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Risk factors for extensive ulcerative colitis and ulcerative proctitis: a population based case-control study. 总被引:3,自引:1,他引:2
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To examine socioeconomic factors, dietary and other personal habits, and medical history as risk factors for ulcerative colitis, we studied 167 (98%) of all prevalent cases of ulcerative colitis diagnosed in Uppsala county from 1945 to 1964 and 167 age and sex matched population controls. Ulcerative colitis patients were less likely than controls to be current cigarette, pipe, or cigar smokers (odds ratio (OR) = 0.44; 95% confidence limits (CL) = 0.25-0.78), but more likely to have symptoms induced by drinking milk (OR = 4.63; 95% CL = 2.15-9.93). Patients with ulcerative colitis do not differ in most of the socioeconomic, dietary and personal habits compared with the background population. 相似文献
4.
Kristina A. Theis Louise Murphy Jennifer M. Hootman Charles G. Helmick Edward Yelin 《Arthritis care & research》2007,57(3):355-363
Objective
To estimate the national prevalence of arthritis‐attributable work limitation (AAWL) among persons ages 18–64 with doctor‐diagnosed arthritis and examine correlates of AAWL.Methods
Using the 2002 National Health Interview Survey, we estimated the prevalence of AAWL (limited in whether individuals work, the type of work they do, or the amount of work they do) and correlates of AAWL in univariable and multivariable‐adjusted logistic regression analyses. Survey data were analyzed in SAS and SUDAAN to account for the complex sample design.Results
A total of 5.3% of all US adults ages 18–64 reported AAWL; in this age group, AAWL is reported by ~30% of those who report arthritis. The prevalence of AAWL was highest among people ages 45–64 years (10.2%), women (6.3%), non‐Hispanic blacks (7.7%), people with less than a high school education (8.6%), and those with an annual household income <$20,000 (12.6%). AAWL was substantially increased among people with arthritis‐attributable activity limitations (multivariable‐adjusted odds ratio [OR] 9.1, 95% confidence interval [95% CI] 7.1–11.6). The multivariable‐adjusted likelihood of AAWL was moderately higher among non‐Hispanic blacks (OR 1.6, 95% CI 1.2–2.3), Hispanics (OR 1.8, 95% CI 1.2–2.6), and people with high levels of functional/social/leisure limitations (OR 1.8, 95% CI 1.4–2.3) and was decreased among those with a college education (OR 0.6, 95% CI 0.4–0.8).Conclusion
AAWL is highly prevalent, affecting millions of Americans and one‐third of adults with doctor‐diagnosed arthritis. Findings suggest the need for more targeted research to better understand the natural history, success of interventions, and effects of policy on AAWL. Public health interventions, including self‐management education programs, may be effective in countering AAWL. 相似文献5.
CG Teo 《Oral diseases》2002,8(S2):88-90
Oral hairy leukoplakia (OHL) and Kaposi's sarcoma (KS) are commonly encountered in the HIV-infected patient. A unique feature of OHL is non-cytolytic high level of replication of Epstein–Barr virus (EBV) in the glossal epithelium. The expression of viral-encoded anti-apoptotic proteins concomitant to replicative proteins probably underlies this phenomenon. The question of whether OHL arises from activation of EBV latent in the tongue, or from superinfection by endogenous EBV shed via non-glossal sites or by exogenous EBV remains unresolved. Human herpesvirus 8 (HHV8) is now seen as necessary but not sufficient cause of KS. Expression of HHV8-encoded oncogenic proteins in endothelial cells probably explains the aberrant proliferation of these cells in KS lesions. Studies into why KS is so commonly observed at the palate in HIV-infected patients may provide important clues to its pathogenesis. 相似文献
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Ulcerative colitis and colorectal cancer. A population-based study 总被引:40,自引:0,他引:40
BACKGROUND. The risk of colorectal cancer is increased among patients with ulcerative colitis. The magnitude of this increase in risk and the effects of the length of follow-up, the extent of disease at diagnosis, and age at diagnosis vary substantially in different studies. METHODS. To provide accurate estimates of the risk of colorectal cancer among patients with ulcerative colitis, we studied a population-based cohort of 3117 patients given a diagnosis of ulcerative colitis from 1922 through 1983 who were followed up through 1984. RESULTS. Ninety-two cases of colorectal cancer occurred in 91 patients. As compared with the expected incidence, the incidence of colorectal cancer in the cohort was increased (standardized incidence ratio [ratio of observed to expected cases] = 5.7; 95 percent confidence interval, 4.6 to 7.0). Less extensive disease at diagnosis was associated with a lower risk; for patients with ulcerative proctitis, the standardized incidence ratio was 1.7 (95 percent confidence interval, 0.8 to 3.2); for those with left-sided colitis, 2.8 (95 percent confidence interval, 1.6 to 4.4); and for those with pancolitis (extensive colitis, or inflammation of the entire colon), 14.8 (95 percent confidence interval, 11.4 to 18.9). Age at diagnosis and the extent of disease at diagnosis were strong and independent risk factors for colorectal cancer. For each increase in age group at diagnosis (less than 15 years, 15 to 29 years, 30 to 39 years, 40 to 49 years, 50 to 59 years, and greater than or equal to 60 years), the relative risk of colorectal cancer, adjusted for the extent of disease at diagnosis, decreased by about half (adjusted standardized incidence ratio = 0.51; 95 percent confidence interval, 0.46 to 0.56). The absolute risk of colorectal cancer 35 years after diagnosis was 30 percent for patients with pancolitis at diagnosis and 40 percent for those given this diagnosis at less than 15 years of age. CONCLUSIONS. Close surveillance and perhaps even prophylactic proctocolectomy should be recommended for patients given a diagnosis of pancolitis, especially those who are less than 15 years of age at diagnosis. 相似文献
9.
