千岛湖次生林优势种种群结构与分布格局

为了揭示亚热带地区常绿阔叶林次生演替机理,以砍伐后自然恢复40余年的浙江千岛湖姥山岛次生林为研究对象,分析了该群落优势种的种群结构、存活曲线和空间分布格局。结果表明:1)群落中重要值最大的是马尾松(Pinus massoniana)种群,达到50.47%,其后依次是石栎(Lithocarpusglabra)、苦槠(Castanopsis sclerophylla)和青冈(Cyclobalanopsis glauca)。2)马尾松的种群结构呈纺锤型,但1、2径级个体数极少,幼龄个体储备严重不足,已呈衰退趋势;石栎、苦槠、青冈的种群结构呈金字塔型。3)从静态生命表看,马尾松种群小径级的死亡率为负值,也说明马尾松种群幼苗严重缺乏,种群呈衰退趋势。4)马尾松种群的存活曲线为凸型,石栎、苦槠和青冈种群则近似直线型。5)4种优势种种群总体和各级个体的空间分布格局均呈聚集分布。总体来看,马尾松种群为稳定型趋向衰退型,而石栎、苦槠和青冈种群为稳定增长型,群落会继续向针阔混交林方向演替,进而演替成为常绿阔叶林。     

High‐Performance Fiber‐Shaped All‐Solid‐State Asymmetric Supercapacitors Based on Ultrathin MnO2 Nanosheet/Carbon Fiber Cathodes for Wearable Electronics

Flexible fiber‐shaped supercapacitors have shown great potential in portable and wearable electronics. However, small specific capacitance and low operating voltage limit the practical application of fiber‐shaped supercapacitors in high energy density devices. Herein, direct growth of ultrathin MnO₂ nanosheet arrays on conductive carbon fibers with robust adhesion is exhibited, which exhibit a high specific capacitance of 634.5 F g^?1 at a current density of 2.5 A g^?1 and possess superior cycle stability. When MnO₂ nanosheet arrays on carbon fibers and graphene on carbon fibers are used as a positive electrode and a negative electrode, respectively, in an all‐solid‐state asymmetric supercapacitor (ASC), the ASC displays a high specific capacitance of 87.1 F g^?1 and an exceptional energy density of 27.2 Wh kg^?1. In addition, its capacitance retention reaches 95.2% over 3000 cycles, representing the excellent cyclic ability. The flexibility and mechanical stability of these ASCs are highlighted by the negligible degradation of their electrochemical performance even under severely bending states. Impressively, as‐prepared fiber‐shaped ASCs could successfully power a photodetector based on CdS nanowires without applying any external bias voltage. The excellent performance of all‐solid‐state ASCs opens up new opportunity for development of wearable and self‐powered nanodevices in near future.     

Therapeutic Efficacy of Percutaneous Radiofrequency Ablation versus Microwave Ablation for Hepatocellular Carcinoma

The aim of this study was to investigate the therapeutic efficacy of percutaneous radiofrequency (RF) ablation versus microwave (MW) ablation for hepatocellular carcinoma (HCC) measuring ≤5 cm in greatest diameter. From January 2006 to December 2006, 78 patients had undergone RF ablation whereas 77 had undergone MW ablation. Complete ablation (CA), local tumour progression (LTP) and distant recurrence (DR) were compared. The overall survival curves were calculated with the Kaplan-Meier technique and compared with the log-rank test. The CA rate was 83.4% (78/93) for RF ablation and 86.7%(91/105 for MW ablation. The LTP rate was 11.8% (11/93) for RF ablation and 10.5% (11/105) for MW ablation. DR was found in 51 (65.4%) in the RF ablation and 62 (80.5%) in the MW ablation. There was no significant difference in the 1-, 3-, and 5-year overall survival rates (P = 0.780) and the 1-, 3-, and 5-year disease-free survival rates (P = 0.123) between RF and MW ablation. At subgroup analyses, for patients with tumors ≤3.0 cm, there was no significant difference in the 1-, 3-, and 5-year overall survival rates (P = 0.067) and the corresponding disease-free survival rates(P = 0.849). For patients with tumor diameters of 3.1–5.0 cm, the 1-, 3-, and 5-year overall survival rates were 87.1%, 61.3%, and 40.1% for RF ablation and 85.4%, 36.6%, and 22% for MW ablation, with no significant difference (P = 0.068). The corresponding disease-free survival rates were 74.2%, 54.8%, and 45.2% for the RF ablation group and 53.3%, 26.8%, and 17.1% for the MW ablation group. The disease-free survival curve for the RF ablation group was significantly better than that for the MW ablation group (P = 0.018). RF ablation and MW ablation are both effective methods in treating hepatocellular carcinomas, with no significant differences in CA, LTP, DR, and overall survival.     

Conservation needs of amphibians in China: A review

The conservation status of all the amphibians in China is analyzed, and the country is shown to be a global priority for conservation in comparison to many other countries of the world. Three Chinese regions are particularly rich in amphibian diversity: Hengduan, Nanling, and Wuyi mountains. Salamanders are more threatened than frogs and toads. Several smaller families show a high propensity to become seriously threatened: Bombinatoridae, Cryptobranchidae, Hynobiidae and Salamandridae. Like other parts of the world, stream-breeding, high-elevation forest amphibians have a much higher likelihood of being seriously threatened. Habitat loss, pollution, and over-harvesting are the most serious threats to Chinese amphibians. Over-harvesting is a less pervasive threat than habitat loss, but it is more likely to drive a species into rapid decline. Five conservation challenges are mentioned with recommendations for the highest priority research and conservation actions.     

