喀斯特小流域土壤有机碳空间异质性及储量估算方法

为了准确估算土壤有机碳储量,利用网格法采集2755个土壤剖面,共计23536个土壤样品,研究了喀斯特小流域土壤有机碳含量分布特征,并以"土壤类型法"为基准,对土壤分布面积、石砾含量、岩石裸露率、土层厚度等指标进行修正,合理的优化了土壤有机碳储量计算公式,探索出一种专属于喀斯特地区土壤有机碳储量的估算方法,结果表明:不同土层深度和土壤类型下土壤有机碳含量存在明显差异,土壤有机碳含量随着土层深度的增加而逐渐减小,不同土属的有机碳含量减小的幅度有所差异,不同坡位和坡向的有机碳含量大小为:阳坡阴坡,坡中上部坡顶坡中坡中下坡坡底,不同土地利用方式下土壤有机碳含量大小顺序为:林地灌草地旱地水田;土壤有机碳含量与坡度、海拔、岩石裸露率均呈极显著正相关关系,与土层厚度、土壤容重呈显著负相关;喀斯特地区土壤异质性较大,不同修正指标对土壤有机碳储量估算的影响程度为:土壤厚度岩石裸露率石砾含量土壤有机碳含量土壤容重;通过修正后的计算公式估算出普定后寨河小流域表层20 cm土壤有机碳密度区间为3.53—5.44 kg/m~2,平均值为:1.24 kg/m~2,100 cm土壤有机碳密度区间为4.44—14.50 kg/m~2,平均值为12.12 kg/m~2,土壤有机碳储量为5.39×10~5t。     

Dysregulation of ferroptosis may involve in the development of non-small-cell lung cancer in Xuanwei area

The Xuanwei area of Yunnan Province, China, is one of the regions suffering from the highest occurrence and mortality rate of lung cancer in the world. Local residents tend to use bituminous coal as domestic fuel, which causes serious indoor air pollution and is established as the main carcinogen. After the local government carried out furnace and stove reform work, lung cancer rate including incidence and mortality among residents remains high. We herein wonder if there are specific mechanisms at protein level for the development of non-small-cell lung cancer (NSCLC) in this area. We investigated the changes of protein profiling in tumour of the patients from Xuanwei area. Tandem mass tag (TMT) was employed to screen the differential proteins between carcinoma and para-carcinoma tissues. We identified a total of 422 differentially expressed proteins, among which 162 proteins were significantly up-regulated and 260 were downregulated compared to para-carcinoma tissues. Many of the differentially expressed proteins were related to extracellular matrix (ECM)-receptor interaction, focal adhesion, PI3K/AKT pathway and ferroptosis. Further experiments on the two differential proteins, thioredoxin 2 (TXN2) and haptoglobin (HP), showed that the change of their expressions could make the lung cancer cell lines more resistant to erastin or RSL-induced ferroptosis in vitro, and promote the growth of tumour in nude mice. In conclusion, this study revealed that aberrant regulation of ferroptosis may involve in the development of lung cancer in Xuanwei area.     

CpG联合铝佐剂对HCV免疫原体液免疫作用的影响

目的:探讨胞苷酸鸟苷寡脱氧核苷酸(CpG ODN)联合铝佐剂对丙型肝炎病毒(HCV)重组免疫原的体液免疫作用。方法:采用高交叉HCV-HVR1和E1重组蛋白与CpG ODN、铝佐剂组合,免疫BALB/c小鼠后以ELISA、酶联免疫斑点测定、流式细胞术、免疫沉淀等方法检测相关体液免疫指标和免疫血清多抗的交叉反应性。结果:CpG联合铝佐剂激发了最高的特异性抗体滴度;佐剂通过提高抗体分泌细胞数量、增加脾脏中记忆B细胞数量、增加脾淋巴细胞IL-6、IL-10分泌浓度实现体液免疫增效;CpG则能提高免疫效率,联合铝佐剂时显著提高浆细胞数量;12份HCV阳性血清中有10份可与多抗HVR1 IgG发生免疫沉淀。结论:CpG和铝佐剂联合应用具有协同作用,多抗HVR1 IgG具有较好的交叉反应性。     

Heat Shock Protein 70 Prevents Hyperoxia-Induced Disruption of Lung Endothelial Barrier via Caspase-Dependent and AIF-Dependent Pathways

