接受昆虫分类文章的SCI昆虫学源期刊名录

对SCI及期刊影响因子作了简要介绍,列出接受昆虫分类文章的SCI昆虫学源期刊名录及其影响因子,以便于昆虫分类学工作者投稿、阅读文献及订阅杂志。     

昆虫学及部分相关学科SCI收录期刊介绍

本文以表格形式介绍了SCI收录的42种昆虫学核心期刊的英文刊名、中文刊名、出版国和最新影响因子,并将其中影响因子最高的前20种期刊及我国进入SCI—E的1种昆虫学期刊进行了全面的揭示,包括英文刊名、汉译刊名、出版周期、原版刊号、最新影响因子、国际标准刊号、出版地、出版者、联系地址、最新期刊网址、期刊描述等全方位的期刊信息。期刊描述内容包括：创刊年及期刊的发展、刊载的主要内容、网站可免费获取的该刊目次和文摘及全文信息等。     

2006—2009年《动物学研究》发表论文被SCI期刊引用情况

近期,本所图书馆通过Web of Knowledge中的Web of Science,在SCI-e上检索到2006—2009年《动物学研究》发表论文共有65篇被SCI期刊引用,其引用的SCI期刊有71种(见附录1),总引次数为109     

《SCI》源期刊昆虫学杂志简介

对于大多数昆虫学家乃至生物学家而言 ,比较熟悉的大型国际检索期刊当为美国《生物学文摘》(Biological Abstracts,BA)、英国《动物学记录》(Zoological Record,ZR)等 ,而对综合性检索期刊《SCI》了解较少。近年来 ,我国不少科研和教学单位刮起了《SCI》风 ,在晋职、评奖、立项时常常以《SCI》期刊源文章为重要的评价指标 ,而且 ,此风愈刮愈烈 ,大有漫卷全国之势。虽然不同的单位与个人对此现象有不同的看法 ,但多在国际上影响因子较高的期刊上发表文章 ,无疑会对提高我国的学术影响力起到积极作用。本文作者对有关昆虫学《SCI》期…     

2010年SCI收录的昆虫学期刊及相关期刊2009年的影响因子

<正>截止2010年6月20日,SCI共收录昆虫学期刊86种;其中核心或内圈期刊42种,扩展或外圈期刊44种,总数比2009年同期增加4种。核心期刊的数量与期刊均与去年相同,扩展期     

生物多样性保护及其相关学科SCI收录期刊介绍

将SCI收录的12种生物多样性保护核心期刊及中国进入科学引文索引和科学引文索引扩展版的10种相关期刊进行了全面的揭示,包括英文刊名、汉译刊名、出版周期、原版刊号、最新影响因子、国际标准刊号、出版地、出版者、联系地址、最新期刊网址,期刊描述等全方位的期刊信息。期刊描述内容包括:期刊的创刊年以及期刊的发展,期刊主要内容及使用的语言,网站可免费获取的该刊目次和文摘及全文信息等。     

Cell Research期刊征订单

CellResearch为中国科学院上海生命科学研究院主办,以全英文刊登国内外细胞生物学及其相关领域的原创性研究论文、综述、快报和述评的国际性期刊。已被Index Medicus,Medline,SCI（SciSearch ISI Web of Science）,BIOSIS,CA,VINIT以及《中国科学引文数据库》、《万方数据库》（光盘版,网络版）、《中国英文版科技期刊数据库》、《中文科技期刊数据库》、《中国学术期刊》（光盘版,网络版）、     

2011年SCI收录的昆虫学期刊及相关期刊2010年的影响因子

<正>截止2011年6月28日,SCI共收录昆虫学期刊89种;其中核心或内圈期刊42种,扩展或外圈期刊47种,总数比2010年同期增加3种。核心期刊的数量与期刊均与去年相同,扩展期刊新增了南非的《非洲无脊椎动物》、马来西亚的《亚洲蚁学》及新西兰的《新西兰昆虫学家》3种期刊。2010年各昆虫学期刊的影响因子见表1;表中各刊的名字按字母顺序排列,部分近2年新加入的期刊尚未有影响因子。     

