 (PDHA1) by blocking pyruvate binding through a novel mechanism in addition to Ser-293 phosphorylation. In addition, we found that multiple oncogenic tyrosine kinases directly phosphorylate PDHA1 at Tyr-301, and Tyr-301 phosphorylation of PDHA1 is common in EGF-stimulated cells as well as diverse human cancer cells and primary leukemia cells from human patients. Moreover, expression of a phosphorylation-deficient PDHA1 Y301F mutant in cancer cells resulted in increased oxidative phosphorylation, decreased cell proliferation under hypoxia, and reduced tumor growth in mice. Together, our findings suggest that phosphorylation at distinct serine and tyrosine residues inhibits PDHA1 through distinct mechanisms to impact active site accessibility, which act in concert to regulate PDC activity and promote the Warburg effect.