Exposure of pulmonary artery endothelial cells (PAECs) to hyperoxia results in a compromise in endothelial monolayer integrity, an increase in caspase-3 activity, and nuclear translocation of apoptosis-inducing factor (AIF), a marker of caspase-independent apoptosis. In an endeavor to identify proteins involved in hyperoxic endothelial injury, we found that the protein expression of heat-shock protein 70 (Hsp70) was increased in hyperoxic PAECs. The hyperoxia-induced Hsp70 protein expression is from hspA1B gene. Neither inhibition nor overexpression of Hsp70 affected the first phase barrier disruption of endothelial monolayer. Nevertheless, inhibition of Hsp70 by using the Hsp70 inhibitor KNK437 or knock down Hsp70 using siRNA exaggerated and overexpression of Hsp70 prevented the second phase disruption of lung endothelial integrity. Moreover, inhibition of Hsp70 exacerbated and overexpression of Hsp70 prevented hyperoxia-induced apoptosis, caspase-3 activation, and increase in nuclear AIF protein level in PAECs. Furthermore, we found that Hsp70 interacted with AIF in the cytosol in hyperoxic PAECs. Inhibition of Hsp70/AIF association by KNK437 correlated with increased nuclear AIF level and apoptosis in KNK437-treated PAECs. Finally, the ROS scavenger NAC prevented the hyperoxia-induced increase in Hsp70 expression and reduced the interaction of Hsp70 with AIF in hyperoxic PAECs. Together, these data indicate that increased expression of Hsp70 plays a protective role against hyperoxia-induced lung endothelial barrier disruption through caspase-dependent and AIF-dependent apoptotic pathways. Association of Hsp70 with AIF prevents AIF nuclear translocation, contributing to the protective effect of Hsp70 on hyperoxia-induced endothelial apoptosis. The hyperoxia-induced increase in Hsp70 expression and Hsp70/AIF interaction is contributed to ROS formation.     

Reciprocal regulation of cilia and autophagy via the MTOR and proteasome pathways

Primary cilium is an organelle that plays significant roles in a number of cellular functions ranging from cell mechanosensation, proliferation, and differentiation to apoptosis. Autophagy is an evolutionarily conserved cellular function in biology and indispensable for cellular homeostasis. Both cilia and autophagy have been linked to different types of genetic and acquired human diseases. Their interaction has been suggested very recently, but the underlying mechanisms are still not fully understood. We examined autophagy in cells with suppressed cilia and measured cilium length in autophagy-activated or -suppressed cells. It was found that autophagy was repressed in cells with short cilia. Further investigation showed that MTOR activation was enhanced in cilia-suppressed cells and the MTOR inhibitor rapamycin could largely reverse autophagy suppression. In human kidney proximal tubular cells (HK2), autophagy induction was associated with cilium elongation. Conversely, autophagy inhibition by 3-methyladenine (3-MA) and chloroquine (CQ) as well as bafilomycin A₁ (Baf) led to short cilia. Cilia were also shorter in cultured atg5-knockout (KO) cells and in atg7-KO kidney proximal tubular cells in mice. MG132, an inhibitor of the proteasome, could significantly restore cilium length in atg5-KO cells, being concomitant with the proteasome activity. Together, the results suggest that cilia and autophagy regulate reciprocally through the MTOR signaling pathway and ubiquitin-proteasome system.     

HLA-DRB1 shared epitope genotyping using the revised classification and its association with circulating autoantibodies,acute phase reactants,cytokines and clinical indices of disease activity in a cohort of South African rheumatoid arthritis patients

Introduction  

The revised shared epitope (SE) concept in rheumatoid arthritis (RA) is based on the presence (S) or absence (X) of the SE RAA amino acid motif at positions 72 to 74 of the third hypervariable region of the various human leucocyte antigen (HLA)-DRB1 alleles. The purpose of this study was to investigate SE subtypes on the basis of the American College of Rheumatology 1987 revised criteria for the classification of RA in a cohort of South African RA patients (n = 143) and their association with clinical and circulating biomarkers of disease activity (autoantibodies, acute phase reactants and cytokines).     

