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Summary Males ofDiprion similis respond to both the (+)-2R,3R,7R and (–)-2S,3S,7S enantiomers of its sex pheromone, erythro-3,7-dimethyl pentadecan-2-yl propionate. A mixture of the 2 enantiomers induces a response similar to that of the individual components.Acknowledgments. C.L. was supported by a NERC Fellowship. 相似文献
83.
Summary Physalaemin, which excites an identifiable molluscan giant neurone (the TAN, tonically autoactive neurone), lost the effect after the trypsin treatment. Unexpectedly, this peptide shows an inhibitory effect on the same neurone after chymotrypsin treatment. Deamino-dicarba-(d-d-)oxytocin and d-d-Arg-vasotocin, which excite another identifiable neurone (the PON, periodically oscillating neurone) continue to show the effect after chymotrypsin treatment (6 h). But d-d-Arg-vasotocin losts the effect on the PON after trypsin treatment.The authors thank Dr Sadaaki Iwanaga of Osaka University and Dr Atsuo Inoue of Daiichi Pharmaceutical Co. for their helpful advice, and Miss Hiroko Tamura for her technical assistance. 相似文献
84.
Effect of RES-blockade on bone marrow cells was studied serially after irradiation in LPS-resistant mice. Injection of carbon particles reduced damage and accelerated recovery of marrow hemopoietic stem cells, indicating that LPS-resistant mice can react normally to RES-blockade. 相似文献
85.
Nude mice were inoculated with BMA1 cells. These are cells which produce granulocyte-macrophage colony stimulating factor (GM-CSF); They are derived from mouse bone marrow stromal cells transfected with adenovirus 5 DNA. Progressive neutrophilia developed as the tumor grew, but disappeared quickly after local tumor excision. Media conditioned with tumor cells had GM-CSF but neither erythropoietin nor burst-promoting activity. In all the tumors which developed, focal areas of bone formation were found among fibrosarcomatous tissues. 相似文献
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I. Yokoi H. Takeuchi A. Sakai A. Mori 《Cellular and molecular life sciences : CMLS》1977,33(3):363-366
Summary An identifiable giant neurone, PON (periodically oscillating neurone), of Achatina fulica Férussac, inhibited by erythro--hydroxy-L-glutamic acid, was also inhibited by 2 relatives of -hydroxy glutamic acid, ibotenic acid and quisqualic acid. These substances similarly showed the effect on the neurone even in the chloride-free medium.The authors wish to thank Professor Emeritus T. Takemoto of Tohoku University, Dr H. Iwasaki of Takeda Chemical Co. and Professor C. H. Eugster of Zurich University for the donation of precious substances, and Miss H. Tamura for technical assistance. 相似文献
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Amyloid beta-protein deposition in tissues other than brain in Alzheimer's disease 总被引:21,自引:0,他引:21
Alzheimer's disease is the most common cause of progressive intellectual failure in aged humans. The filamentous brain lesions which define the disease occur within neurons (neurofibrillary tangles), in extracellular cerebral deposits (amyloid plaques) and in meningocerebral blood vessels (amyloid angiopathy). They are found in lesser numbers in the brains of virtually all old humans. A protein with a relative molecular mass (Mr) of approximately 4,000, designated amyloid beta-protein or amyloid A4 protein, is the subunit of the vascular and plaque amyloid filaments in individuals with Alzheimer's disease, normal ageing and trisomy 21 (Down's syndrome). The amyloid beta-protein is a small fragment of a membrane-associated glycoprotein, encoded by a gene on human chromosome 21 which is telomeric to a genetic defect that causes at least some cases of familial Alzheimer's disease. Until now, the pathological lesions of the disease have been found only in the brain, although reports of phenotypic abnormalities in non-neural tissues have suggested that Alzheimer's disease may be a widespread, systemic disorder. Here we report the detection of amyloid beta-protein deposits in non-neural tissues and blood vessels of Alzheimer's disease patients, including skin, subcutaneous tissue and intestine. The protein was also present in non-neural tissues in a proportion of aged, normal subjects. Our findings indicate that a principal feature of the disease process is expressed subclinically in tissues other than brain. The occurrence of amyloid beta-protein deposits in multiple tissues suggests that the protein may be produced locally in numerous organs or may, as in other human amyloidoses, be derived from a common circulating precursor. These observations affect the rationale for many experiments analysing the amyloid beta-protein precursor and its messenger RNAs in Alzheimer's disease brain tissue and have major implications for the pathogenesis and treatment of the disease. 相似文献