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991.
Temporins, anti-infective peptides with expanding properties 总被引:2,自引:1,他引:1
Mangoni ML 《Cellular and molecular life sciences : CMLS》2006,63(9):1060-1069
Antimicrobial peptides are effector molecules of the innate immune response of all pluricellular organisms, providing them
with first-line defence against pathogens. Amphibian skin secretions represent one of the richest natural sources for such
peptide antibiotics, and temporins, a large family of antimicrobial peptides from frog skin, are among the smallest ones found
in nature to date. Their functional role and modes of action have been described, along with their interesting and unique
properties. These properties make temporins good molecules for an in-depth understanding of host defence peptides in general.
Furthermore, they are attractive templates for the future design of new therapeutics against infectious diseases with new
modes of action, urgently needed due to the increasing resistance of microorganisms to the available drugs.
Received 8 November 2005; received after revision 19 December 2005; accepted 18 January 2006 相似文献
992.
2003年9月至2005年11月,在广西药用植物园、柳江种植基地和南宁郊区等一点红[Emilia sonchifolia(L.)DC.]的种植区调查研究一点红真菌性病害.结果鉴定了6种真菌性病害, 即:斑点病(Corynespora cassiicola)、灰霉病(Botrytis cinerea)、黑斑病(Alternaria longipes)、斑枯病(Septoria glycines)、炭疽病(Colletotrichum sp.)和锈病(Coleosporium sp.),其中斑点病、灰霉病、黑斑病和斑枯病的病原鉴定是采用传统分类与分子生物学分类相结合的方法进行. 相似文献
993.
目的:探讨风湿性心脏病(以下简称风心病)合并妊娠剖宫产的麻醉处理及围术期的综合治疗。方法:对33例妊娠合并风心病剖宫产的临床资料进行回顾性分析。28例产妇选用腰麻-硬脊膜外联合麻醉(简称硬脊麻),2例选用硬膜外麻醉(简称硬外麻),1例因术前出现严重心衰及2例需同时行瓣膜置换+取栓术而行全身麻醉(全麻)。术前、术中积极防治心衰,对已行换瓣术后的产妇围术期合理应用抗凝剂。结果:麻醉过程多数平稳,新生儿除全麻的2例病例Apgar评分在2—3分外,其余均在8分以上,母婴均安全度过围手术期,无1例死亡。仅一例因宫腔出现活动性出血,止血效果差而行全宫切除术,余病例无出现围术期大出血危情。结论:硬脊麻用于风心病合并妊娠剖宫产手术是安全有效的,术前、术中积极正确地防治心衰、改善心功能等综合治疗及围术期合理应用抗凝剂,可降低母婴死亡率。 相似文献
994.
Improper protein folding (misfolding) can lead to the formation of disordered (amorphous) or ordered (amyloid fibril) aggregates.
The major lens protein, α-crystallin, is a member of the small heat-shock protein (sHsp) family of intracellular molecular
chaperone proteins that prevent protein aggregation. Whilst the chaperone activity of sHsps against amorphously aggregating
proteins has been well studied, its action against fibril-forming proteins has received less attention despite the presence
of sHsps in deposits found in fibril-associated diseases (e.g. Alzheimer’s and Parkinson’s). In this review, the literature
on the interaction of αB-crystallin and other sHsps with fibril-forming proteins is summarized. In particular, the ability
of sHsps to prevent fibril formation, their mechanisms of action and the possible in vivo consequences of such associations are discussed. Finally, the fibril-forming propensity of the crystallin proteins and its
implications for cataract formation are described along with the potential use of fibrillar crystallin proteins as bionanomaterials.
Received 13 June 2008; received after revision 29 July 2008; accepted 05 August 2008 相似文献
995.
Monocytes and their pathophysiological role in Crohn’s disease 总被引:1,自引:1,他引:0
Zhou L Braat H Faber KN Dijkstra G Peppelenbosch MP 《Cellular and molecular life sciences : CMLS》2009,66(2):192-202
Our immune system shows a stringent dichotomy, on the one hand displaying tolerance towards commensal bacteria, but on the
other hand vigorously combating pathogens. Under normal conditions the balance between flora tolerance and active immunity
is maintained via a plethora of dynamic feedback mechanisms. If, however, the balancing act goes faulty, an inappropriate
immune reaction towards an otherwise harmless intestinal flora causes disease, Crohn’s disease for example. Recent developments
in the immunology and genetics of mucosal diseases suggest that monocytes and their derivative cells play an important role
in the pathophysiology of Crohn’s disease. In our review, we summarize the recent studies to discuss the dual function of
monocytes - on the one hand the impaired monocyte function initiating Crohn’s disease, and on the other hand the overactivation
of monocytes and adaptive immunity maintaining the disease. With a view to developing new therapies, both aspects of monocyte
functions need to be taken into account.
Received 1 June 2008; received after revision 24 July 2008; accepted 13 August 2008 相似文献
996.
