伊洛河流域草本植物群落物种多样性

生物多样性沿环境梯度的变化是生物多样性研究的重要内容,环境梯度包含了多种环境因子(海拔高度、水热条件、人类扰动等)的综合。以伊洛河流域草本植物群落为对象,沿河从入黄河口到河源地选取典型样地调查研究伊洛河流域草本植物群落物种多样性及其分布格局。结果表明:物种丰富度和Shannon-Wiener多样性指数沿河均稍呈"S"型曲线变化,不同群落类型中分布格局差别不大,各群落类型中的物种丰富度和多样性均呈现出中游丘陵山地交界区最高,上游河源区次之,下游平原地区最低的趋势;β多样性指数的变化趋势与α多样性较一致,总体上呈现出中游丘陵山地区物种更替速率较快,平原区更替较慢;在流域内上游河源地属于自然植被区,人为干扰较轻,具有较高的物种多样性,物种替代主要受物种的竞争扩散能力和生境条件的制约;在下游平原农业区,人类活动强烈,区域内以人工生态系统为主,物种组成简单,物种替代具有跳跃性的特征,主要受人类活动的制约;在中游从自然生态系统向农业生态系统的过渡区域,人类活动的扰动有一定的强度,导致该区域内自然分布种和伴人种混合生长,具有较高的物种多样性和较快的物种替代速率。总体上伊洛河流域草本植物群落物种多样性分布格局强烈的受到人类活动的影响,物种替代速率较高。     

Increased IGF2BP3 expression promotes the aggressive phenotypes of colorectal cancer cells in vitro and vivo

Previous literatures reported insulin-like growth factor-2 messenger RNA-binding protein 3 (IGF2BP3) is a poor prognostic marker for colorectal cancer (CRC) patients. However, basic research on the effect and biological role of IGF2BP3 in CRC was still scare. Real-time quantitative polymerase chain reaction and western blot analysis were used to examine IGF2BP3 expression level in tumors and paired normal tissues from CRC patients. Tissue microarrays with 192 CRC patients were subjected to immunohistochemical staining to analyze the prognostic value of IGF2BP3. Proliferation assays, migration assays, and xenograft tumor formation in nude mice were performed to assess the biological role of IGF2BP3 in CRC cells. IGF2BP3 expression was significantly upregulated in tumor tissues compared with the matched normal tissues both in messenger RNA and protein level and was associated with worse prognosis. IGF2BP3 knockdown made cell cycle arrest to impair the proliferation ability of CRC cells and further inhibited the xenograft tumor growth in nude mice, also inhibited the migration ability of CRC cells via inducing epithelial–mesenchymal transition. Therefore, the research demonstrated that increased IGF2BP3 expression promoted the aggressive phenotypes of CRC cells. Targeted IGF2BP3 could be a novel and effective gene therapy for CRC patients to make a better prognosis.     

Caveolin-1 knockdown increases the therapeutic sensitivity of lung cancer to cisplatin-induced apoptosis by repressing Parkin-related mitophagy and activating the ROCK1 pathway

Chemotherapy is the first-line treatment option for patients with lung cancer. However, therapeutic resistance occurs through an incompletely understood mechanism. Our research wants to investigate the influence of Caveolin-1 (Cav-1) on the therapeutic sensitivity of lung cancer in vitro. Results in this study demonstrated that Cav-1 levels were markedly inhibited in A549 lung cancer cells after exposure to cisplatin. Knockdown of caveolin further enhanced cisplatin-triggered cancer death in A549 cells. The functional investigation demonstrated that Cav-1 inhibition amplified the mitochondrial stress signaling induced by cisplatin, as evidenced by the mitochondrial reactive oxygen species burst, cellular metabolic disruption, mitochondrial membrane potential reduction, and mitochondrial caspase-9-related apoptosis activation. At the molecular level, cav-1 augmented cisplatin-mediated mitochondrial damage by inhibiting Parkin-related mitochondrial autophagy. Mitophagy activation effectively attenuated the promotive impact of Cav-1 knockdown on mitochondrial damage and cell death. Furthermore, our data indicated that Cav-1 affected Parkin-related mitophagy by activating the Rho-associated coiled-coil kinase 1 (ROCK1) pathway; inhibition of the ROCK1 axis prevented cav-1 knockdown-mediated cell death and mitochondrial damage. Taken together, our results provide ample data illuminate the necessary action exerted by Cav-1 on affecting cisplatin-related therapeutic resistance. Silencing of Cav-1 inhibited Parkin-related mitophagy, thus amplifying cisplatin-mediated mitochondrial apoptotic signaling. This finding identifies the Cav-1/ROCK1/Parkin/mitophagy axis as a potential target to overcome cisplatin-related resistance in lung cancer cells.     