2012年SCI收录的昆虫学期刊及相关期刊2011年的影响因子

<正>截止2012年6月28日,SCI共收录昆虫学期刊90种;其中核心或内圈期刊41种,扩展或外圈期刊49种,总数比去年同期增加1种。扩展期刊新增了美国的《昆虫学研究》和英国的《系统与应用蜱螨学》2种期刊;以前属于核心期刊的《农业和城市昆虫学杂志》今年6月份则被剔除在收录范围之外,因此,今年收录的核心期刊的数量比去年减少了1种。     

信息中心招聘“生命科学期刊社”社长

<正>中科院上海生命科学信息中心是中科院上海生命科学研究院成员单位之一,统一管理10多种中英文生命科学期刊,其中,《Cell Research》是我国生物学一流的旗舰期刊,2008年该刊SCI影响因子为4.535,在我国科技期刊走向国际前沿中具有示范作用。为了进一步打造高水平的生命科学学术期刊集群,为我国学术期刊跨越发展起到引领作用,中科院决定在上海生命     

Clinical correlates of frequency analyses of cardiovascular control after spinal cord injury

Spinal cord injury (SCI) has profound effects on cardiovascular autonomic function due to injury to descending autonomic pathways, and cardiovascular diseases are the leading causes of morbidity and mortality after SCI. Evaluation of cardiovascular autonomic dysfunction after SCI and appraisal of simple noninvasive autonomic assessments that are clinically meaningful would be useful to SCI clinicians and researchers. We aimed to assess supine and upright cardiovascular autonomic function from frequency analyses of heart rate and blood pressure variability (HRV and BPV) after SCI. We studied 26 subjects with chronic cervical or thoracic SCI and 17 able-bodied controls. We continuously recorded R-R interval (RRI, by ECG) and beat-to-beat blood pressure (by Finometer) in supine and seated positions. Cardiovascular control was assessed from spectral analysis of RRI and blood pressure time series. Cardiac baroreflex control was assessed from cross-spectral analyses of low-frequency spectra. Supine and upright low-frequency HRV and BPV were reduced in cervical SCI subjects, as were total BPV and HRV. Supine high-frequency HRV was reduced in thoracic SCI subjects. Cardiac baroreflex delay was increased in cervical SCI subjects. Supine frequency domain indexes were correlated with sympathetic skin responses, orthostatic cardiovascular responses, and plasma catecholamine levels. SCI results in reduced sympathetic drive to the heart and vasculature and increased baroreflex delay in cervical SCI subjects and reduced cardiac vagal tone in thoracic SCI subjects. Frequency analyses of autonomic function are related to clinical measures of autonomic control after SCI and provide useful noninvasive clinical tools with which to assess autonomic completeness of injury following SCI.     

Spinal cord injury causes bone loss through peroxisome proliferator‐activated receptor‐γ and Wnt signalling

It has long been recognized that spinal cord injury (SCI) leads to a loss of bone mineral. However, the mechanisms of bone loss after SCI remain poorly understood. The aim of this study was to investigate whether SCI causes a shift in skeletal balance between osteoblastogenesis and adipogenesis. Eighty male Sprague‐Dawley rats at 6 weeks of age were randomly divided into two groups: sham‐operated (SHAM) group and SCI group. The rats were killed after 3 weeks, 3 months and 6 months, and their femora, tibiae and humeri were collected for mesenchymal stem cells (MSCs) culture, bone mineral density (BMD) measurement, RNA analysis and Western Blot analysis. Osteogenic and adipogenic differentiation potential of MSCs from SCI rats and SHAM rats was evaluated. We found increased marrow adiposity in sublesional tibiae of SCI rats. SCI caused increased peroxisome proliferator‐activated receptor‐γ (PPARγ) expression and diminished Wnt signalling in sublesional tibiae. Interestingly, in MSCs from SCI rats treated with the PPARγ inhibitor GW9662, the ratios of RANKL to OPG expression were significantly decreased. On the contrary, in MSCs from SCI rats treated with the PPARγ ligand troglitazone, the ratios of RANKL to OPG expression in SCI rats were significantly increased. High expression of PPARγ may lead to increased bone resorption through the RANKL/OPG axis after SCI. In addition, high expression also results in the suppression of osteogenesis and enhancement of adipogenesis in SCI rats. SCI causes a shift in skeletal balance between osteoblastogenesis and adipogenesis, thus leading to bone loss after SCI.     

