全文获取类型
收费全文 | 232篇 |
免费 | 48篇 |
专业分类
儿科学 | 1篇 |
基础医学 | 73篇 |
临床医学 | 6篇 |
内科学 | 59篇 |
神经病学 | 109篇 |
外科学 | 4篇 |
综合类 | 1篇 |
预防医学 | 25篇 |
肿瘤学 | 2篇 |
出版年
2009年 | 1篇 |
2007年 | 1篇 |
2003年 | 2篇 |
2002年 | 4篇 |
2001年 | 3篇 |
2000年 | 3篇 |
1999年 | 3篇 |
1998年 | 5篇 |
1997年 | 3篇 |
1996年 | 4篇 |
1995年 | 4篇 |
1994年 | 7篇 |
1993年 | 6篇 |
1992年 | 15篇 |
1991年 | 24篇 |
1990年 | 16篇 |
1989年 | 13篇 |
1988年 | 13篇 |
1987年 | 10篇 |
1986年 | 19篇 |
1985年 | 20篇 |
1984年 | 9篇 |
1983年 | 9篇 |
1982年 | 10篇 |
1981年 | 14篇 |
1980年 | 5篇 |
1979年 | 5篇 |
1978年 | 11篇 |
1977年 | 4篇 |
1976年 | 1篇 |
1975年 | 2篇 |
1974年 | 4篇 |
1973年 | 4篇 |
1972年 | 2篇 |
1971年 | 3篇 |
1970年 | 3篇 |
1969年 | 6篇 |
1967年 | 4篇 |
1966年 | 2篇 |
1965年 | 3篇 |
1964年 | 1篇 |
1958年 | 1篇 |
1956年 | 1篇 |
排序方式: 共有280条查询结果,搜索用时 15 毫秒
41.
Korean hemorrhagic fever virus (KHFV) has been adapted to the Wistar and Fisher strains of rats. Infection was detected by the appearance of specific antigen in the lung tissue of the infected rats at 14 to 64 days after inoculation and by the appearance of circulating antibodies in ther serum which reacted specifically with KHFV antigen in the lungs of infected Apodemus agrarius subsp. coreae 3 weeks after inoculation. Distribution of antigen in rat tissues as determined by immunofluorescent staining was the same as that in Apodemus mice except that antigen was present in the spleens of rats. Adaptation of KHFV to the laboratory rat provides an animal model that is free of wild rodent viruses and is readily available for use in studies on the characterization of KHFV. 相似文献
42.
43.
The sequential development of spongiform change and gliosis of scrapie in the golden Syrian hamster 总被引:1,自引:0,他引:1
C L Masters R G Rohwer M C Franko P Brown D C Gajdusek 《Journal of neuropathology and experimental neurology》1984,43(3):242-252
The lesion profiles of spongiform change and gliosis in the hamster occurring after intracerebral (IC) inoculation of scrapie virus, are calculated and compared to the lesion profile of spongiform change of scrapie in mice and of scrapie and Creutzfeldt-Jakob disease (CJD) in the squirrel monkey. The profile of scrapie in hamsters differs considerably from that of a closely related strain of scrapie in mice, and both differ from scrapie and CJD in the squirrel monkey. These differences emphasize the effect of the host on the distribution of pathological changes in these unconventional virus infections. The sequential development of the lesions in the hamster shows that the earliest changes are detectable before the onset of clinical disease 49-57 days after inoculation, as assessed by light microscopy. Gliosis is detectable by indirect immunofluorescence 35-39 days after inoculation by use of a monoclonal antibody directed against astrocytes. 相似文献
44.
A new case of Creutzfeldt-Jakob disease associated with human growth hormone therapy in New Zealand 总被引:2,自引:0,他引:2
M Croxson P Brown B Synek M G Harrington R Frith G Clover J Wilson D C Gajdusek 《Neurology》1988,38(7):1128-1130
A clinically atypical, neuropathologically verified case of Creutzfeldt-Jakob disease is described in a 32-year-old New Zealand woman with idiopathic hypopituitarism who had been treated in late adolescence (1970 to 1973) with human growth hormone processed from pooled cadaveric pituitary glands. 相似文献
45.
S Bahmanyar R K Liem J W Griffin D C Gajdusek 《Journal of neuropathology and experimental neurology》1984,43(4):369-375
The antineurofilament antibodies found in the serum of a chimpanzee with experimental Creutzfeldt-Jakob disease reacted specifically with the 200,000-dalton polypeptide of the purified neurofilament triplet. They also reacted strongly with thoroughly characterized neurofilament swellings of proximal axons of spinal cord motoneurons from beta,beta' iminodipropionitrile (IDPN)-intoxicated rats. 相似文献
46.
