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91.
The provision of renal replacement therapy for adults in England and Wales: recent trends and future directions 总被引:1,自引:7,他引:1
Roderick PJ; Ferris G; Feest TG 《QJM : monthly journal of the Association of Physicians》1998,91(8):581-587
We assessed the level of provision of renal replacement therapy for adults
in England and Wales. All autonomous main renal units in England (n = 52)
and Wales (n = 5) were surveyed in 1996. Data for England were compared to
the 1993 National Renal Review. The acceptance rate in England 1995 was 82
(80-85) per million population (p.m.p.) compared with 67 (65-70) p.m.p. in
1991-2. The rate in 1995 in Wales was 109 (98- 122) p.m.p. The prevalence
rate in England was 476 p.m.p. at end-1995 compared to 393 p.m.p. in 1993,
in Wales it was 487 p.m.p. The number of main renal units in England did
not rise between 1993 and 1995; capacity was increased by use of more
treatment shifts and temporary haemodialysis stations, and by opening more
satellite units. The main growth was in hospital haemodialysis. There was
an uneven geographical distribution of services. Patients accepted were
older with more comorbidity. The use of better-quality processes of
dialysis increased. The steady-state position for RRT will not be reached
for over a decade. Health authorities will face continued pressure to fund
increases in quantity and quality improvements. A stronger evidence base of
the effectiveness of therapies, and a national registry to monitor the
equity and cost-effectiveness of services are needed.
相似文献
92.
Coagulation parameters of CPD fresh-frozen plasma and CPD cryoprecipitate-poor plasma after storage at 4 degrees C for 28 days 总被引:1,自引:0,他引:1
A pilot study was performed on the storage of plasma and cryosupernatant plasma at 4 degrees C for up to 28 days. Eight bags, four of CPD fresh-frozen plasma (FFP) and four of CPD cryosupernatant plasma (CSP, plasma without cryoprecipitate), were sampled during storage for assays of pH; factors V, VIII, IX, and XI; fibrinogen; prothrombin time; activated partial thromboplastin time (APTT); plasma protein electrophoresis; viscosity; and C1q binding. No changes were found in viscosity or the plasma protein electrophoretic pattern, and there was no detectable immune complex formation. The fibrinogen concentration remained constant, and the prothrombin time showed a gradual increase of 2.5 seconds for both groups of plasma. The labile coagulation factor V decreased gradually for FFP and CSP to 58 and 64 percent of its initial value, respectively (51 +/− 8% and 54 +/− 6% of the value of fresh pooled plasma). Factor VIII decreased to 36 percent of its initial value in FFP (48 +/− 14% of fresh pooled plasma). In CSP, factor VIII decreased after 28 days to 7 percent of its initial value (7 +/− 1% of fresh pooled plasma). The APTT increased for FFP from 28 to 35.8 +/− 1.1 seconds and for CSP from 36 to 49.5 +/− 4.9 seconds. The only chemical change observed for both plasmas was a rise in pH, from 7.27 to 7.56, after 28 days. The results of this pilot study indicate that FFP can be stored at 4 degrees C for 28 days with sufficient recovery of coagulation factors to maintain hemostasis.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
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96.
Thrombosis in inflammatory bowel disease: clinical setting, procoagulant profile and factor V Leiden 总被引:7,自引:0,他引:7
Jackson LM; O'Gorman PJ; O'Connell J; Cronin CC; Cotter KP; Shanahan F 《QJM : monthly journal of the Association of Physicians》1997,90(3):183-188
Patients with inflammatory bowel disease have an increased frequency of
thromboembolism, and microvascular thrombosis has been proposed as a
contributory pathogenic factor. The mechanism of enhanced procoagulant
activity is not understood. We examined the clinical setting of
thromboembolic events in 52 patients with Crohn's disease or ulcerative
colitis, and assessed the procoagulant laboratory profile, including Factor
V Leiden, in a subset of 20 patients to identify procoagulant risk factors.
