Blockade of L-type voltage-gated Ca channel inhibits ischemia-induced neurogenesis by down-regulating iNOS expression in adult mouse

Neurogenesis in the adult mammalian hippocampus may contribute to repairing the brain after injury. The signals that regulate neurogenesis in the dentate gyrus following ischemic stroke insult are not well known. We have previously reported that inducible nitric oxide synthase (iNOS) expression is necessary for ischemia-stimulated neurogenesis in the adult dentate gyrus. Here, we show that mice subjected to 90 min of middle cerebral artery occlusion (MCAO) significantly increased the number of new neurons and up-regulated iNOS expression in the dentate gyrus. Blockade of the L-type voltage-gated Ca(2+) channel (L-VGCC) prevented neurogenesis in the dentate gyrus and subventricular zone (SVZ), and down-regulated iNOS expression in the dentate gyrus after cerebral ischemia. This study suggests that Ca(2+) influx through L-VGCC is involved in ischemia-induced neurogenesis by up-regulating iNOS expression.     

黏附分子在肿瘤发生及发展中的作用

细胞黏附分子是以配体和受体相结合的形式,介导细胞与细胞间或细胞与基质间相互作用的一类分子,参与机体的多种重要生理和病理过程.近年来,在对肿瘤发生和发展的研究中发现,黏附分子可通过多种途径影响肿瘤的生长、浸润及转移过程.因此.对黏附分子在肿瘤发生和发展中作用及机制的深入研究,可为肿瘤早期诊断提供重要的分子指标和发现新的治疗靶标.并为进而形成临床诊疗新策略提供重要理论支持.现就几种重要黏附分子在肿瘤生长与转移中的作用进行综述.     

囊萼紫草属与滇紫草属花粉形态比较研究

本文借助光学显微镜和扫描电镜研究了囊萼紫草属3种和滇紫草属12种植物的花粉形态。囊萼紫草属的花粉为哑铃形或茧形,中等大小,P／E比为1．6一1．67,三孔沟,内孔横长;具小刺状纹饰。滇紫草属的花粉为近长球形或近卵球形,P／E为l—1．23;三孔沟或三合沟孔,内孔一般纵长,具皱波状纹饰,在皱波上具密集的小瘤或微颗粒。从花粉形态的角度,本文支持把囊萼紫草属从滇紫草属(广义)中分离出来的观点。值得注意的是,在滇紫草属的花粉中首次观察到了一种比较少见且特化的花粉即单极三合沟孔的花粉。     

Semaphorin 3B is a 1,25-Dihydroxyvitamin D3-induced gene in osteoblasts that promotes osteoclastogenesis and induces osteopenia in mice

The vitamin D endocrine system is important for skeletal homeostasis. 1,25-Dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] impacts bone indirectly by promoting intestinal absorption of calcium and phosphate and directly by acting on osteoblasts and osteoclasts. Despite the direct actions of 1,25(OH)(2)D(3) in bone, relatively little is known of the mechanisms or target genes that are regulated by 1,25(OH)(2)D(3) in skeletal cells. Here, we identify semaphorin 3B (SEMA3B) as a 1,25(OH)(2)D(3)-stimulated gene in osteoblastic cells. Northern analysis revealed strong induction of SEMA3B mRNA by 1,25(OH)(2)D(3) in MG-63, ST-2, MC3T3, and primary osteoblastic cells. Moreover, differentiation of these osteogenic cells enhanced SEMA3B gene expression. Biological effects of SEMA3B in the skeletal system have not been reported. Here, we show that osteoblast-derived SEMA3B alters global skeletal homeostasis in intact animals and osteoblast function in cell culture. Osteoblast-targeted expression of SEMA3B in mice resulted in reduced bone mineral density and aberrant trabecular structure compared with nontransgenic littermates. Histomorphometry studies indicated that this was likely due to increased osteoclast numbers and activity. Indeed, primary osteoblasts obtained from SEMA3B transgenic mice stimulated osteoclastogenesis to a greater extent than nontransgenic osteoblasts. This study establishes that SEMA3B is a 1,25(OH)(2)D(3)-induced gene in osteoblasts and that osteoblast-derived SEMA3B impacts skeletal biology in vitro and in vivo. Collectively, these studies support a putative role for SEMA3B as an osteoblast protein that regulates bone mass and skeletal homeostasis.     

