侵袭性真菌深部感染的早期实验室诊断

目的探讨假丝酵母菌甘露聚糖抗原和假丝酵母菌IgG/IgM抗体、曲霉半乳甘露聚糖抗原和烟曲霉IgG抗体在侵袭性真菌病早期临床诊断中的应用价值。方法收集已确诊侵袭性假丝酵母菌病患者18例,侵袭性烟曲霉病患者6例,单纯细菌感染患者20例,浅部真菌感染患者20例,健康体检者(正常对照组)20例,通过酶联免疫吸附法(ELISA)检测患者血清甘露聚糖和假丝酵母菌IgG/IgM抗体以及曲霉半乳甘露聚糖抗原和烟曲霉IgG抗体浓度,计算各指标的灵敏度、特异度、阳性预测值、阴性预测值和受试者工作特征(ROC)曲线下面积。结果甘露聚糖抗原和假丝酵母菌IgG/IgM抗体联合测定的敏感度为66.7%,特异度为83.3%,阴性预测值为100.0%,阳性预测值为85.7%,ROC曲线下面积为0.992(95%CI:0.974~1.000);半乳甘露聚糖抗原和烟曲霉IgG抗体联合测定的敏感度为66.7%,特异度为95.0%,阴性预测值为98.2%,阳性预测值为100.0%,ROC曲线下面积为0.978(95%CI:0.934~1.000)。结论甘露聚糖抗原和假丝酵母菌IgG/IgM抗体、半乳甘露聚糖抗原和烟曲霉IgG抗体联合检测对深部真菌感染的早期诊断具有重要意义。     

Theoretical studies on the Mo-catalyzed asymmetric intramolecular Pauson-Khand-type [2?+?2?+?1] cycloadditions of 3-allyloxy-1-propynylphosphonates

Density functional theory (DFT) was used to investigate the Mo-catalyzed intramolecular Pauson-Khand reaction of 3-allyloxy-1-propynylphosphonates. All intermediates and transition states were optimized completely at the B3LYP/6-31 G(d,p) level [LANL2DZ(f) for Mo]. In the Mo-catalyzed intramolecular Pauson-Khand reaction, the C–C oxidative cyclization reaction was the chirality-determining step, and the reductive elimination reaction was the rate-determining step. The carbonyl insertion reaction into the Mo–C(sp(3)) bondwas easier than into the Mo–C=C bond. And the dominant product predicted theoretically was of (S)-chirality, which agreed with experimental data. This reaction was solventd ependent, and toluene was the best among the three solvents toluene, CH3CN, and THF.     

Diversity,structure and function of the coiled‐coil domains of plant NLR immune receptors

Plant nucleotide‐binding, leucine‐rich repeat receptors (NLRs) perceive pathogen avirulence effectors and activate defense responses. Nucleotide‐binding, leucine‐rich repeat receptors are classified into coiled‐coil (CC)‐containing and Toll/interleukin‐1 receptor (TIR)‐containing NLRs. Recent advances suggest that NLR CC domains often function in signaling activation, especially for induction of cell death. In this review, we outline our current understanding of NLR CC domains, including their diversity/classification and structure, their roles in cell death induction, disease resistance, and interaction with other proteins. Furthermore, we provide possible directions for future work.     

LncRNA-135528 inhibits tumor progression by up-regulating CXCL10 through the JAK/STAT pathway

Spontaneous tumor regression can be observed in many tumors, however, studies related to the altered expression of lncRNA in spontaneous glioma regression are limited, and the potential contributions of lncRNAs to spontaneous glioma regression remain unknown. To investigate the biological roles of lncRNA-135528 in spontaneous glioma regression. The cDNA fragment of lncRNA-135528 was obtained by rapid-amplification of cDNA ends (RACE) technology and cloned into the plvx-mcmv-zsgreen-puro vector. Additionally, we stably silenced or overexpressed lncRNA-135528 in G422 cells by transfecting with siRNA against lncRNA-135528 or lncRNA-135528 overexpression plasmid. Then, we examined lncRNA-135528 overexpressing and lncRNA-135528 silencing on glioma cells and its effects on CXCL10 and JAK/STAT pathways. The main findings indicated that lncRNA-135528 promoted glioma cell apoptosis, inhibited cell proliferation and arrested cell cycle progression; the up-regulation of lncRNA135528 led to significantly increased CXCL10 levels and the differential expression of mRNA associated with JAK/STAT pathway in glioma cells. lncRNA-135528 can inhibit tumor progression by up-regulating CXCL10 through the JAK/STAT pathway.     

Fasting up‐regulates ferroportin 1 expression via a Ghrelin/GHSR/MAPK signaling pathway

The significant positive correlation between ghrelin and iron and hepcidin levels in the plasma of children with iron deficiency anemia prompted us to hypothesize that ghrelin may affect iron metabolism. Here, we investigated the effects of fasting or ghrelin on the expression of hepcidin, ferroportin 1 (Fpn1), transferrin receptor 1 (TfR1), ferritin light chain (Ft‐L) proteins, and ghrelin, and also hormone secretagogue receptor 1 alpha (GHSR1α) and ghrelin O‐acyltransferase (GOAT) mRNAs in the spleen and/or macrophage. We demonstrated that fasting induces a significant increase in the expression of ghrelin, GHSR1α, GOAT, and hepcidin mRNAs, as well as Ft‐L and Fpn1 but not TfR1 proteins in the spleens of mice in vivo. Similar to the effects of fasting on the spleen, ghrelin induced a significant increase in the expression of Ft‐L and Fpn1 but not TfR1 proteins in macrophages in vitro. In addition, ghrelin was found to induce a significant enhancement in phosphorylation of ERK as well as translocation of pERK from the cytosol to nuclei. Furthermore, the increased pERK and Fpn1 induced by ghrelin was demonstrated to be preventable by pre‐treatment with either GHSR1α antagonist or pERK inhibitor. Our findings support the hypothesis that fasting upregulates Fpn1 expression, probably via a ghrelin/GHSR/MAPK signaling pathway.     

Knockdown of RPL34 inhibits the proliferation and migration of glioma cells through the inactivation of JAK/STAT3 signaling pathway

Ribosomal protein L34 (RPL34), belonging to the L34E family of ribosomal proteins, was reported to be dysregulated in several types of cancers and plays important roles in tumor progression. However, the expression and roles of RPL34 in human glioma remain largely unknown. Thus, the objective of this study was to investigate the expression and role of RPL34 in glioma. We report here that RPL34 is highly expressed in human glioma tissues and cell lines. Knockdown of RPL34 markedly inhibited the proliferation, migration, and invasion, as well as prevented the epithelial-mesenchymal transition phenotype in glioma cells. Further, mechanistic analysis showed that knockdown of RPL34 significantly downregulated the levels of p-JAK and p-STAT3 in glioma cells. Taken together, our findings indicated that knockdown of RPL34 inhibits the proliferation and migration of glioma cells through the inactivation of JAK/STAT3 signaling pathway. Thus, RPL34 may serve as a potential therapeutic target for the treatment of glioma.