47.
Neuritic degeneration is a prominent ultrastructural feature of scrapie in hamsters. To investigate the morphogenesis of neuritic degeneration, we examined brain tissues from hamsters infected with the 263K strain of scrapie virus and from age-matched controls at varying intervals following intracerebral inoculation. Dystrophic neurites--defined as dendrites, axonal preterminals, and myelinated axons containing mitochondria and pleomorphic, electron-dense inclusion bodies--were found as early as 2 weeks postinoculation. Their numbers increased with the incubation period, and their highest density was observed at the terminal stage of disease. Occasionally, small clusters of these structures formed neuritic plaques. Such dystrophic neurites were only rarely seen in brains of uninfected hamsters. Experimental scrapie thus provides an animal model for human neuroaxonal dystrophies. In addition, since this model allows predictable formation of brain amyloid, it may serve as a model for the study of neuronal aging and Alzheimer's disease. 相似文献
48.
R M Garruto C C Plato N C Myrianthopoulos M S Schanfield D C Gajdusek 《American journal of medical genetics》1983,14(2):289-298
Blood group frequencies, immunoglobulin allotypes, and dermatoglyphic patterns were determined on patients with amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia (PD), two chronic, degenerative, neurologic disorders of unknown cause found commonly among the Chamorros of the Mariana Islands, in an attempt to identify a specific genetic or phenetic marker associated with either disorder. With the exception of the Kidd system, no significant differences were found in blood group frequencies nor in immunoglobulin allotypes between ALS patients, PD patients, and unaffected controls. The dermatoglyphic analysis demonstrated that ALS patients had higher frequencies of palmar patterns and accessory triradii in the IV interdigital area, and PD patients had significantly higher frequencies of complete simian creases and of palmar patterns in the thenar/I interdigital area than unaffected controls. The frequencies of the remaining dermatoglyphic traits showed no significant differences. We conclude that none of the marker systems tested show a particular pattern of association in patients and controls or a genetic predisposition to either disorder, and that early identification of at-risk individuals remains elusive. 相似文献
49.
Pamela E. Rodgers-Johnson Ralph M. Garruto D. Carleton Gajdusek 《Trends in neurosciences》1988,11(12):526-532
Tropical myeloneuropathies are a group of neurological disorders known to occur in subtropical and tropical regions. Many aetiologies have been postulated and investigated over the past 100 years, but no single cause has been found. Recent studies suggest that human T-cell lymphotropic virus HTLV-I is the causative agent of one of these tropical myeloneuropathies, endemic tropical spastic paraparesis, and of a related disorder in southern Japan called HTLV-I-associated myelopathy. Endemic tropical spastic paraparesis is now being reported from geographical and climatic regions that were previously thought to be free of these disorders. 相似文献
50.
Neuronal degeneration and neurofilament accumulation in the trigeminal ganglia in Creutzfeldt-Jakob disease 总被引:2,自引:0,他引:2
D C Guiroy S K Shankar C J Gibbs J A Messenheimer S Das D C Gajdusek 《Annals of neurology》1989,25(1):102-106
We report the pathological and immunohistochemical changes in the first-order neurons in the trigeminal ganglia in Creutzfeldt-Jakob disease (CJD). Degenerative changes consisted of cytoplasmic vacuolation and fenestration, abundant satellite cells, neurofilament accumulation in neurons, and axonal dystrophy with spheroid formation and torpedolike structures arising from the neuronal cytoplasm. Dystrophic axons, axonal spheroids, and some ganglion cells were labeled with monoclonal antibodies to a phosphorylated epitope of neurofilaments (200 kDa). Polyclonal antibodies to purified scrapie-associated fibril/prion protein (molecular weight 27-30 kDa) extracted from scrapie-infected hamster brains, as well as polyclonal and monoclonal antibodies to a synthetic 15-amino acid polypeptide of the 27- to 30-kDa protein, demonstrated variable immunoreactivity with degenerating neurons in the CJD cases, but not in the controls. Furthermore, some of the satellite cells and dystrophic axons were stained by the antibodies to the synthetic peptide. These data indicate that the first-order neurons of the trigeminal ganglia may form a route by which the CJD agent may travel from the brain to the periphery or vice versa. As in other chronic neurodegenerative diseases, disturbances of neuroaxonal transport seem to occur in CJD. 相似文献