Cellular-scale transport in deformed skeletal muscle following spinal cord injury

Deep tissue injury (DTI) is a severe pressure ulcer initiating in weight-bearing skeletal muscles. Being common in spinal cord injury (SCI) patients, DTI is associated with mechanical cell damage and ischaemia. Muscle microanatomy in SCI patients is characterised by reduced myofibre sizes and smaller, fewer capillaries. We hypothesise that these changes influence mass transport in SCI muscles, making DTI more probable. Using multiphysics models of microscopic cross-sections through normal and SCI muscles, we studied effects of the following factors on transport of glucose and myoglobin (potential biomarker for early DTI detection): (i) abnormal SCI muscle microanatomy, (ii) large tissue deformations and (iii) ischaemia. We found that the build-up of concentrations of glucose and myoglobin is slower for SCI muscles, which could be explained by the pathological SCI microanatomy. These findings overall suggest that microanatomical changes in muscles post-SCI play an important role in the vulnerability of the SCI patients to DTI.     

Direct Evidence for Calpain Involvement in Apoptotic Death of Neurons in Spinal Cord Injury in Rats and Neuroprotection with Calpain Inhibitor

To demonstrate calpain involvement in neurodegeneration in rat spinal cord injury (SCI), we examined SCI segments for DNA fragmentation, neurons for calpain overexpression, neuronal death, and neuroprotection with calpain inhibitor (E-64-d). After the induction of SCI (40 g cm force) on T12, rats were treated within 15 min with vehicle (DMSO) or E-64-d. Sham animals underwent laminectomy only. Animals were sacrificed at 24 h, and five 1-cm long spinal cord segments were collected: two rostral (S1 and S2), one lesion (S3), and two caudal segments (S4 and S5). Agarose gel electrophoresis of DNA samples isolated from the SCI segments showed both random and internucleosomal DNA fragmentation indicating occurrence of necrosis as well as apoptosis mostly in the lesion, moderately in caudal, and slightly in rostral segments from SCI rats. Treatment of SCI rats with E-64-d (1 mg/kg) reduced DNA fragmentation in all segments. The lesion and adjacent caudal segments (S3 and S4) were further investigated by in situ double-immunofluorescent labelings that showed increase in calpain expression in neurons in SCI rats and decrease in calpain expression in SCI rats treated with E-64-d. In situ combined TUNEL and double-immunofluorescent labelings directly detected co-localization of neuronal death and calpain overexpressin in SCI rats treated with only vehicle while attenuation of neuronal death in SCI rats treated with E-64-d. Previous studies from our laboratory indirectly showed neuroprotective effect of E-64-d in SCI rats. Our current results provide direct in situ evidence for calpain involvement in neuronal death and neuroprotective efficacy of E-64-d in lesion and penumbra in SCI rats. Special issue in honor of Naren Banik.     

Sensory function above lesion level in spinal cord injury patients with and without pain

Patients with spinal cord injury (SCI) may or may not develop central neuropathic pain despite having cord lesions of apparently the same site, extension and nature. The consequences of the cord lesion in the central nervous system and the mechanisms underlying pain are unclear. In this study, we examined sensory detection and pain thresholds above injury level in 17 SCI patients with central neuropathic pain, in 18 SCI patients without neuropathic pain, and in 20 control subjects without injury and pain. The SCI pain group had significantly higher cold and warm detection thresholds compared with the SCI pain free group and controls and higher tactile detection thresholds compared with the SCI pain free group. No difference in pain or pain tolerance thresholds was seen among pain and pain free SCI patients. These data suggest changes in somatosensory function in dermatomes rostral to the segmental injury level linked to the presence of central neuropathic pain in SCI patients. The results are discussed in relation to current concepts of pain inhibitory and facilitating systems.     

