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91.
The genetic defect in the p67phox-deficient form of chronic granulomatous disease (CGD) follows an autosomal recessive pattern of inheritance. When genomic DNA from normal individuals is digested with HindIII and probed with p67phox cDNA an allelic restriction fragment length polymorphism (RFLP) of 4.0 kb or 2.3 kb is detected. We cloned and characterized the p67phox gene using the cDNA and sequenced the exon/intron boundaries, mapping 16 exons on the 40-kb gene. The polymorphic region was then sequenced to identify the inheritance pattern of amniocentesis-derived fetal cells by genomic amplification. The proband, a 9-year-old female patient with p67phox-deficient CGD, and her phenotypically normal mother are homozygous for the RFLP marker, whereas the father and two brothers are heterozygous. The fetus was shown to be heterozygous as well, showing it had inherited at least one normal p67phox gene from the father and that it was predicted to have a normal phenotype. Cord blood samples at birth showed normal oxidative function. Amplification allows rapid detection of the inheritance pattern for fetal diagnosis in informative families. We report the genomic structure of p67phox and an amplification-based method for detection of the marker on chromosome 1q25, used here for prenatal diagnosis of CGD. 相似文献
92.
Summary: Activation of platelets and the coagulation pathway are factors which may contribute to the progression of renal disease in IgA nephropathy (IgAN). Of 21 patients with IgAN and serum creatinines between 1.6 and 3.0 mg/dL, 10 were assigned to treatment with dipyridamole and low-dose warfarin (keeping the thrombotest between 30 and 50%) and 11 to no treatment in a prospective randomized 3-year study. At entry into the trial, patients in the treatment group were younger (35 ± 6 years vs 42 ± 9 years) and had worse histological scores for tubular atrophy (1.7 ± 0.7 vs 1.1 ± 0.5) and arteriolar hyperplasia (1.4 ± 0.7 vs 0.7 ± 0.8) than those in the non-treatment group. There were no differences in serum creatinine values, creatinine clearances, urinary protein excretions, serum albumins or urinary erythrocyte counts. At the end of the trial, patients on treatment did not experience a significant increase in serum creatinine values (1.9 ± 0.3 mg/dL to 2.5 ± 1.2) or reduction in creatinine clearances (52 ± 20mL/min to 52 ± 27). Untreated patients, however, experienced a significant rise in serum creatinine values (2.1 ± 0.5 mg/dL to 3.3 ± 1.1, P < 0.01) and a fall in creatinine clearances (51 ± 26 mL/min to 31 ± 22, P = 0.06). There was no significant change in the proteinuria in either group (treatment group: 1.2 ± 1.2 g/day to 1.3 ± 1.1, non-treatment group: 1.9 ± 1.4 to 1.5 ± 1.1) and there was also no change in serum albumins and urinary erythrocyte counts. Four untreated and one treated patient developed end-stage renal failure during the course of the trial. This study suggests that treatment of patients with IgAN and renal impairment with dipyridamole and low-dose warfarin retards the deterioration of renal function, as measured by the serum creatinine and creatinine clearance. 相似文献
93.
94.