Integrating economic input–output life cycle assessment with risk assessment for a screening-level analysis

Goal, Scope, and Background  The paper describes the integration of the economic input–output life cycle assessment (EIO-LCA) model and the environmental fate and transport model (CHEMGL) with a risk assessment tool. Utilizing the EIO-LCA, instead of a traditional LCA, enables a rapid, screening-level analysis of an emerging chemical of concern, decabromodiphenyl ether (DecaBDE). The risk assessment in this study is evaluated based on the mass of chemical released, estimated concentrations, exposure, and chemical toxicity. Methods  The relative risk from ten economic sectors identified within the EIO-LCA model, 55 chemicals utilized in those sectors and DecaBDE along with four potential DecaBDE breakdown products, were evaluated for the life cycle stages and exposure pathways. The relative risk (expressed as toluene equivalents) of the different chemicals, sectors, and life cycle stages were compared to assess those representing the greatest overall relative risks to humans (via inhalation and ingestion) and fish. Results  The greatest overall risk to human health resulted from the manufacturing and production stages. For fish, the manufacturing stage represented virtually all of the risk. Of the 56 chemicals evaluated, DecaBDE represented the majority of the total risk to humans. However, DecaBDE posed the least risk compared to its potential breakdown products. Discussion  The risk to humans from ingestion, which represented the greatest risk, from the production, manufacturing, and consumption stages can be controlled and reduced through various safety precautions in the workplace. Additionally, the increasing concentration of DecaBDE in anaerobic compartments represents a threat to humans and fish via the higher risk DecaBDE breakdown products. Conclusions  Overall, the manufacturing and production life cycle stages pose the greatest risk to humans and fish. The sediment compartment received the highest DecaBDE concentration for the production, manufacturing, and consumption stages. This case study demonstrates that the integrated EIO-LCA with risk assessment is suitable for screening-level analysis of emerging chemicals due to rapid life cycle inventory analysis. Recommendations  The production and manufacturing stages allow for greater industry control and government regulation, compared to the consumption stage, because there are fewer point sources. This integrated life cycle methodology may allow chemical designers to evaluate each stage and assess areas where risks can be minimized.     

Positive Effects of Biochar on the Degraded Forest Soil and Tree Growth in China: A Systematic Review

Soil degradation threatens the forest sustainable productivity, particularly in afforestation system. Biochar derived from agroforestry waste or biomass can potentially improve the degraded forest soil and promote the tree growth. To expand the application of biochar for forestry productivity improvement, we here reviewed the effects and the underlying mechanisms of biochar on the degraded forest soil and tree growth. Totally 96 studies that conducted from pot to field investigations in China were summarized. The result suggested that biochar generally exerted positive effects on restoration of degraded forest soil such as that with compaction, acidification or soil erosion, which are mainly manifested by improving soil porosity, increasing pH, enhancing erosion resistance and mitigating greenhouse gas emissions. Furthermore, biochar incorporation promoted the growth of tested trees in most cases, which effect was mainly attributing to directly supplying nutrients, improving soil physio-chemical properties, enhancing the root’s nutrient absorption capacity, and enlarging the living space. In summary, current studies demonstrate that biochar has a unique potential for improving degraded forest soils and promoting tree growth. However, investigations on the underlying mechanisms and the long-term effects should be strengthened.     

Bibliometric analysis of Journal of Plant Ecology during 2017–2021

Issue Section: Editorial Journal of Plant Ecology (JPE) was founded in 2008. It is sponsored by the Botanical Society of China and the Institute of Botany, Chinese Academy of Sciences, and published by Oxford University Press, UK. JPE publishes diverse types of articles that fall into the broad scope of plant ecology, including plant ecophysiology, population ecology, community ecology, ecosystem ecology, landscape ecology, conservation ecology, evolutionary ecology, theoretical ecology and global change ecology.     

Cecal microbial transplantation attenuates hyperthyroid-induced thermogenesis in Mongolian gerbils

Endothermic mammals have a high energy cost to maintain a stable and high body temperature (T_b, around 37°C). Thyroid hormones are a major regulator for energy metabolism and T_b. The gut microbiota is involved in modulating host energy metabolism. However, whether the interaction between the gut microbiota and thyroid hormones is involved in metabolic and thermal regulations is unclear. We hypothesized that thyroid hormones via an interaction with gut microbiota orchestrate host thermogenesis and T_b. l -thyroxine-induced hyperthyroid Mongolian gerbils (Meriones unguiculatus) increased resting metabolic rate (RMR) and T_b, whereas Methimazole-induced hypothyroid animals decreased RMR. Both hypothyroid and hyperthyroid animals differed significantly in faecal bacterial community. Hyperthyroidism increased the relative abundance of pathogenic bacteria, such as Helicobacter and Rikenella, and decreased abundance of beneficial bacteria Butyricimonas and Parabacteroides, accompanied by reduced total bile acids and short-chain fatty acids. Furthermore, the hyperthyroid gerbils transplanted with the microbiota from control donors increased type 2 deiodinase (DIO2) expression in the liver and showed a greater rate of decline of both serum T3 and T4 levels and, consequently, a more rapid recovery of normal RMR and T_b. These findings indicate that thyroid hormones regulate thermogenesis depending on gut microbiota and colonization with normal microbiota by caecal microbial transplantation attenuates hyperthyroid-induced thermogenesis. This work reveals the functional consequences of the gut microbiota-thyroid axis in controlling host metabolic physiology and T_b in endotherms.