Arif JM; Gairola CG; Glauert HP; Kelloff GJ; Lubet RA; Gupta RC 《Carcinogenesis》1998,19(8):1515-1517
The present study investigated the effects of dietary oltipraz on cigarette
smoke-related lipophilic DNA adduct formation. Female Sprague- Dawley rats
were exposed daily to sidestream cigarette smoke in a whole- body exposure
chamber 6 h/day for 4 consecutive weeks. One group of rats was maintained
on control diet while another group received the same diet supplemented
with either a low (167 p.p.m.) or high (500 p.p.m.) dose of oltipraz,
starting 1 week prior to initiation of smoke exposure until the end of the
experiment. Analysis of lipophilic DNA adducts by the nuclease P1-mediated
32P-post-labeling showed up to five smoke-related adducts. Adduct no. 5
predominated in both the lung and the heart while adduct nos 3 and 2
predominated in the trachea and bladder, respectively. Quantitative
analysis revealed that the total adduct level was the highest in lungs
(270+/-68 adducts/10(10) nucleotides), followed by trachea (196+/-48
adducts/10(10) nucleotides), heart (141+/-22 adducts/10(10) nucleotides)
and bladder (85+/-16 adducts/10(10) nucleotides). High dose oltipraz
treatment reduced the adduct levels in lungs and bladder by >60%, while
the reduction in lungs in the low-dose group was approximately 35%. In
trachea, the effect of low and high dietary oltipraz on smoke DNA adduction
was equivocal, while smoke-related DNA adducts in the heart were minimally
inhibited by high-dose oltipraz. In a repeat experiment that employed a
3-fold lower dose of cigarette smoke, oltipraz (500 p.p.m.) was found to
inhibit the formation of DNA adducts in rat lungs and trachea by 80 and
65%, respectively. These data clearly demonstrate a high efficacy of
oltipraz in inhibiting the formation of cigarette smoke-induced DNA adducts
in the target tissues.
相似文献
10.
Mutation of the p53 tumor suppressor gene in spontaneously occurring osteosarcomas of the dog 总被引:8,自引:0,他引:8
Inactivation of the p53 tumor suppressor gene has been implicated in the
pathogenesis of numerous human cancers, including osteosarcomas.
Appendicular osteosarcomas of the dog appear to be a good model for their
human equivalent with regard to biologic behavior, epidemiology and
histopathology. We individually screened exons 5-8 of the p53 gene for
mutations in 15 canine appendicular osteosarcomas using 'Cold' SSCP to
compare the role of this gene in human and canine osteosarcoma
tumorigenesis. Seven of the tumors (47%) exhibited point mutations, with
one tumor possessing two mutations within different exons. Of these, seven
were missense mutations and the eighth was a 'silent' mutation potentially
affecting the exon 6-7 splicing region. Five of the missense mutations were
located in highly conserved regions IV and V, while another corresponded
with the highly conserved codon 220 mutational hotspot located outside the
conserved domains. The locations and types of mutations were nearly
identical to those reported in human cancer. These findings provide strong
evidence of the involvement of p53 mutations in the development of canine
appendicular osteosarcomas. Canine osteosarcomas appear to be a promising
model for their human equivalent on a clinical, pathologic, and molecular
level.
相似文献