Autoimmune diseases are a leading cause of disability and are increasing in incidence in industrialized countries. How people
develop autoimmune diseases is not completely understood, but is related to an interaction between genetic background, environmental
agents, autoantigens and the immune response. Molecular mimicry continues to be an important hypothesis that explains how
an infection with an environmental agent results in autoimmune disease of the nervous system and other target organs. Although
molecular mimicry has yet to be unequivocally proven, in the past several years there has been a sharpening of its definition
with better experimental data implicating it as a cause of neurological disease in humans.
Received 9 July 2007; received after revision 15 November 2007; accepted 27 November 2007 相似文献
997.
Rosenstiel P Jacobs G Till A Schreiber S 《Cellular and molecular life sciences : CMLS》2008,65(9):1361-1377
NOD-like receptors (NLRs) comprise a family of cytosolic proteins that have been implicated as ancient cellular sentinels
mediating protective immune responses elicited by intracellular pathogens or endogenous danger signals. Genetic variants in
NLR genes have been associated with complex chronic inflammatory barrier diseases (e.g. Crohn disease, bronchial asthma). In
this review, we focus on the molecular pathophysiology of NLRs in the context of chronic inflammatory diseases and pinpoint
recent advances in the evolutionary understanding of NLR biology. We propose that the field of NLRs may serve as a prototype
for how a comprehensive understanding of an element of the immunological barrier will eventually lead to the development of
targeted diagnostic, therapeutic and/or preventive strategies.
Received 29 October 2007; received after revision 10 December 2007; accepted 19 December 2007 相似文献
998.
Parkinson’s disease (PD) is characterized by the death of dopaminergic neurons and the presence of Lewy bodies in the substantia
nigra pars compacta. The mechanisms involved in the death of neurons as well as the role of Lewy bodies in the pathogenesis
of the disease are still unclear. Lewy bodies are made of aggregated proteins, in which α-synuclein represents their major
component. α-Synuclein interacts with synphilin-1, a protein that is also present in Lewy bodies. When expressed in cells,
synphilin-1 forms inclusions together with α-synuclein that resemble Lewy bodies. Synphilin-1 is ubiquitylated by various
E3 ubiquitin-ligases, such as SIAH, parkin and dorfin. Ubiquitylation of synphilin-1 by SIAH is essential for its aggregation
into inclusions. We recently identified a new synphilin-1 isoform, synphilin-1A, that is toxic to neurons, aggregation-prone
and accumulates in detergent-insoluble fractions of brains from α-synucleinopathy patients. Synphilin-1A inclusions recruit
both α-synuclein and synphilin-1. Aggregation of synphilin-1 and synphilin-1A seems to be protective to cells. We now discuss
several aspects of the neurobiology and pathology of synphilin-1 isoforms, focusing on possible implications for PD.
Received 26 July 2007; received after revision 19 September 2007; accepted 15 October 2007 相似文献
999.
Double KL Dedov VN Fedorow H Kettle E Halliday GM Garner B Brunk UT 《Cellular and molecular life sciences : CMLS》2008,65(11):1669-1682
Neuromelanin and lipofuscin are two pigments produced within the human brain that, until recently, were considered inert cellular waste products of little interest to neuroscience. Recent research has increased our understanding of the nature and interactions of these pigments with their cellular environment and suggests that these pigments may, indeed, influence cellular function. The physical appearance and distribution of the pigments within the human brain differ, but both accumulate in the aging brain and the pigments share some structural features. Lipofuscin accumulation has been implicated in postmitotic cell aging, while neuromelanin is suggested to function as an iron-regulatory molecule with possible protective functions within the cells which produce this pigment. This review presents comparative aspects of the biology of neuromelanin and lipofuscin, as well as a discussion of their hypothesized functions in brain and their possible roles in aging and neurodegenerative disease. 相似文献
1000.
Delgado M Pérez-Miguelsanz J Garrido F Rodríguez-Tarduchy G Pérez-Sala D Pajares MA 《Cellular and molecular life sciences : CMLS》2008,65(13):2080-2090
Wilson's disease is characterized by longterm hepatic accumulation of copper leading to liver disease with reduction of S-adenosylmethionine synthesis. However, the initial changes in this pathway remain unknown and constitute the objective of the present study. Using the Long Evans Cinnamon rat model, early alterations were detected in the mRNA and protein levels, as well as in the activities of several enzymes of the methionine cycle. Notably, the main change was a redox-mediated 80% decrease in the mRNA levels of the methionine adenosyltransferase regulatory subunit as compared to the control group. Moreover, changes in S-adenosylmethionine, S-adenosylhomocysteine, methionine and glutathione levels were also observed. In addition, in vitro experiments show that copper affects the activity and folding of methionine adenosyltransferase catalytic subunits. Taken together, these observations indicate that early copper accumulation alters methionine metabolism with a pattern distinct from that described previously for other liver diseases. 相似文献