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51.
Y Y Zhu W Lee E Botvinick M Dae K Chatterjee J Danforth T Ports 《American heart journal》1988,116(4):1071-1080
In order to determine their significance during dipyridamole perfusion scintigraphy, symptomatic, ECG, and scintigraphic findings were related to each other, to the hemodynamic response, and to angiographic findings in 73 consecutive patients having coronary angiography within 3 months of scintigraphy. The group having induced "cardiac" pain differed from the group without induced pain only in their higher incidence of induced ischemic ST changes, the "marked" hemodynamic response, and their lower incidence of an "absent" hemodynamic response (all p less than 0.01). Induced ST depression was found only in patients with coronary disease. In this population, dipyridamole-induced pain was a moderately specific marker and induced ST abnormalities a more highly specific marker for coronary disease. However, both were insensitive for coronary disease diagnosis. If induced pain or ST abnormalities in the presence of significant coronary disease were accepted as indicators of ischemia, then scintigraphic abnormalities appeared to be produced by dipyridamole in roughly equal incidence by ischemic and nonischemic mechanisms. Induced ischemia related frequently to an exaggerated hypotensive response with no change in double product, suggesting its cause to be an induced increase in myocardial oxygen demand. Dipyridamole-induced image defects were noted even in the absence of a peripheral hemodynamic response. This indicates that the peripheral response does not always correlate with its central coronary effect and an absent peripheral hemodynamic response does not necessarily invalidate scintigraphic results. 相似文献
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Bhatia Ansh Gaur Prithvi Sanjeevkumar Zimba Olena Chatterjee Tulika Nikiphorou Elena Gupta Latika 《Clinical rheumatology》2022,41(3):861-867
Clinical Rheumatology - Instagram allows for graphical and visual information exchange. This paper aims to explore the current landscape of rheumatology on Instagram and analyse the accounts... 相似文献
55.
Denny John Prabir Chatterjee Shruti Murthy Ramesh Bhat Baba Maiyaki Musa 《The Indian journal of tuberculosis》2018,65(3):208-217
Background
In India, multidrug-resistant tuberculosis (MDR-TB) patients are usually treated in hospitals. Decentralised care model, however, has been suggested as a possible alternative by the World Health Organization (WHO). In the “End TB Strategy”, the WHO highlights, as one of the key targets for 2035, that ‘no TB-affected families should face catastrophic hardship due to the tuberculosis’. Removal of financial barriers to health-care access and mitigation of catastrophic expenditures are therefore considered vital to achieve the universal health coverage (UHC) goal. Since forgoing healthcare due to the financial constraints is a known fact in India, decentralised care as an intervention choice (as against hospital-based care) might enhance equity provided it is an affordable choice. Thus, an economic evaluation was conducted, from the perspective of the national health system in India, to assess the cost-effectiveness of decentralised care compared to centralised care for MDR-TB.Methods
This study uses a decision-analytic model with a follow-up of two years to assess the expected costs of the decentralised versus the centralised approaches for MDR-TB treatment. A published systematic review of observational studies yielded the MDR-TB treatment outcomes, which included treatment success, treatment default, treatment failure, and mortality parameters. It was observed that these parameters did not vary significantly between the two alternatives. Treatment costs included the following costs: hospital admission costs, clinic costs, visits to laboratory and MDR-TB centre, drug therapy, injections and food. Costs data of drugs, diagnosis, hospital stay and travel to public facilities, based on a simple market survey, were taken from a recently published study on MDR-TB expenditures in the Chhattisgarh state of India. Potential cost savings related to the implementation of decentralised MDR-TB care for all patients who initiated MDR-TB treatment in India were additionally estimated.Results
Estimated average expected total treatment cost was US$ 3390.56 for the hospital-based model and US$ 1724.1 for the decentralised model for a patient treated for MDR-TB in India, generating potential savings of US$1666.50 per case, with ICER US$ 2382.68 per QALY gained. One of the primary drivers of this difference was the significantly more intensive (thus expensive) stay charges in the hospital. If the costs and treatment probabilities are extrapolated to the whole country, with 48114 MDR-TB patients initiated on treatment in 2017, decentralised care would have additional 1058 patients cured, gain additional 3824 QALYs, and avert 2165 deaths, as compared to centralised care, in India. At various scenarios of coverage rates of decentralised and centralised care the cost difference would range between 23% and 94% for the country.Conclusion
Our study provides evidence of cost savings for MDR-TB patients if patients choose decentralised treatment in comparison to suggested hospitalisation of these patients for centralised treatment with similar outcomes. The economic evaluation presented in this study expected significant efficiency gains in choice of two treatment options and the cost savings may improve equity. In India, treatment of MDR-TB using decentralised care is expected to result in similar patient outcomes at markedly reduced public health costs compared with centralised care. 相似文献56.