Accumulation of trace elements in agricultural topsoil under different geological background

For establishing rational farming mechanism, it is essential to know the relative contribution of different geological background and anthropogenic activities to trace elements in agricultural soil. In this paper, 282 surface soil samples were collected based on the different geological background. Five harmful trace elements (As, Cd, Cr, Hg and Pb) were analyzed. The results indicated most of trace elements contents were far beyond the threshold of uncultivated soil background, which indicate anthropogenic input strongly influenced on trace elements in agricultural soil. In addition, correlation analysis showed trace element contents exhibited high relationships with soil pH, C/N and physical clay (<0.01 mm) (p?<?0.05). The principal component analysis showed that the first component included Cd, Cr and Hg, while Pb and As formed the second component. Furthermore, in the agricultural topsoil derived from carbonate rock, the high background values of trace elements and alkaline condition made the enrichments of Cd, Cr and Hg were the most significant. In the agricultural topsoil derived from red residua, the Pb and As contents was the highest values among the soil categories, partly because the type of soil had amount of physical clay (<0.01 mm). In the agricultural topsoil derived from shale, the pH or physical clay had significant relationship with Cd, Pb, Hg and As (p?<?0.01). In the agricultural topsoil derived from sand stone, the acid condition and loose texture might account for the lowest values of Cd, Cr, Pb and As content to some extent.     

��-Actin Association with Endothelial Nitric-oxide Synthase Modulates Nitric Oxide and Superoxide Generation from the Enzyme

Protein-protein interactions represent an important post-translational mechanism for endothelial nitric-oxide synthase (eNOS) regulation. We have previously reported that β-actin is associated with eNOS oxygenase domain and that association of eNOS with β-actin increases eNOS activity and nitric oxide (NO) production. In the present study, we found that β-actin-induced increase in NO production was accompanied by decrease in superoxide formation. A synthetic actin-binding sequence (ABS) peptide 326 with amino acid sequence corresponding to residues 326–333 of human eNOS, one of the putative ABSs, specifically bound to β-actin and prevented eNOS association with β-actin in vitro. Peptide 326 also prevented β-actin-induced decrease in superoxide formation and increase in NO and l-citrulline production. A modified peptide 326 replacing hydrophobic amino acids leucine and tryptophan with neutral alanine was unable to interfere with eNOS-β-actin binding and to prevent β-actin-induced changes in NO and superoxide formation. Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-β-actin association, decreased NO production, and increased superoxide formation in COS-7 cells. Disruption of eNOS-β-actin interaction in endothelial cells using ABS peptide 326 resulted in decreased NO production, increased superoxide formation, and decreased endothelial monolayer wound repair, which was prevented by PEG-SOD and NO donor NOC-18. Taken together, this novel finding indicates that β-actin binding to eNOS through residues 326–333 in the eNOS protein results in shifting the enzymatic activity from superoxide formation toward NO production. Modulation of NO and superoxide formation from eNOS by β-actin plays an important role in endothelial function.     

Substructural specificity and polyvalent carbohydrate recognition by the Entamoeba histolytica and rat hepatic N- acetylgalactosamine/galactose lectins

Both the Entamoeba histolytica lectin, a virulence factor for the causative agent of amebiasis, and the mammalian hepatic lectin bind to N-acetylgalactosamine (GalNAc) and galactose (Gal) nonreducing termini on oligosaccharides, with preference for GalNAc. Polyvalent GalNAc- derivatized neoglycoproteins have >1000-fold enhanced binding affinity for both lectins (Adler,P., Wood,S.J., Lee,Y.C., Lee,R.T., Petri,W.A.,Jr. and Schnaar,R.L.,1995, J. Biol. Chem ., 270, 5164-5171). Substructural specificity studies revealed that the 3-OH and 4-OH groups of GalNAc were required for binding to both lectins, whereas only the E.histolytica lectin required the 6-OH group. Whereas GalNAc binds with 4-fold lower affinity to the E.histolytica lectin than to the mammalian hepatic lectin, galactosamine and N-benzoyl galactosamine bind with higher affinity to the E. histolytica lectin. Therefore, a synthetic scheme for converting polyamine carriers to poly-N-acyl galactosamine derivatives (linked through the galactosamine primary amino group) was developed to test whether such ligands would bind the E.histolytica lectin with high specificity and high affinity. Contrary to expectations, polyvalent derivatives including GalN6lys5, GalN4desmosine, GalN4StarburstTMdendrimer, and GalN8StarburstTMdendrimer demonstrated highly enhanced binding to the mammalian hepatic lectin but little or no enhancement of binding to the E.histolytica lectin. We propose that the mammalian hepatic lectin binds with greatest affinity to GalNAc "miniclusters," which mimic branched termini of N-linked oligosaccharides, whereas the E.histolytica lectin binds most effectively to "maxiclusters," which may mimic more widely spaced GalNAc residues on intestinal mucins.