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排序方式: 共有905条查询结果,搜索用时 15 毫秒
1.
Characterization of nephropathy induced by immunization with high molecular weight dextran 总被引:1,自引:0,他引:1
Pasi A; Dendorfer U; Holthofer H; Nelson P; Tazzari S; Armelloni S; Fornasieri A; D'Amico G; Schlondorff D 《Nephrology, dialysis, transplantation》1997,12(9):1849-1855
Background. Injection of DEAE dextran into Lewis rats
can produce proteinuria and has been reported as a model of IgA
nephropathy. Methods. Cationic diethyl aminoethyl
(DEAE) dextran of molecular weight 500 KDa was injected into male Lewis
rats. After a pre-immunization period of 3 weeks, the animals were divided
into two groups: group 1 (n=14) received daily i.v. injections of 3.5 mg of
antigen, group 2 (n=14) was injected with 1.5 mg three times per week for a
total period of 6 weeks. I.v. treatment was initiated with gradually
increasing doses of DEAE dextran in both groups for 1 week, after which the
maintenance dose was reached. Results. We observed the
appearance of proteinuria in a nephrotic range after 5 weeks of i.v.
injections in group 1 (urinary excretion: 332±83 mg/24 h,
controls: 53±14 mg/24 h). In group 2, the proteinuria was almost
equal to protein excretion of healthy rats of the same weight
(67±20 mg/24 h). The serum and urine creatinine were normal. By
light microscopy of kidney biopsies, the presence of focal and segmental
proliferation of mesangial cells after 6 weeks of i.v. injections was
identified. Immunohistochemistry revealed no deposition of IgA, IgM, IgG,
or C3. Using anti-ED1 antibodies, there was no evidence of interstitial
infiltration of monocytes/macrophages after 6 weeks of i.v. injections.
Staining for proliferating cell nuclear antigen (PCNA) did not show the
presence of proliferating cells either in glomeruli or in the interstitium.
Staining with FITC-WGA lectin revealed focal and segmental loss of the
negative charge in the capillary wall. By electron microscopy there was
deposition of dextran in the basal membrane and segmental and focal damage
of the podocyte foot processes. As the chemokine RANTES may be involved in
glomerular injury, we examined the kidneys of proteinuric and
non-proteinuric rats for the presence of RANTES. By indirect
immunofluorescence only the proteinuric rats showed RANTES deposition in
mesangium. Conclusions. Injection of rats with DEAE
dextran leads to dose-dependent proteinuria without deposition of immune
complexes but with podocyte damage. This is associated with local
expression of the chemokine RANTES which may play a role in proteinuria of
glomerular disease. 相似文献
2.
Acute IP injection of benzyl alcohol but not benzaldehyde (0.5 g/kg) caused aversion to voluntary drinking of 5% ethanol solution by male rats with preference to ethanol. Benzyl alcohol noncompetitively inhibited hepatic alcohol dehydrogenase of rats maintained for a short term on 5% ethanol compared to control. The results suggest an adverse interaction between benzyl alcohol and ethanol underlying the observed aversion to ethanol. 相似文献
3.
4.
Serological evidence that dry heating of clotting factor concentrates prevents transmission of non-A, non-B hepatitis 总被引:1,自引:0,他引:1
S J Skidmore K J Pasi S J Mawson M D Williams F G Hill 《Journal of medical virology》1990,30(1):50-52
A new test for antibodies specific for an agent causing non-A, non-B hepatitis (NANBH) was used to screen 45 children with coagulation disorders who received factor concentrates. It was found that the test results correlated with clinical evidence of NANBH and that heat treatment of concentrates (80 degrees C for 72 hours) appears to have prevented transmission of NANBH. 相似文献
5.
Apolipoprotein B gene DNA polymorphisms are associated with macro- and microangiopathy in non-insulin-dependent diabetes mellitus 总被引:2,自引:0,他引:2
Olavi Ukkola Markku J. Savolainen Pasi I. Salmela Kai von Dickhoff Y. Antero Kesäniemi 《Clinical genetics》1993,44(4):177-184
Ukkola O, Savolainen MJ, Salmela PI, von Dickhoff K, Kesäniemi YA. Apolipoprotein B gene DNA polymorphisms are associated with macro-and microangiopathy in non-insulin-dependent diabetes mellitus. Clin Genet 1993: 44: 177–184. © Munksgaard, 1993 The relationship between diabetic macroangiopathy or microangiopathy and apolipoprotein B (apoB) polymorphism was studied in 139 male and 129 female patients with non-insulin-dependent diabetes (NIDDM) mellitus, comprising consecutive patients with poor diabetic control (HBA1 13.2%\pm2.7 (SD)) referred to our hospital. Plasma cholesterol and triglyceride concentrations were higher in the patients who were homozygous for the X2 allele (presence of Xba I cleavage site). Patients with the X1 allele (absence of Xba I cleavage site) tended to have a higher frequency of macroangiopathy, although the differences were not statistically significant. There was no difference in the prevalence of microangiopathy between the groups. In subjects with only an R1 allele (= R +; homozygous for the presence of EcoR I cleavage site) the prevalence of coronary heart disease (CHD) was observed to be high (61.9%) as compared to the subjects possessing an R2 allele (= R —; homozygous or heterozygous for the absence of the EcoR I cleavage site) (46.7%; p<0.02). When the polymorphisms Xba I (subjects homozygous for the absence of the cutting site = X +; subjects homozygous or heterozygous for the presence of the cutting site = X —) and EcoR I were combined, the prevalence of macroangiopathy was observed to be high in X + R + (80.0%) as compared with X + R- (44.2%), X-R+ (56.8%) and X-R- (50.0%) (p<0.03). The prevalence of macroangiopathy tended to be particularly high in patients with the apoprotein E4 allele (phenotype E4\4 or E4/3), combined with either X+ or R +. Our findings suggest that variation at the apoB locus is one of the factors involved in predisposing diabetic patients to the development of arterial disease. As in previous studies the effect of the variation at the apoB gene on circulating lipid levels was observed. The data also support a role for the e4 allele of the apolipoprotein E gene as an important determinant of macroangiopathy in NIDDM. 相似文献
6.