The mechanisms by which adreno-corticoid hormones regulate Na+, K+-ATPase in adult kidney were studied in adrenalectomized (Adx) rats. Five days after adrenalectomy, Na+, K+-ATPase activity was significantly reduced in the renal cortex homogenate (C = 13.0±0.8 vs. Adx = 7.1±0.7 μmol Pi mg-1 protein h-1) and in renal microsomes (C = 30.3 ± 1.9 vs Adx = 14.6 ± 1.3 μmol Pi mg-1 protein h-1). Glucocorticoid replacement treatment of adrenalectomized rats with betamethasone (20 μg kg-1 body wt twice daily for 5 days) effectively counteracted the observed reduction in Na+, K+-ATPase activity. In cortical homogenate the protein level of α1 and β1 subunits measured in immunoblots was not significantly different in Adx and control rats, indicating that 5 days after adrenalectomy the α1 and β1 subunits were present in renal cortical cells to almost normal extent but could not be assembled into a transmembrane functional unit. In support of this conclusion we found that the protein level of both the α1 and β1 subunits was significantly lower (P < 0.001 for both subunits) in microsomes from Adx than in control rats. The mRNA abundance for α1 and β1 subunits were not lower in Adx as compared to control rats 1 and 5 days after surgery. However, if Adx rats were given a single dose of betamethasone (600 μg kg-1 body wt), a significant 2-fold increase in both α1 and β1 mRNAs was observed (P < 0.05 for both subunits). These data suggest that glucocorticoids can upregulate the mRNA of both Na+, K+-ATPase subunits but that the low renal Na+, K+-ATPase activity in adult Adx rats is mainly due to loss of glucocorticoid regulation of the post-translational processing of the enzyme. 相似文献
95.
商陆多糖Ⅰ联合白细胞介素2对小鼠脾细胞杀瘤活性的影响 总被引:2,自引:0,他引:2
商陆多糖Ⅰ(PAP-I),0.3~3μg·ml-1和小鼠脾细胞培养3~5d可显著增强其杀伤P815肿瘤细胞活性及IL-2(250~500IU·ml-1)诱导的LAK细胞活性,最适浓度为1μg·ml-1。PAP-I及IL-2和脾细胞培养的上清液对P815肿瘤细胞无细胞毒作用,但能增强脾细胞及LAK细胞杀瘤活性。PAP-I,5,10及50mg·kg-1,ip可增强脾细胞杀伤P815和L929细胞的活性及IL-2诱导的LAK细胞活性。 相似文献
96.
97.
Choudhary Ratan K. Kaur Harmanjot Choudhary Shanti Verma Ramneek 《Proceedings of the National Academy of Sciences, India. Section B.》2017,87(1):167-172
Proceedings of the National Academy of Sciences, India Section B: Biological Sciences - India is the largest producer of buffalo milk in the world. Buffalo milk is rich in minerals like calcium and... 相似文献
98.
Lymph node enlargement due to cysticercus infestation has not been reported in human subjects. A 7-y-old girl presented with seizures and a right submandibular lymph node enlargement. Investigations showed inflammatory granulomas in the brain. Fine needle aspiration cytology from submandibular lymph node and enzyme-linked immunosorbent assay of serum and cerebrospinal fluid showed the presence of cysticercosis infestation. The case underlines the potential of fine needle aspiration cytology for establishing diagnosis in patients having enlarged lymph nodes. 相似文献
99.
Jarolim P; Rubin HL; Brabec V; Chrobak L; Zolotarev AS; Alper SL; Brugnara C; Wichterle H; Palek J 《Blood》1995,85(3):634-640
To elucidate the molecular basis of band 3 deficiency in a recently defined subset of patients with autosomal dominant hereditary spherocytosis (HS), we screened band 3 cDNA for single-strand conformation polymorphism (SSCP). In 5 of 17 (29%) unrelated HS subjects with band 3 deficiency, we detected substitutions R760W, R760Q, R808C, and R870W that were all coinherited with the HS phenotype. The involved arginines are highly conserved throughout evolution. To examine whether or not the product of the mutant allele is inserted into the membrane, we studied one HS subject who was doubly heterozygous for the R760Q mutation and the K56E (band 3sMEMPHIS) polymorphism that results in altered electrophoretic mobility of the band 3 Memphis proteolytic fragments. We detected only the band 3MEMPHIS in the erythrocyte membrane indicating that the protein product of the mutant, R760Q, band 3 allele is absent from the red blood cell membrane. These findings suggest that the R760Q substitution, and probably the other arginine subsitutions, produce band 3 deficiency either by precluding incorporation of the mutant protein into the red blood cell membrane or by leading to loss of mutant protein from differentiating erythroid precursors. 相似文献
100.