Using three overlapped RILs to dissect genetically clustered QTL for fiber strength on Chro.D8 in Upland cotton

Fiber strength is an important trait among cotton fiber qualities due to ongoing changes in spinning technology. Major quantitative trait loci (QTL) for fiber quality enable molecular marker-assisted selection (MAS) to effectively improve fiber quality of cotton cultivars. We previously identified a major QTL for fiber strength derived from 7235 in Upland cotton. In the present study, in order to fine-map fiber strength QTL, we chose three recombinant inbred lines (RIL), 7TR-133, 7TR-132, and 7TR-214, developed from a cross between 7235 and TM-1 for backcrossing to TM-1 to develop three large mapping populations. Phenotypic data for fiber strength traits were collected in Nanjing (JES/NAU) and Xinjiang (BES/XJ) in 2006 and 2007. Three simple sequence repeat (SSR) genetic linkage maps on Chro.24(D8) were constructed using these three backcrossed populations. The SSR genetic maps were constructed using 907 individuals in (7TR-133 × TM-1)F₂ (Pop A), 670 in (7TR-132 × TM-1)F₂ (Pop B), and 940 in (7TR-214 × TM-1)F₂ (Pop C). The average distance between SSR loci was 0.62, 1.7, and 0.56 cM for the three maps. MapQTL 5 software detected five-clustered QTL (2.5 < LOD < 29.8) on Chro.D8 for fiber strength following analysis of three RIL backcrossed F₂/F_2:3 progenies at JES/NAU and BES/XJ over 2 years. Five QTL for fiber strength exhibited a total phenotypic variance (PV) of 28.8–59.6%.     

Metabolic adaptation to a disruption in oxygen supply during myocardial ischemia and reperfusion is underpinned by temporal and quantitative changes in the cardiac proteome

Despite decades of intensive research, there is still no effective treatment for ischemia/reperfusion (I/R) injury, an important corollary in the treatment of ischemic disease. I/R injury is initiated when the altered biochemistry of cells after ischemia is no longer compatible with oxygenated microenvironment (or reperfusion). To better understand the molecular basis of this alteration and subsequent incompatibility, we assessed the temporal and quantitative alterations in the cardiac proteome of a mouse cardiac I/R model by an iTRAQ approach at 30 min of ischemia, and at 60 or 120 min reperfusion after the ischemia using sham-operated mouse heart as the baseline control. Of the 509 quantified proteins identified, 121 proteins exhibited significant changes (p-value<0.05) over time and were mostly clustered in eight functional groups: Fatty acid oxidation, Glycolysis, TCA cycle, ETC (electron transport chain), Redox Homeostasis, Glutathione S-transferase, Apoptosis related, and Heat Shock proteins. The first four groups are intimately involved in ATP production and the last four groups are known to be important in cellular antioxidant activity. During ischemia and reperfusion, the short supply of oxygen precipitates a pivotal metabolic switch from aerobic metabolism involving fatty acid oxidation, TCA, and phosphorylation to anaerobic metabolism for ATP production and this, in turn, increases reactive oxygen species (ROS) formation. Therefore the implication of these 8 functional groups suggested that ischemia-reperfusion injury is underpinned in part by proteomic alterations. Reversion of these alterations to preischemia levels took at least 60 min, suggesting a refractory period in which the ischemic cells cannot adjust to the presence of oxygen. Therefore, therapeutics that could compensate for these proteomic alterations during this interim refractory period could alleviate ischemia-reperfusion injury to enhance cellular recovery from an ischemic to a normoxic microenvironment. Among the perturbed proteins, Park7 and Ppia were selected for further investigation of their functions under hypoxia. The results show that Park7 plays a key role in regulating antioxidative stress and cell survival, and Ppia may function in coping with the unfolded protein stress in the I/R condition.     

Distinct role of matrix metalloproteinase-3 in kidney injury molecule-1 shedding by kidney proximal tubular epithelial cells

Tubulointerstitial injury is a common pathway in progressive renal impairment and human proximal tubular epithelial cells (PTEC) play a crucial role in this process. Kidney injury molecule-1 (KIM-1) has received increasing attention due to its potential utility as the therapeutic target and biomarker for kidney injury. This study aims to explore the underlying mechanism regulating the release of KIM-1. Cultured primary human PTEC expressed and released KIM-1 from the apical surface through an ectodomain shedding process mediated by matrix metalloproteinase (MMP), independent of gene expression and protein synthesis. The constitutive KIM-1 shedding by PTEC was enhanced in a dose- and time-dependent manner by human serum albumin (HSA) or tumor necrosis factor-α (TNF-α), two important physiological stimuli found during kidney injury. Data from PCR array screening of MMPs gene expression in PTEC following activation by HSA or TNF-α, and from blocking experiments using either synthetic MMP inhibitors or MMP gene knockdown by siRNA, revealed that the constitutive and accelerated shedding of KIM-1 in cultured PTEC was mediated by MMP-3. Furthermore, the up-regulation of MMP-3 and KIM-1 release by PTEC was associated with generation of reactive oxygen species. In a mouse model of acute kidney injury induced by ischemia and reperfusion, increased expression of MMP-3 and KIM-1 as well as their co-localization were observed in kidney from ischemic but not in sham-operated mice. Taken together, these in vitro and in vivo evidences suggest that MMP-3 plays an inductive role in KIM-1 shedding by PTEC.