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591.
Muscle LIM protein: expressed in slow muscle and induced in fast muscle by enhanced contractile activity 总被引:5,自引:0,他引:5
Schneider Achim G.; Sultan Karim R.; Pette Dirk 《American journal of physiology. Cell physiology》1999,276(4):C900
To identify earlychanges in gene expression during the fast-to-slow transition inducedby chronic low-frequency stimulation, total RNA wasextracted from 12-h-stimulated tibialis anterior (TA) muscles of ratsand amplified by differential display RT-PCR. Among the signals ofdifferentially expressed mRNAs, a cDNA ~300 bp in length, which wasalmost undetectable in control TA muscles but prominent in stimulatedTA and normal soleus muscles, was identified. This cDNA was cloned andidentified as corresponding to the mRNA of the muscle LIM protein(MLP). Its differential expression in control, stimulated TA, andsoleus muscles was verified by Northern blotting. Antibodies againstMLP were used to identify by immunoblot analysis a protein of 22 kDa,the predicted molecular mass of MLP. Immunohistochemistry revealedstrong reactivity for MLP in all fibers of normal soleus muscle andfaint staining of some type IIA and type I fibers in control TA muscle.These fibers increased in number and staining intensity in4-day-stimulated TA muscle. MLP thus seems to play an essential roleduring the rearrangement of cytoskeletal and/or myofibrillar structuresin transforming adult muscle fibers. 相似文献
592.
A. M. N. Sultan 《Molecular and cellular biochemistry》1988,79(2):113-118
Summary The utilization of D-3-HB and the production of acetoacetate by the perfused rat heart were investigated over a wide range
of DL-3-HB concentrations. The rate of D-3-HB utilization is concentration dependent, and shows saturation kinetics. The oxidized
amount of D-3-HB when D-3-HB as a sole substrate, accounts at a maximum for 50% of the total oxygen consumption, which suggest
the contribution of the endogenous substrate as fuel source along with D-3-HB. The proportion of the D-3-HB consumed that
is oxidized rather than released as acetoacetate increases from 70% to 93% as the concentration of D-3-HB falls from 6.99
mM to 0.30 mM. 相似文献
593.
594.
The subcellular localization of Factor VIII/von Willebrand protein (VIII R:Ag) is studied with monoclonal antibody and gold immunocytochemical technique. Monoclonal antibody against purified VIII R:Ag is brightly fluorescent on megakaryocytes and platelets. In E.M., gold immunolabeling is performed on thin cell sections of human megakaryocytes and platelets. Different embedding materials are used to preserve the antigenicity : Epon embedded megakaryocytes show a high concentration of VIII R:Ag in alpha-granules using 4F9 monoclonal antibody. In comparison, lowicryl K4M embedded material does not improve the same specificity, only a few platelets granules were stained. This subcellular localization, in full agreement with biochemical results appears visualized for the first time in E.M. 相似文献
595.
A. H. Sultan M. A. Kamm C. N. Hudson C. I. Bartram 《BMJ (Clinical research ed.)》1994,308(6933):887-891
OBJECTIVES--To determine (i) risk factors in the development of third degree obstetric tears and (ii) the success of primary sphincter repair. DESIGN--(i) Retrospective analysis of obstetric variables in 50 women who had sustained a third degree tear, compared with the remaining 8553 vaginal deliveries during the same period. (ii) Women who had sustained a third degree tear and had primary sphincter repair and control subjects were interviewed and investigated with anal endosonography, anal manometry, and pudendal nerve terminal motor latency measurements. SETTING--Antenatal clinic in teaching hospital in inner London. SUBJECTS--(i) All women (n = 8603) who delivered vaginally over a 31 month period. (ii) 34 women who sustained a third degree tear and 88 matched controls. MAIN OUTCOME MEASURES--Obstetric risk factors, defecatory symptoms, sonographic sphincter defects, and pudendal nerve damage. RESULTS--(i) Factors significantly associated with development of a third degree tear were: forceps delivery (50% v 7% in controls; P = 0.00001), primiparous delivery (85% v 43%; P = 0.00001), birth weight > 4 kg (P = 0.00002), and occipito-posterior position at delivery (P = 0.003). No third degree tear occurred during 351 vacuum extractions. Eleven of 25 (44%) women who were delivered without instruments and had a third degree tear did so despite a posterolateral episiotomy. (ii) Anal incontinence or faecal urgency was present in 16 women with tears and 11 controls (47% v 13%; P = 0.00001). Sonographic sphincter defects were identified in 29 with tears and 29 controls (85% v 33%; P = 0.00001). Every symptomatic patient had persistent combined internal and external sphincter defects, and these were associated with significantly lower anal pressures. Pudendal nerve terminal motor latency measurements were not significantly different. CONCLUSIONS--Vacuum extraction is associated with fewer third degree tears than forceps delivery. An episiotomy does not always prevent a third degree tear. Primary repair is inadequate in most women who sustain third degree tears, most having residual sphincter defects and about half experiencing anal incontinence, which is caused by persistent mechanical sphincter disruption rather than pudendal nerve damage. Attention should be directed towards preventive obstetric practice and surgical techniques of repair. 相似文献
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598.
Faisal Thayyullathil Anees Rahman Cheratta Ameer Alakkal Karthikeyan Subburayan Siraj Pallichankandy Yusuf A. Hannun Sehamuddin Galadari 《Cell death & disease》2021,12(1)
Ferroptosis is a type of regulated cell death characterized by ROS accumulation and devastating lipid peroxidation (LPO). The role of acid sphingomyelinase (ASM), a key enzyme in sphingolipid metabolism, in the induction of apoptosis has been studied; however, to date its role in ferroptosis is unclear. In this study, we report that ASM plays a hitherto unanticipated role in promoting ferroptosis. Mechanistically, Erastin (Era) treatment results in the activation of ASM and generation of ceramide, which are required for the Era-induced reactive oxygen species (ROS) generation and LPO. Inhibition of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) or removal of intracellular ROS, significantly reduced Era-induced ASM activation, suggesting that NADPH oxidase-derived ROS regulated ASM-initiated redox signaling in a positive feedback manner. Moreover, ASM-mediated activation of autophagy plays a critical role in ferroptosis inducers (FINs)-induced glutathione peroxidase 4 (GPX4) degradation and ferroptosis activation. Genetic or pharmacological inhibition of ASM diminishes Era-induced features of autophagy, GPX4 degradation, LPO, and subsequent ferroptosis. Importantly, genetic activation of ASM increases ferroptosis in cancer cells induced by various FINs. Collectively, these findings reveal that ASM plays a novel role in ferroptosis that could be exploited to improve pathological conditions that link to ferroptosis.Subject terms: Lipid peroxides, Cancer models, Macroautophagy, Lipid signalling 相似文献