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61.
Summary The numerical density of neurons and glial cells was estimated in visual area 18 of the adult human cerebral cortex and compared with that of area 17. Blocks of areas 17 and 18 came from the same brains and this allowed the comparison of 1) neuronal and glial numerical densities through the whole cortical depth with calculation of the neuron/glia ratio, 2) neuronal and glial numbers under one square millimeter of cortical surface, and 3) neuronal numerical densities in three groups of identified layers. The mean neuronal density is approximately 40000 neurons/mm3 in area 17 and 31500/m3 in area 18. The mean glial density is around 27000/mm3 in area 17 and 32000/mm3 in area 18. This gives a neuron/glia ratio of approximately 1.5 in area 17 and of 1.0 in area 18, but the total cellular density is similar in both areas. There are about 90000 neurons and 64000 glial cells under one square millimeter of cortical surface in area 17, and some 73000 neurons and 74000 glial cells in area 18. The higher neuronal density in area 17 is found through the whole depth of cortex and does not seem to be more pronounced in layer IVc of area 17 compared to layer IV in area 18 than in the groups of layers II–III and V–VI.  相似文献   
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OBJECTIVE—A pilot study of the density ofdendritic spines on pyramidal neurons in layer III of human temporaland frontal cerebral neocortex in schizophrenia.
METHODS—Postmortem material from a groupof eight prospectively diagnosed schizophrenic patients,five archive schizophrenic patients, 11 non-schizophrenic controls,and one patient with schizophrenia-like psychosis, thought to be due tosubstance misuse, was impregnated with a rapid Golgi method. Spineswere counted on the dendrites of pyramidal neurons in temporaland frontal association areas, of which the soma was in layer III(which take part in corticocortical connectivity) and which met strictcriteria for impregnation quality. Altogether 25 blocks were studied inthe schizophrenic group and 21 in the controls. If more than one blockwas examined from a single area, the counts for that area wereaveraged. All measurements were made blind: diagnoses were onlydisclosed by a third party after measurements were completed. Possibleconfounding affects of coexisiting Alzheimer's disease were taken intoaccount, as were the effects of age at death and postmortem interval.
RESULTS—There was a significant (p<0.001)reduction in the numerical density of spines in schizophrenia (276/mmin control temporal cortex and 112/mm in schizophrenic patients, and299 and 101 respectively in the frontal cortex). An analysis ofvariance, taking out effects of age at death and postmortem interval,which might have explained the low spine density for some of theschizophrenic patients, did not affect the significance of the results.
CONCLUSION—The results support theconcept of there being a defect in the fine structure of dendritesof pyramidal neurons, involving loss of spines, in schizophreniaand may help to explain the loss of cortical volume without loss ofneurons in this condition, although the effect of neuroleptic drugscannot be ruled out.

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64.
The distribution of cytochrome oxidase activity was studied in the cerebral cortex of two species of cetaceans, the harbour porpoise Phocoena phocoena, and the bottlenose dolphin Tursiops truncatus. Two main patterns of distribution of cytochrome oxidase were detected. The first, characteristic of the visual and auditory cortices of the lateral and suprasylvian gyri, is typified by a peak density in layer III, contrasting with low levels in layers II, V and VI. The second is found in wide areas of the limbic lobe, the insular cortex, the temporal operculum and the occipital cortex. In these regions, distribution of cytochrome oxidase is more uniform, with little difference between layers III, V and VI. A transitional pattern is found in the most dorsal parts of the limbic lobe, the parietal operculum, the ectosylvian gyrus and in orbitofrontal cortex. As areas of high cytochrome oxidase activity have been described in various land mammals to correspond to zones of major excitatory input and, in particular, to characterise the cortical layers that receive thalamocortical afferents, we propose that the thalamocortical input to cetacean sensory cortex, in which a typical layer IV is absent, may be mainly to layer III. This view is supported by the high density of neurons positive for the inhibitory transmitter gamma-aminobutyric acid that is also found in layer III of cetacean cortex, another typical feature of thalamocortical recipient zones.  相似文献   
65.