Synthesis and photoluminescence study of di‐dendron dendrimers derived from mono‐Boc‐protected ethylenediamine cores

This work is focused on the synthesis and optical properties of cone‐shaped structural feature di‐dendron polyamidoamine dendrimers up to the third generation with mono‐Boc‐protected ethylenediamine (EDA) as a core. Strong UV absorbance spectra and fluorescence spectra from di‐dendron dendrimers with different terminal groups (‐NH₂, ‐COOCH₃) were studied under different conditions by varying experimental parameters such as concentration and pH. The optical density and fluorescence intensities increased when di‐dendron dendrimers generation number increased from 0.5 to 3.0. It was confirmed that the concentration of di‐dendron dendrimers plays an important role in fluorescence intensity. The increase in fluorescence intensity was linear in low concentration regions, but the intensity increased slowly in high concentration regions. The results also showed a rapid increase in fluorescence intensity at low pH. The formation of a fluorescence‐emitting moiety had a close relationship to protonated tertiary amine groups in di‐dendron dendrimers derived from mono‐Boc‐protected EDA cores. Furthermore, the formation of fluorescent chemical species was irreversible. Copyright © 2010 John Wiley & Sons, Ltd.     

Remodeling of Hyperpolarization-Activated Current,Ih, in Ah-Type Visceral Ganglion Neurons Following Ovariectomy in Adult Rats

Hyperpolarization-activated currents (I_h) mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels modulate excitability of myelinated A− and Ah-type visceral ganglion neurons (VGN). Whether alterations in I_h underlie the previously reported reduction of excitability of myelinated Ah-type VGNs following ovariectomy (OVX) has remained unclear. Here we used the intact nodose ganglion preparation in conjunction with electrophysiological approaches to examine the role of I_h remodeling in altering Ah-type neuron excitability following ovariectomy in adult rats. Ah-type neurons were identified based on their afferent conduction velocity. Ah-type neurons in nodose ganglia from non-OVX rats exhibited a voltage ‘sag’ as well as ‘rebound’ action potentials immediately following hyperpolarizing current injections, which both were suppressed by the I_h blocker ZD7288. Repetitive spike activity induced afterhyperpolarizations lasting several hundreds of milliseconds (termed post-excitatory membrane hyperpolarizations, PEMHs), which were significantly reduced by ZD7288, suggesting that they resulted from transient deactivation of I_h during the preceding spike trains. Ovariectomy reduced whole-cell I_h density, caused a hyperpolarizing shift of the voltage-dependence of I_h activation, and slowed I_h activation. OVX-induced I_h remodeling was accompanied by a flattening of the stimulus frequency/response curve and loss of PEMHs. Also, HCN1 mRNA levels were reduced by ∼30% in nodose ganglia from OVX rats compared with their non-OVX counterparts. Acute exposure of nodose ganglia to 17beta-estradiol partly restored I_h density and accelerated I_h activation in Ah-type cells. In conclusion, I_h plays a significant role in modulating the excitability of myelinated Ah-type VGNs in adult female rats.     

Hyperuricemia as an Independent Predictor of Vascular Complications and Mortality in Type 2 Diabetes Patients: A Meta-Analysis

Background

Recent data have suggested that serum uric acid (SUA) level is positively associated with the development of type 2 diabetes (T2DM). Whether SUA is also independently associated with the development of vascular complications and mortality in T2DM is controversial.

