Lipids Modulate the Increase of BK Channel Calcium Sensitivity by the β1 Subunit

Co-expression of the auxiliary β1 subunit with the pore forming α subunit of BK dramatically alters apparent calcium sensitivity. Investigation of the mechanism underlying the increase in calcium sensitivity of BK in smooth muscle has concentrated on the energetic effect of β1′s interaction with α. We take a novel approach, exploring whether β1 modification of calcium sensitivity reflects altered interaction between the channel protein and surrounding lipids. We reconstituted hSlo BK α and BK α+β1 channels into two sets of bilayers. One set contained POPE with POPS, POPG, POPA and POPC, where the length of acyl chains is constant, but surface charge differs. The second set is a series of neutral bilayers formed from DOPE with phosphatidylcholines (PCs) of varying acyl chain lengths: C (14∶1), C (18∶1), C (22∶1) and C (24∶1), and with brain sphingomyelin (SPM), in which surface charge is constant, but bilayer thickness varies. The increase in calcium sensitivity caused by the β1 subunit was preserved in negatively charged lipid bilayers but not in neutral bilayers, indicating that modification of apparent Ca²⁺ sensitivity by β1 is modulated by membrane lipids, requiring negatively charged lipids in the membrane. Moreover, the presence of β1 reduces BK activity in thin bilayers of PC 14∶1 and thick bilayers containing SPM, but has no significant effect on activity of BK in PC 18∶1, PC 22∶1 and PC 24∶1 bilayers. These data suggest that auxiliary β1 subunits fine-tune channel gating not only through direct subunit-subunit interactions but also by modulating lipid-protein interactions.     

Neurexophilin 1 Gene Polymorphism in Chickens and Its Variation Among Species

Neurexophilin 1 (nxph1) has been considered a potential candidate marker for sperm storage in chicken sperm storage tubules. In this work, one mutation of chicken nxph1 was detected. We analyzed 18 nxph1 gene sequences from 18 species. The coding sequence length of the zebra fish nxph1 gene is 819 bp; that of the other species is 816 bp. Amino acid alignment analysis revealed that the gene product is a conserved protein, especially in mammals. The sequences of mammals are highly conserved. We found 202 conserved amino acids (70–271), and there were only eight mutations in the remaining 69 amino acids. That level of conservation could be due to the nxph1 gene having been subjected to substantial constraints or strong purifying selection during millions of years of evolution.     

Carbon budgets of wetland ecosystems in China

Wetlands contain a large proportion of carbon (C) in the biosphere and partly affect climate by regulating C cycles of terrestrial ecosystems. China contains Asia's largest wetlands, accounting for about 10% of the global wetland area. Although previous studies attempted to estimate C budget in China's wetlands, uncertainties remain. We conducted a synthesis to estimate C uptake and emission of wetland ecosystems in China using a dataset compiled from published literature. The dataset comprised 193 studies, including 370 sites representing coastal, river, lake and marsh wetlands across China. In addition, C stocks of different wetlands in China were estimated using unbiased data from the China Second Wetlands Survey. The results showed that China's wetlands sequestered 16.87 Pg C (315.76 Mg C/ha), accounting for about 3.8% of C stocks in global wetlands. Net ecosystem productivity, jointly determined by gross primary productivity and ecosystem respiration, exhibited annual C sequestration of 120.23 Tg C. China's wetlands had a total gaseous C loss of 173.20 Tg C per year from soils, including 154.26 Tg CO₂‐C and 18.94 Tg CH₄‐C emissions. Moreover, C stocks, uptakes and gaseous losses varied with wetland types, and were affected by geographic location and climatic factors (precipitation and temperature). Our results provide better estimation of the C budget in China's wetlands and improve understanding of their contribution to the global C cycle in the context of global climate change.     