A Pasi P Kulling D Voellmy C Gramsch P Mehraein M H?ni F S Messiha 《Physiology & behavior》1989,46(1):13-16
The regional levels' profile of human beta-endorphin (beta h-EP) was studied in the brainstem and the cerebellum of 16 infant victims of "Sudden Infant Death Syndrome" and other death causes. An immunoaffinity chromatography procedure based on a monoclonal antibody directed specifically against the N-terminus of beta-EP was used to extract this peptide from the tissue samples. Beta-EP was then assessed quantitatively by means of a very sensitive solid phase radioimmunoassay (using a polyclonal antibody specific for the C-terminus of beta-EP) developed especially for the study presented here. 相似文献
7.
8.
N. Hutri-Kähönen Mika Kähönen Pasi Jolma Xiumin Wu Juhani Sand Isto Nordback Pauli Ylitalo Pertti Arvola Ilkka Pörsti 《Naunyn-Schmiedeberg's archives of pharmacology》1999,359(4):322-330
The majority of the findings concerning arterial physiology and pathophysiology originate from studies with experimental
animals, while only limited information exists about the functional characteristics of human arteries. Therefore, the aim
of the present work was to compare the control of vascular tone in vitro in mesenteric arterial rings of corresponding size
(outer diameter 0.75–1 mm) from humans and Wistar-Kyoto rats. The relaxations to acetylcholine (ACh) were clearly less marked
in the mesenteric arteries of humans when compared with rats. How-ever, when calcium ionophore A23187 was used as the vasodilator,
the endothelium-mediated relaxations did not significantly differ between these species. The NO synthase inhibitor N
G-nitro-l-arginine methyl ester (l-NAME) attenuated the relaxations to ACh and A23187 in both groups. The endothelium-independent
relaxations to the β-adrenoceptor agonist isoprenaline and the nitric oxide (NO)-donor nitroprusside were somewhat lower in
human arteries, while vasodilation induced by the K+ channel opener cromakalim was similar between humans and rats. Arterial contractile sensitivity to noradrenaline and serotonin
was slightly lower in human vessels, whereas contractile sensitivity to KCl was similar between these species. The contractions
induced by cumulative addition of Ca2+ with noradrenaline as the agonist were effectively inhibited in both groups by the calcium channel blocker nifedipine, the
effect of which was clearly more pronounced in human arteries. In conclusion, the control of vascular tone of isolated arteries
of corresponding size from humans and rats appeared to be rather similar. The most marked differences between these species
were the impaired endothelium-mediated dilation to ACh and the more pronounced effect of nifedipine on the Ca2+-induced contractions in human arteries.
Received: 1 October 1998 / Accepted: 4 January 1999 相似文献
9.
10.
Saila Antila Ullamari Pesonen Lasse Lehtonen Pasi Tapanainen Hanna Nikkanen Katja Vaahtera Harry Scheinin 《European journal of pharmaceutical sciences》2004,23(3):213-222
OBJECTIVE: The purpose of this study was to investigate the pharmacokinetics of levosimendan and to determine the primary pharmacokinetic parameters of the pharmacologically active metabolite OR-1896 in rapid and slow acetylators. METHODS: Levosimendan was administered as a constant rate (0.1 microg/(kg min)) i.v. infusion for 24h in six rapid and six slow acetylators based on N-acetyltransferase 2 genotyping. At the end of the infusion, a small amount (2.5 microg/kg) of (13)C-labeled OR-1896 was administered by i.v. infusion for 10 min. Blood samples were taken at predefined sampling points 14 days post-infusion and levosimendan and its metabolite concentrations were determined by LC-MS/MS. RESULTS: Steady-state concentrations of levosimendan were achieved within 4-8h and no differences were found in the pharmacokinetics of the parent compound between the rapid and slow acetylators. The maximum concentrations of amino phenylpyridazinone metabolite OR-1855 and N-acetylated conjugate OR-1896 were observed approximately 24h after terminating the infusion. AUC of OR-1896 was approximately 3.5 times higher in the rapid acetylators compared to the slow acetylators (P = 0.002, 95% confidence interval for group ratio from 2.0 to 8.2). The mean +/- S.D. fraction of levosimendan metabolized to OR-1896 was 6.8 +/- 2.8% in the rapid and 4.3 +/- 2.4% in the slow acetylators (P = 0.12). (13)C-OR-1855 concentrations were detected in plasma after administration of (13)C-OR-1896 indicating deacetylation from OR-1896 to OR-1855. CONCLUSIONS: Plasma OR-1896 levels during and after levosimendan treatment are dependent on the acetylation status of the subject-rapid acetylators having 3.5 times higher concentrations than slow acetylators. 相似文献