Patients who developed thrombosis tended to be young; 60% of thrombotic
events occurred in patients under 50 years. Multiple thromboembolic
episodes occurred in 13% and unusual sites of thrombosis (e.g.
intracardiac, cerebral, inominate veins) in 11%. No risk factor was
identifiable in 52% of cases and two-thirds of thromboses occurred in an
out-patient setting. The mortality rate was 8%. Evidence for inflammatory
disease activity was found in only 45% of patients with ulcerative colitis
at the time of the thromboembolic event, in contrast to 89% of those with
Crohn's disease. Assays for specific coagulation defects were negative in
all cases tested (protein S, C were normal in 17/17; anti-thrombin III,
anti-phospholipid antibodies and activated protein C resistance were
negative in 20/20, and only 1/20 patients was found to be heterozygous for
Factor V leiden. Thrombosis in inflammatory bowel disease is important
because it occurs in a young population, often in unusual sites, and has a
high mortality. The development of thrombosis is related to active
inflammatory disease in most patients with Crohn's disease but apparently
not in those with ulcerative colitis. Since approximately half of the
patients had no other identifiable risk factor, there remains a substantial
group of patients with IBD who develop thrombosis for unknown reasons.
相似文献
97.
98.
Genetic factors affecting the consistency and magnitude of changes in plasma cholesterol in response to dietary challenge 总被引:3,自引:0,他引:3
Humphries SE; Talmud PJ; Cox C; Sutherland W; Mann J 《QJM : monthly journal of the Association of Physicians》1996,89(9):671-680
We examined the role of common genetic variation in determining the
consistency and magnitude of change in plasma total cholesterol (TC) levels
in response to two separate changes from a high-saturated (SFA) to a
low-saturated/high-polyunsaturated-fat (PUFA) diet, in a group of
free-living healthy men and women. Consistent responders were defined as
those whose mean difference in the change in TC was within one SD of the
mean for all participants, and the remainder were defined as variable
responders. DNA was obtained from 55 individuals and genotype determined at
the apolipoprotein (apo) B locus (signal peptide, SP), apoCIII (C1100-T)
and lipoprotein lipase (LPL) gene loci (HindIII). In the 38 consistent
responders, the apoBSP24 allele was significantly more common than in the
17 individuals with a variable response (0.29 vs. 0.12; p < 0.05). No
other polymorphism showed a significant frequency difference between
groups. In the group as a whole, the correlation between the change in TC
level in response to the first and second dietary change was 0.28 (p =
0.05), but those with one or more apoB SP24 alleles and those with the
apoCIII genotype CC had a significantly higher correlation than those with
other genotypes (0.46 (p = 0.05) vs. 0.12 (NS) and 0.31 (p = 0.05) vs. 0.02
(NS), respectively). In the group as a whole, mean response left TC 10%
higher on the SFA than on the PUFA diet, and neither apoB nor apoCIII
genotypes affected the magnitude of this response. However, individuals
with the LPL HindIII genotype H+ H+ had a significantly smaller change in
mean TC in response to diet than those with one or more H- allele (9.3% vs.
14.4%; p = 0.03). Thus variation at the apoB and apoCIII loci affects the
consistency of response to change in dietary fat content, while variation
at the LPL gene locus affects magnitude of response.
相似文献
99.
Wierzbicki AS; Lumb PJ; Semra YK; Crook MA 《QJM : monthly journal of the Association of Physicians》1998,91(4):291-294
Lipid targets can be difficult to attain in familial hypercholesterolaemia.
