Late Quaternary environmental and climate history of Rauer Group, East Antarctica

The Rauer Group is an archipelago in Prydz Bay, East Antarctica. The ice-free islands and the surrounding shallow marine areas provide valuable archives for the reconstruction of the late Pleistocene and Holocene environmental and climatic history of the region. Two sediment records from two marine inlets of Rauer Group have been studied for their sedimentological, geochemical, and biological characteristics. Radiocarbon ages from one of the inlets indicate ice-free conditions within the last glacial cycle, probably during the second half of Marine Isotope Stage 3. Subsequent ice sheet coverage of Rauer Group during the Last Glacial Maxiumum (LGM) can be inferred from a till layer recovered in one of the basins. The inlets became ice-free prior to 11,200 cal yr BP, when biogenic sedimentation started. Deglacial processes in the catchments, however, influenced the inlets until ~ 9200 cal yr BP as evidenced by the input of minerogenic material. Marine productivity under relatively open water conditions indicates an early Holocene climate optimum until 8200 cal yr BP, which is followed by a cooler period with increased sea ice. Warmer conditions are inferred for the mid Holocene, when both basins experienced an input of freshwater between ~ 5700-3500 cal yr BP, probably due to ice-sheet melting and increased precipitation on the islands. Neoglacial cooling in the late Holocene since c. 3500 cal yr BP is reflected by an increase in sea ice in both inlets.     

自由基与细胞凋亡

细胞凋亡是指细胞在生理和病理情况下的一种死亡模式,广泛涉及到肿瘤、衰老和退行性病变等一系列疾病．最近有实验表明自由基与细胞凋亡有密切的关系．凋亡细胞内活性氧自由基（ROS）生成增加,同时消除ROS的能力下降.大多数凋亡障碍的细胞表现出ROS分子大量减少,若调节细胞内ROS含量,死亡率能随之改变;离子辐射能通过经自由基引起细胞的凋亡,培养细胞在无血清或撤除生长因子后发生的死亡也大多与细胞内自由基代谢酶如过氧化氢酶等的活性变化有关.提示自由基是参与调节细胞凋亡的重要因素之一.     

The Effect of Bovine IFN-α on the Immune Response in Guinea Pigs Vaccinatedwith DNA Vaccine of Foot-and-Mouth Disease Virus

Foot-and-mouth disease virus (FMDV) belongs to thegenus Aphthovirus of the family Picornavidae. The FMDVgenome is a copy of positive-sense, single-stranded RNA,which contains one large open reading frame (ORF). TheORF is translated into a polypeptide, which undergoesautoproteolytic cleavage to produce the structural and non-structural proteins and ultimately forms mature viral pro-teins [1,2]. FMD is caused by the FMDV, which is a highly conta-gious vesicular disease of cloven-hoofe…     

Red cell genotyping and the future of pretransfusion testing

The ABO blood group, based on molecular biological detection technology, has the advantages of simple operation, high sensitivity, and standardized result interpretation, and is not affected by sample immunological characteristics. However, clinically, performance verification, clinical application scope, quality management, abnormal result processing, and other issues associated with the ABO blood group molecular detection technology are relatively complex, and there is a lack of unified norms and standards. Therefore, from the perspective of the whole process of ABO molecular biology detection, this study aims to provide standardized opinions on important links affecting the detection results, common problems encountered in the detection process, and the assessment and treatment of abnormal results. Finally, a Chinese expert consensus on molecular biological technology based on genotyping and sequencing detection was put forward, which standardizes the detection process, improves the accuracy of results, and promotes the development of technology and broader clinical application.     

兰州市北山不同林地春夏季土壤纤毛虫群落特征

为了研究兰州市北山绿化工程的植被恢复状况,于2016年4月和7月,对北山罗九公路绿化工程区的人工林及荒坡、半荒坡共6个样点进行野外调查采样,分析土壤纤毛虫群落组成及其影响因素。研究结果表明:(1)春季有10纲21目34科44属80种,夏季10纲21目38科54属104种。春夏季的优势类群均为尖毛科(Plagiocampidae),优势种为膨胀肾形虫(Colpoda inflate)和盘状肾形虫(Colpoda patella)。(2)土壤纤毛虫的丰度、物种数和多样性指数夏季高于春季,且人工林样点的土壤纤毛虫的丰度、物种数和多样性指数均高于荒坡;(3)春季土壤有机碳、土壤温度和电导率是影响土壤纤毛虫物种数分布的主要环境因子;夏季土壤有机碳、土壤温度及pH是影响土壤纤毛虫物种数分布的主要因子。总体而言,人工林土壤恢复较荒坡、半荒坡好,而人工林中杨树林和侧柏林的土壤环境质量较优。     

Upregulation of long noncoding TNFSF10 contributes to osteoarthritis progression through the miR-376-3p/FGFR1 axis

Osteoarthritis (OA) is a common joint disease with high morbidity, but there is still no definitive treatment for it. Long noncoding RNAs (lncRNAs) have been confirmed to play key roles in OA progression. This work was done to investigate the roles and action mechanism of lncRNA TNFSF10 in OA. The messenger RNA levels of TNFSF10 in articular cartilage samples from patients or chondrocytes were detected by Quantitative real-time PCR assay (qRT-PCR). The effects of TNFSF10 on chondrocytes were evaluated on the basis of cell growth, apoptosis, and inflammation. Then, the interaction between TNFSF10 and miR-376-3p was explored by dual-luciferase reporter test, RNA-binding protein immunoprecipitation, and RNA pull-down assay. Finally, various cell experiments, Western blot analysis, and qRT-PCR were performed to study the interaction among TNFSF10, miR-376-3p, and fibroblast growth factor receptor 1 (FGFR1). It was found that TNFSF10 was upregulated in OA cartilages and stimulated cell proliferation, antiapoptosis, and inflammation for chondrocytes. In addition, TNFSF10 acted as a competing endogenous RNA to downregulate miR-376-3p, and the influence of TNFSF10 on chondrocytes was partly reversed by miR-376-3p. Moreover, FGFR1, as a target of miR-376-3p, had reversal functions on the outcomes mediated by miR-376-3p. The further analysis displayed that there was a negative relationship between TNFSF10 and miR-376-3p as well as miR-376-3p and FGFR1, while FGFR1 was positively related with TNFSF10. Altogether, TNFSF10 overexpression probably stimulated proliferation and inflammation, and inhibited apoptosis by regulating the miR-376-3p/FGFR1 axis, implying that its increase contributed to OA progression. Our study provided a new potential biomarker or therapeutic target-TNFSF10, which was helpful to develop an efficient approach to cure OA.     

