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181.
A Banerjee AT Kalghatgi GS Saiprasad A Nagendra BN Panda SK Dham A Mahen KD Menon MA Khan 《Medical Journal Armed Forces India》2005,61(1):16-21
Background
Between 04 Mar 2002 to 21 Mar 2002, 31 cases of pneumonia were admitted at a military hospital in South India. Most of these cases were young recruits. The out break was investigated to ascertain the cause and suggest preventive measures.Methods
Detailed epidemiological history was taken from all 31 cases and 100 controls. Case sheets, laboratory reports and chest radiographs were studied. Laboratory investigations included sputum examination by Gram stain and blood cultures on brain heart infusion broth. Cultures grown on liquid media were subcultured on solid media. The regimental centre was visited to note the living and environmental conditions.Results
Epidemiological investigations revealed overcrowding in the regimental centre. The space per recruit was below recommended standards. 51.6% of recruits who contacted pneumonia were sleeping on double deckers as compared to 21% of healthy controls. Blood culture was positive for Streptococcus pneumoniae in 25.8% of the cases. Chest radiograph showed consolidation typical of lobar pneumonia in 67% of the cases.Conclusion
The outbreak of pneumococcal pneumonia occurred due to overcrowding. Chilly weather conditions and stress were contributing factors.Key Words: Military recruits, Outbreak, Overcrowding, Pneumococcal, Pneumonia 相似文献182.
183.
Symptomatic vascular malformations: ethanol embolotherapy 总被引:5,自引:0,他引:5
Yakes WF; Haas DK; Parker SH; Gibson MD; Hopper KD; Mulligan JS; Pevsner PH; Johns JC Jr; Carter TE 《Radiology》1989,170(3):1059
184.
Williams RJ; Henderson LM; Naidoo Y; Cassim B; Elson CJ; Bhoola KD 《Rheumatology (Oxford, England)》1997,36(4):420-425
Polymorphonuclear leucocytes (PMNs) from the synovial fluid of patients
with rheumatoid arthritis (RA) showed reduced tissue kallikrein and kinin
immunoreactivity in comparison with blood PMNs from healthy individuals as
judged visually using confocal microscopy. Similarly, synovial fluid PMNs
exhibited reduced tissue kallikrein immunoreactivity as compared with blood
PMNs from the same RA patients. Blood PMNs stimulated to degranulate in
vitro also displayed less immunostaining for tissue kallikrein and kinin
than non-stimulated PMNs. By contrast, no difference in kininogen
immunostaining was detected between RA synovial fluid PMNs and blood PMNs
from healthy people. It is considered that the results support the
hypothesis that tissue kallikrein, released from the granules of RA
synovial fluid PMNs, cleaves the kinin moiety from multifunctional
kininogen protein on the surface of the PMNs.
相似文献
185.
Automated biopsy devices: a blinded evaluation 总被引:4,自引:1,他引:3
186.
187.
Diaphanography as a means of detecting breast cancer 总被引:1,自引:0,他引:1
188.
Heckel D; Comtesse N; Brass N; Blin N; Zang KD; Meese E 《Human molecular genetics》1998,7(12):1859-1872
189.
Acquired hypoprothrombinemia due to non-neutralizing antibodies to prothrombin: mechanism and management 总被引:1,自引:0,他引:1
A patient developed bleeding due to an acute acquired specific prothrombin deficiency. Unlike previously described patients, this patient had no evidence of an associated lupus anticoagulant. Prothrombin activity and antigen were decreased concordantly and the patient's plasma did not neutralize the activity of added prothrombin or interfere with its measurement by electroimmunoassay. Nevertheless, immunoelectrophoresis and experiments using 125I-prothrombin revealed a prothrombin-binding antibody. The residual prothrombin in the patient's plasma was in the form of a prothrombin-antibody complex. Administration of adrenal corticosteroids was associated with a rise in prothrombin activity and cessation of bleeding, but circulating prothrombin was still bound to the antibody. This suggests that non- neutralizing antibodies to prothrombin cause plasma prothrombin deficiency because of a rapid clearance of prothrombin-antibody complexes, which is slowed by adrenal corticosteroids. The antibody had a relatively low affinity for prothrombin (Kd 5 to 8 X 10(-7)) and was transient. It is possible, therefore, that the antibody arose not to prothrombin itself, but to an antigen sharing an epitope with prothrombin. 相似文献
190.
Identification of the amino acid mutations associated with human erythrocyte spectrin alpha II domain polymorphisms 总被引:1,自引:0,他引:1
Four distinct spectrin alpha II domain polymorphisms are known to occur in several nonwhite populations. Type 1 is essentially the only form found in whites and is also the most common form in nonwhites. In contrast to most other spectrin mutations that are single-base substitutions, two of the alpha II domain polymorphisms, types 2 and 3, are particularly unusual because they appear to involve 4-Kd insertions relative to type 1. We have identified the mutations responsible for these polymorphisms using biochemical approaches and a computer database of spectrin-domain peptides separated by two-dimensional gels. The type 3 mutation is characterized by an apparent 4-Kd increase in alpha II domain peptides with no change in pI. This apparent molecular weight increase is a sodium dodecyl sulfate (SDS) gel artifact resulting from an Arg-->His mutation at residue 22 of the domain. The type 4 polymorphism shows a basic charge shift with no apparent change in molecular weight on gels. This charge shift results from a mutation of Thr-->Arg at position 174 of the domain. This mutation appears to be linked to a "silent" mutation at position 130 from an Ile-->Val. Support for possible linkage was obtained from analysis of three unrelated donors with the type 2 polymorphism. The type 2 polymorphism shows both the charge shift characteristic of the type 4 mutation and the apparent size shift that defines the type 3 polymorphism. Analysis of type 2 peptides confirmed that the two mutations described above for type 4 as well as the mutation at residue 22 observed in type 3 occur simultaneously in type 2. The observation that the type 2 polymorphism is a composite of the type 3 and 4 mutations is especially surprising because the type 2 polymorphism occurs far more frequently than either the type 3 or 4 forms. The basis for apparent linkage between the mutations at residues 130 and 174, which are encoded by different exons, is also not clear. Identification of the mutations described here permits design of genetic screening analyses that can be applied to larger populations to evaluate this potential linkage. 相似文献