Methods

A computerized literature search of MEDLINE, Embase and PubMed database was conducted and the odds ratio (OR) or hazard ratio (HR) for per 0.1mmol/l increase in SUA in each study was calculated. Cochrane’s Q and I² statistics were used to evaluate heterogeneity among studies and pooling OR and HR with 95% confidence intervals (CIs) were calculated using random-effects models and fixed-effects models. The pooled analysis was performed using Stata 10.0.

Results

Our search yielded 9 eligible articles (16 ORs and HRs) including 20,891 T2DM patients. Pooled estimates for the relationship suggested that each 0.1 mmol/l increase in SUA resulted in a 28% increase in the risk of diabetic vascular complications and a 9% increase in the risk of diabetic mortality. In stratification-analysis, the positive relationship between SUA and vascular complications remained significant irrespective of mean age, adjustment for metabolic variables and medications. However, it was inconsistent in different populations (significantly positive in the Asian but not in Australian and Italian population) and sample sizes (significantly positive in the relatively large sample size [≥1000] but non-significant in the small sample size [<1000]).

Conclusions

Results of this meta-analysis supported elevated SUA as an independent predictor of vascular complications and mortality in T2DM patients. SUA-lowering therapies might be helpful for prevention and treatment of vascular complications in this population.     

Insights on the robust variance estimator under recurrent-events model

Recurrent events are common in medical research for subjects who are followed for the duration of a study. For example, cardiovascular patients with an implantable cardioverter defibrillator (ICD) experience recurrent arrhythmic events that are terminated by shocks or antitachycardia pacing delivered by the device. In a published randomized clinical trial, a recurrent-event model was used to study the effect of a drug therapy in subjects with ICDs, who were experiencing recurrent symptomatic arrhythmic events. Under this model, one expects the robust variance for the estimated treatment effect to diminish when the duration of the trial is extended, due to the additional events observed. However, as shown in this article, that is not always the case. We investigate this phenomenon using large datasets from this arrhythmia trial and from a diabetes study, with some analytical results, as well as through simulations. Some insights are also provided on existing sample size formulae using our results.     

REDD1 attenuates cardiac hypertrophy via enhancing autophagy

Cardiac hypertrophy is a major risk factor of cardiovascular morbidity and mortality. Autophagy is established to be involved in regulating cardiac hypertrophy. REDD1, a stress-responsive protein, is proved to contribute in autophagy induction. However, the role of REDD1 in cardiac hypertrophy remains unknown. Our study demonstrated that REDD1 knockdown by RNAi exacerbated phenylephrine (PE)-induced cardiac hypertrophy, manifested by increased hypertrophic markers such as ANP and cell surface area. In addition, we discovered that ERK1/2 signaling pathway was involved in the effect of REDD1 on hypertrophy. Moreover, our study showed that REDD1 knockdown impaired autophagy in hypertrophied cardiomyocytes. mTOR, a signaling molecule governing autophagy induction, was activated by the knockdown of REDD1 under PE stress. Importantly, the pro-hypertrophic effect of REDD1 knockdown was significantly reversed by the autophagy enhancer rapamycin. Taken together, we firstly prove that REDD1 is essential for inhibiting cardiac hypertrophy by enhancing autophagy.     

A Novel Degenerated Primer Pair Detects Diverse Genes of Acyl Homoserine Lactone Synthetase in Rhizobiaceae Family

A novel degenerated primer set was designed to amplify acyl homoserine lactone (AHL) synthetase genes from members of the family Rhizobiaceae. The primer set successfully amplified AHL synthetase genes from pure cultures of AHL producers from Rhizobiaceae, but not from AHL producers out of the Rhizobiaceae family, indicating the specificity of this primer set to the Rhizobiaceae family. An inoculation experiment showed that the minimal detectable concentration of AHL producers from the soil was around 2.5 × 10⁷ CFU/g soil. When applying to environmental samples, 7 and 14 different genotypes of AHL synthetase genes were identified in the rhizosphere of Glycine max and Vigna unguiculata, respectively, which revealed complicated and unknown AHL-based quorum-sensing networks in the rhizosphere. This is the first primer set that covers diverse AHL synthetase genes from different genera. It will be a useful culture-independent approach for better understanding of the ecological significance of QS in natural habitats.