Up-Regulation of the Biosynthesis and Release of Substance P through Wnt/β-Catenin Signaling Pathway in Rat Dorsal Root Ganglion Cells

To examine regulatory effects of β-catenin on the biosynthesis and release of substance P, a rat chronic constriction injury (CCI) model and a rat dorsal root ganglion (DRG) cell culture model were used in the present study. The CCI treatment significantly induced the overall expression of β-catenin (158 ± 6% of sham) in the ipsilateral L5 DRGs in comparison with the sham group (109 ± 4% of sham). The CCI-induced aberrant expression of β-catenin was significantly attenuated by oral administration of diclofenac (119 ± 6% of the sham value; 10 mg/kg). Importantly, aberrant nuclear accumulation of β-catenin in cultured DRG cells resulted in up-regulation of the PPT-A mRNA expression and the substance P release. The up-regulation of both the PPT-A mRNA expression and the substance P release by either a GSK-3β inhibitor TWS119 (10 μM) or a Wnt signaling agonist Wnt-3a (100 ng/ml) were significantly abolished by an inhibitor of cyclooxygenase-2 (COX-2; NS-398, 1 μM). Collectively, these data suggest that nociceptive input-activated β-catenin signaling plays an important role in regulating the biosynthesis and release of substance P, which may contribute to the inflammation responses related to chronic pain.     

Overexpression of fibroblast growth factor‐21 (FGF‐21) protects mesenchymal stem cells against caspase‐dependent apoptosis induced by oxidative stress and inflammation

The clinical application of stem cells offers great promise as a potential avenue for therapeutic use in neurodegenerative diseases. However, cell loss after transplantation remains a major challenge, which currently plagues the field. On the basis of our previous findings that fibroblast growth factor 21 (FGF‐21) protected neurons from glutamate excitotoxicity and that upregulation of FGF‐21 in a rat model of ischemic stroke was associated with neuroprotection, we proposed that overexpression of FGF‐21 protects bone marrow‐derived mesenchymal stem cells (MSCs) from apoptosis. To test this hypothesis, we examined whether the detrimental effects of apoptosis can be mitigated by the transgenic overexpression of FGF‐21 in MSCs. FGF‐21 was transduced into MSCs by lentivirus and its overexpression was confirmed by quantitative polymerase chain reaction. Moreover, FGF‐21 overexpression did not stimulate the expression of other FGF family members, suggesting it does not activate a positive feedback system. The effects of hydrogen peroxide (H₂O₂), tumor necrosis factor‐α (TNF‐α), and staurosporine, known inducers of apoptosis, were evaluated in FGF‐21 overexpressing MSCs and mCherry control MSCs. Caspases 3 and 7 activity was markedly and dose‐dependently increased by all three stimuli in mCherry MSCs. FGF‐21 overexpression robustly suppressed caspase activation induced by H₂O₂ and TNF‐α, but not staurosporine. Moreover, the assessment of apoptotic morphological changes confirmed the protective effects of FGF‐21 overexpression. Taken together, these results provide compelling evidence that FGF‐21 plays a crucial role in protecting MSCs from apoptosis induced by oxidative stress and inflammation and merits further investigation as a strategy for enhancing the therapeutic efficacy of stem cell‐based therapies.     

A Motif from Lys216 to Lys222 in Human BUB3 Protein Is a Nuclear Localization Signal and Critical for BUB3 Function in Mitotic Checkpoint

Human BUB3 is a key mitotic checkpoint factor that recognizes centromeric components and recruits other mitotic checkpoint molecules to the unattached kinetochore. The key amino acid residues responsible for its localization are not yet defined. In this study, we identified a motif from Lys²¹⁶ to Lys²²² in BUB3 as its nuclear localization signal. A BUB3 mutant with deletion of this motif (Del216–222) was found to localize to both the cytoplasm and the nucleus, distinct from the exclusively nuclear distribution of wild-type BUB3. Further analysis revealed that residues Glu²¹³, Lys²¹⁶, Lys²¹⁷, Lys²¹⁸, Tyr²¹⁹, and Phe²²¹, but not Lys²²², contribute to nuclear localization. Interestingly, the nuclear localization signal was also critical for the kinetochore localization of BUB3. The deletion mutant Del216–222 and a subtle mutant with four residue changes in this region (E213Q/K216E/K217E/K218E (QE)) did not localize to the kinetochore efficiently or mediate mitotic checkpoint arrest. Protein interaction data suggested that the QE mutant was able to interact with BUB1, MAD2, and BubR1 but that its association with the centromeric components CENP-A and KNL1 was impaired. A motif from Leu⁶¹ to Leu⁶⁵ in CENP-A was found to be involved in the association of BUB3 and CENP-A in cells; however, further assays suggested that CENP-A does not physically interact with BUB3 and does not affect BUB3 localization. Our findings help to dissect the mechanisms of BUB3 in mitotic checkpoint signaling.