To compare atorvastatin with simvastatin- fenofibrate and
simvastatin-cholestyramine therapy, we studied 54 patients with familial
hypercholesterolaemia over periods of 2-6 months on each therapeutic
regimen. The atorvastatin regimen reduced total cholesterol by 41.2 +/-
11.2%, LDL by 45.6 +/- 15.5%, triglycerides by 33.8 +/- 24.8%, and
increased HDL by 2.3 +/- 37.0%. Simvastatin- fenofibrate therapy achieved
reductions of 33.9 +/- 8.5% in cholesterol, 42.0 +/- 12.2% in LDL, 34.7 +/-
38.3% for triglycerides, and a 25.4 +/- 55.1% increase in HDL.
Simvastatin-cholestyramine gave a reduction of 31.3 +/- 11.8% in
cholesterol, 36.0 +/- 14.4% in LDL, 13.7 +/- 36.3% in triglycerides, and a
1.1 +/- 30.3% rise in HDL. The atorvastatin regimen was marginally but not
significantly better than simvastatin-fenofibrate in improving the LDL:HDL
ratio, LDL:apoB and and apolipoprotein B:A1 ratios. Eleven patients (20.4%)
had side- effects: two discontinued atorvastatin due to side-effects; two
patients had rashes; six had myalgia and two had diarrhoea.
Gastrointestinal side-effects were described in 16 (30.1%) patients on
simvastatin-cholestyramine therapy and four cases of myalgia (11.2%) were
seen with simvastatin-fenofibrate. In nine patients on atorvastatin (20.4%)
a 30% or greater fall in HDL was observed, compared to five patients with
resin therapy (9.2%) and two with fibrate therapy (5.5%). There were no
significant differences in liver or muscle biochemistry between the
regimens, but atorvastatin did raise transaminase and creatine kinase
concentrations significantly compared to pre-treatment values (p = 0.001).
Atorvastatin significantly improves the lipid profile in most patients
compared with other regimens. It has a comparable incidence of side-effects
to combination therapy regimens.
相似文献
100.
H-2 effects on cell-cell interactions in the response to single non-H-2 alloantigens. II. H-2 D region control of H-7.1-specific stimulator function in mixed lymphocyte culture and susceptibility to lysis by H-7.1- specific cytotoxic cells 下载免费PDF全文
The relative immunogenicity of the H-7.1 alloantigen has been shown in a previous communication to be regulated by a gene in the D region of the mouse major histocompatibility (H-2) complex. The level of relative immunogenicity was inferred from survival times of H-7.1-incompatible skin grafts donated by donors with different H-2 haplotype origins of H-2D region genes. In this communication we report the results of an extension of these previous investigations into the possible role of H-2D region genes in controlling the capacity of H-7.1-incompatible lymphocytes to stimulate H-7.1-speciflc mixed lymphocyte culture proliferation and generation of cytotoxic effector cells. The results reported herein demonstrate that the H-2D genotype of H-7.1-incompatible stimulator cells determines the relative H-7.1-specific capacity of those lymphocytes to stimulate H-7.1-specific proliferation of in vivo primed responder T cells in secondary mixed lymphocyte culture. H-2D(b)-bearing, H-7.l-incompatible stimulators were significantly more effective in stimulating H-7.1-specific proliferation than H-2D(d)-bearing stimulators. As expected, H-2D(b), H-7.1-in-compatible stimulators were also more effective than H-2D(d) a stimulators in generating H-7.1- specific cytotoxic effector cells. Further, the susceptibility of (51)Cr- labeled, H-7.1-incompatible lymphoblast targets to H-7.1-specific lysis was similarly regulated by an H-2D gene. Reciprocal H-2 restriction (F(1) cells are capable of killing only the cells bearing the immunizing cell parental H-2 haplotype) observed by other investigators for cytolysis of non-H-2-incompatible targets was not observed. H-2D a-bearing, H-7.1- incompatible stimulators stimulated generation of cytotoxic effectors capable of detectably lysing H-2D(b) but not H-2D(a)-bearing, H-7.1- incompatible targets. The impact of these observations on the proposed models for H-2 restriction of non-H-2 histocompatibility antigen-specific cytolysis is discussed. 相似文献