Sensory function above lesion level in spinal cord injury patients with and without pain

Patients with spinal cord injury (SCI) may or may not develop central neuropathic pain despite having cord lesions of apparently the same site, extension and nature. The consequences of the cord lesion in the central nervous system and the mechanisms underlying pain are unclear. In this study, we examined sensory detection and pain thresholds above injury level in 17 SCI patients with central neuropathic pain, in 18 SCI patients without neuropathic pain, and in 20 control subjects without injury and pain. The SCI pain group had significantly higher cold and warm detection thresholds compared with the SCI pain free group and controls and higher tactile detection thresholds compared with the SCI pain free group. No difference in pain or pain tolerance thresholds was seen among pain and pain free SCI patients. These data suggest changes in somatosensory function in dermatomes rostral to the segmental injury level linked to the presence of central neuropathic pain in SCI patients. The results are discussed in relation to current concepts of pain inhibitory and facilitating systems.     

Electroacupuncture modulates the intestinal microecology to improve intestinal motility in spinal cord injury rats

Spinal cord injury (SCI) is a disease involving gastrointestinal disorders. The underlying mechanisms of the potential protective effects of electroacupuncture (EA) and 5-hydroxytryptamine (5-HT) system on SCI remain unknown. We investigated whether EA improves gut microbial dysbiosis in SCI and regulates the 5-HT system. 16S rDNA gene sequencing was applied to investigate alterations in the gut microbiome of the rats. Faecal metabolites and the expression of the 5-HT system were detected. EA and faecal microbiota transplantation (FMT) treatment facilitated intestinal transmission functional recovery and restored the colon morphology of SCI rats. The composition of the intestinal microbiota, including numbers of phylum Proteobacteria, class Clostridia, order Bacteroidales, and genus Dorea, were amplified in SCI rats, and EA and FMT significantly reshaped the intestinal microbiota. SCI resulted in disturbed metabolic conditions in rats, and the EA and FMT group showed increased amounts of catechin compared with SCI rats. SCI inhibited 5-HT system expression in the colon, which was significantly reversed by EA and FMT treatment. Therefore, EA may ameliorate SCI by modulating microbiota and metabolites and regulate the 5-HT system. Our study provides new insights into the pathogenesis and therapy of SCI from the perspective of microbiota and 5-HT regulation.     

Long-term clinical observation of patients with acute and chronic complete spinal cord injury after transplantation of NeuroRegen scaffold

Spinal cord injury (SCI) often results in an inhibitory environment at the injury site. In our previous studies, transplantation of a scaffold combined with stem cells was proven to induce neural regeneration in animal models of complete SCI. Based on these preclinical studies, collagen scaffolds loaded with the patients’ own bone marrow mononuclear cells or human umbilical cord mesenchymal stem cells were transplanted into SCI patients. Fifteen patients with acute complete SCI and 51 patients with chronic complete SCI were enrolled and followed up for 2 to 5 years. No serious adverse events related to functional scaffold transplantation were observed. Among the patients with acute SCI, five patients achieved expansion of their sensory positions and six patients recovered sensation in the bowel or bladder. Additionally, four patients regained voluntary walking ability accompanied by reconnection of neural signal transduction. Among patients with chronic SCI, 16 patients achieved expansion of their sensation level and 30 patients experienced enhanced reflexive defecation sensation or increased skin sweating below the injury site. Nearly half of the patients with chronic cervical SCI developed enhanced finger activity. These long-term follow-up results suggest that functional scaffold transplantation may represent a feasible treatment for patients with complete SCI.