Effect of Purple Sweet Potato Anthocyanins on β-Amyloid-Mediated PC-12 Cells Death by Inhibition of Oxidative Stress

Amyloid-beta peptide (Aβ) is known to induce the redox imbalance, mitochondrial dysfunction and caspase activation, resulting in neuronal cell death. Treatment with antioxidants provided a new therapeutic strategy for Alzheimer’s disease (AD) patients. Here we investigate the effects of purple sweet potato anthocyanins (PSPA), the known strong free radical scavengers, on Aβ toxicity in PC12 cells. The results showed that pretreatment of PC12 cells with PSPA reduced Aβ-induced toxicity, intracellular reactive oxygen species (ROS) generation and lipid peroxidation dose-dependently. In parallel, cell apoptosis triggered by Aβ characterized with the DNA fragmentation and caspase-3 activity were also inhibited by PSPA. The concentration of intracellular Ca²⁺ and membrane potential loss associated with cell apoptosis were attenuated by PSPA. These results suggested that PSPA could protect the PC-12 cell from Aβ-induced injury through the inhibition of oxidative damage, intracellular calcium influx, mitochondria dysfunction and ultimately inhibition of cell apoptosis. The present study indicates that PSPA may be a promising approach for the treatment of AD and other oxidative-stress-related neurodegenerative diseases.     

拟南芥转录因子CBF1和CBF4基因的克隆与序列分析

利用聚合酶链式反应技术(PCR)从拟南芥(Arabidopsis thaliana)植株中扩增出CBF1和CBF4基因,并将其连接到pGEM-Tvector载体上。PCR和酶切鉴定后进行基因测序,结果表明所克隆的CBF1和CBF4基因序列与GenBank中基因序列同源性分别可达99.84%和99.41%,说明这两个片段确为拟南芥CBF1和CBF4基因。     

Selenium Level Surveillance for the Year 2007 of Keshan Disease in Endemic Areas and Analysis on Surveillance Results Between 2003 and 2007

Selenium deficiency is widely accepted as a fundamental cause of Keshan disease (KD). In the present study, the selenium levels of hair and food samples of KD in some endemic areas were measured; the prevalence and incidence of KD for the year 2007 in these areas were surveyed. The results for KD surveillance from 2003 to 2007 were analyzed. The selenium level was measured fluorometrically. In 2007, a total of 19,280 residents were surveyed in 15 provinces. The prevalence and incidence of KD were 3.0% and 4.9‰, respectively. In KD and control subjects, the mean levels of hair selenium were respectively 0.3223 mg/kg and 0.4466 mg/kg. The mean level of staple food selenium was 0.0227?±?0.0144 mg/kg. During the 5 years, the selenium content in hair was always kept at a normal level within inhabitants of KD-endemic areas, but that in staple food was always kept at a lower level. These results indicate that the pathogenic factor has not been drastically eliminated even with the increasing selenium level of internal environment and is still continually damaging public health of KD in endemic areas. Since KD is still a serious threat to public health in its endemic areas, it is of great importance to pay attention to the prevention and control of this disease.     

Abnormalities of white matter microstructure in unmedicated obsessive-compulsive disorder and changes after medication

Background

Abnormalities of myelin integrity have been reported in obsessive-compulsive disorder (OCD) using multi-parameter maps of diffusion tensor imaging (DTI). However, it was still unknown to what degree these abnormalities might be affected by pharmacological treatment.

Objective

To investigate whether the abnormalities of white matter microstructure including myelin integrity exist in OCD and whether they are affected by medication.

Methodology and Principal Findings

Parameter maps of DTI, including fractional anisotropy (FA), axial diffusivity (AD), radial diffusivity (RD) and mean diffusivity (MD), were acquired from 27 unmedicated OCD patients (including 13 drug-naïve individuals) and 23 healthy controls. Voxel-based analysis was then performed to detect regions with significant group difference. We compared the DTI-derived parameters of 15 patients before and after 12-week Selective Serotonin Reuptake Inhibitor (SSRI) therapies. Significant differences of DTI-derived parameters were observed between OCD and healthy groups in multiple structures, mainly within the fronto-striato-thalamo-cortical loop. An increased RD in combination with no change in AD among OCD patients was found in the left medial superior frontal gyrus, temporo-parietal lobe, occipital lobe, striatum, insula and right midbrain. There was no statistical difference in DTI-derived parameters between drug-naive and previously medicated OCD patients. After being medicated, OCD patients showed a reduction in RD of the left striatum and right midbrain, and in MD of the right midbrain.

Conclusion

Our preliminary findings suggest that abnormalities of white matter microstructure, particularly in terms of myelin integrity, are primari ly located within the fronto-striato-thalamo-cortical circuit of individuals with OCD. Some abnormalities may be partly reversed by SSRI treatment.