This study examined the contribution of AmpC over-expression to beta-lactam resistance in clinical isolates of Pseudomonas aeruginosa obtained from a hospital in Houston, TX, USA. Seventy-six non-repeat bloodstream isolates obtained during 2003 were screened for ceftazidime resistance in the presence and absence of clavulanic acid 4 mg/L. AmpC was identified by isoelectric focusing (with and without cloxacillin inhibition); stable derepression was ascertained phenotypically by a spectrophotometric assay (with and without preceding induction by imipenem) using nitrocefin as the substrate, and was confirmed subsequently by quantitative RT-PCR of the ampC gene. The clonal relatedness of the AmpC-over-expressing isolates was assessed by pulsed-field gel electrophoresis. In addition, the ampC and ampR gene sequences were determined by PCR and sequencing. For comparison, two standard wild-type strains (PAO1 and ATCC 27853) and three multidrug-susceptible isolates were used as controls. AmpC over-expression was confirmed in 14 ceftazidime-resistant isolates (overall prevalence rate, 18.4%), belonging to seven distinct clones. The most prevalent point mutations in ampC were G27D, V205L and G391A. Point mutations in ampR were also detected in eight ceftazidime-resistant isolates. AmpC over-expression appears to be a significant mechanism of beta-lactam resistance in P. aeruginosa. Understanding the prevalence and mechanisms of beta-lactam resistance in P. aeruginosa may guide the choice of empirical therapy for nosocomial infections in hospitals.  相似文献   
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67.
We utilised postmortem brain tissue to quantify sections of left and right orbitofrontal cortex (area 11) from nine schizophrenic and eight control patients from the Charing Cross Prospective Schizophrenia Study immunostained for the presence of the kainate receptor (GluR5/6/7). The numerical density of neurons immunopositive for kainate receptor was measured. Other sections from the same blocks were stained with cresyl violet to determine the total neuronal numerical density. All measurements were made blind: diagnoses were only revealed by a third party after measurements were completed. There was a significant reduction (21%) in numerical density of kainate receptor-positive neurons in both cortices in the schizophrenic group (488 cells/mm2) compared to that in the control group (618 cells/mm2) (P=0.033). Nissl-stained tissue showed no significant difference in total neuronal numerical density between control and schizophrenic groups. These observations suggest that there are actually fewer kainate receptor-positive neurons in schizophrenic orbitofrontal cortex. There was no correlation of reduced kainate receptor-positive cell number with age at death, postmortem interval, or other possibly confounding neuropathology. Our results support the concept of there being reduced glutamatergic activity in frontal cortex in schizophrenia.  相似文献   
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69.
Summary The ultrastructure of the dorsal lateral geniculate nucleus (dLGN) of microphthalmic mice is described in affected white homozygotes (mi/mi) and their apparently normal grey littermates. In the dLGN of mi/mi animals populations of apparently normal axon terminals were observed, including some with flattened synaptic vesicles and other small terminals with round vesicles and dark mitochondria (RSD), possibly of cortico-thalamic origin, just as in normal mice. However, no typical large retinal endings with round vesicles and pale mitochondria (RLP) are visible. Instead they appear to be replaced by other large boutons with round vesicles and dark mitochondria (RLD). Eye enucleation does not cause degeneration of these RLD terminals. In apparently normal grey littermates RLP terminals are present and they degenerate when an eye is enucleated. But RLD endings are also found in these animals, and never degenerate after enucleation. The origin of the RLD terminals is unclear but seems not to be cortical. These findings are compared with those of Cullen and Kaiserman-Abramof (1976) in a different strain (ZRDCT-An) of anophthalmic mouse in which they found large replacement terminals similar to our RLD boutons.  相似文献   
70.
The objective of this study was to examine time and temperature of food under actual operating conditions during product flow, from procurement through service, and to seek relationships to the amounts of food consumed during the noon meal by children in Head Start early childhood developmental centers. A process flow model was developed for a conventional foodservice system such as that used in Head Start. The preparation and service of the lunch menus served to 101 3- to 5-year-old children in three centers were studied during a 3-week period for adherence to time and temperature standards. Weight of food consumed was measured and evaluated by a preference ratings panel for acceptability. Food was well accepted, was consumed by the children, and received very good adult preference panel ratings. The largest variations from the time standard were in processing-heating hot vegetables, while the greatest temperature variations were across all process steps for entrées. Deviations from recommended time and temperature standards for handling of milk were significantly correlated with lower consumption of milk.  相似文献   
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