Prenatal diagnosis of thyroid hormone resistance 总被引:4,自引:0,他引:4
Asteria C Rajanayagam O Collingwood TN Persani L Romoli R Mannavola D Zamperini P Buzi F Ciralli F Chatterjee VK Beck-Peccoz P 《The Journal of clinical endocrinology and metabolism》1999,84(2):405-410
A 29-yr-old woman with pituitary resistance to thyroid hormones (PRTH) was found to harbor a novel point mutation (T337A) on exon 9 of the thyroid hormone receptor beta (TRbeta) gene. She presented with symptoms and signs of hyperthyroidism and was successfully treated with 3,5,3'-triiodothyroacetic acid (TRIAC) until the onset of pregnancy. This therapy was then discontinued in order to prevent TRIAC, a compound that crosses the placental barrier, from exerting adverse effects on normal fetal development. However, as the patient showed a recurrence of thyrotoxic features after TRIAC withdrawal, we sought to verify, by means of genetic analysis and hormone measurements, whether the fetus was also affected by RTH, in order to rapidly reinstitute TRIAC therapy, which could potentially be beneficial to both the mother and fetus. At 17 weeks gestation, fetal DNA was extracted from chorionic villi and was used as a template for PCR and restriction analysis together with direct sequencing of the TRbeta gene. The results indicated that the fetus was also heterozygous for the T337A mutation. Accordingly, TRIAC treatment at a dose of 2.1 mg/day was restarted at 20 weeks gestation. The mother rapidly became euthyroid, and the fetus grew normally up to 24 weeks gestation. At 29 weeks gestation mild growth retardation and fetal goiter were observed, prompting cordocentesis. Circulating fetal TSH was very high (287 mU/L) with a markedly reduced TSH bioactivity (B/I: 1.1 +/- 0.4 vs 12.7 +/- 1.2), while fetal FT4 concentrations were normal (8.7 pmol/L; normal values in age-matched fetuses: 5-22 pmol/L). Fetal FT3 levels were raised (7.1 pmol/L; normal values in age-matched fetuses: <4 pmol/L), as a consequence of 100% cross-reactivity of TRIAC in the FT3 assay method. To reduce the extremely high circulating TSH levels and fetal goiter, the dose of TRIAC was increased to 3.5 mg/day. To monitor the possible intrauterine hypothyroidism, another cordocentesis was performed at 33 weeks gestation, showing that TSH levels were reduced by 50% (from 287 to 144 mU/L). Furthermore, a simultaneous ultrasound examination revealed a clear reduction in fetal goiter. After this latter cordocentesis, acute complications occured, prompting delivery by cesarean section. The female neonate was critically ill, with multiple-organ failure and respiratory distress syndrome. In addition, a small goiter and biochemical features ofhypothyroidism were noted transiently and probably related to the prematurity of the infant. At present, the baby is clinically euthyroid, without goiter, and only exhibits biochemical features of RTH. In summary, although further fetal studies in cases of RTH are necessary to determine whether elevated TSH levels with a markedly reduced bioactivity are a common finding, our data suggest transient biochemical hypothyroidism in RTH during fetal development. Furthermore, we advocate prenatal diagnosis of RTH and adequate treatment of the disease in case of maternal hyperthyroidism, to avoid fetal thyrotrope hyperplasia, reduce fetal goiter, and maintain maternal euthyroidism during pregnancy. 相似文献
57.
Initial testing (stage 1) of the tubulin binding agent nanoparticle albumin‐bound (nab) paclitaxel (Abraxane®) by the Pediatric Preclinical Testing Program (PPTP) 下载免费PDF全文
58.
The mouse Pax21Neu
mutation is identical to a human PAX2
mutation in a family with renal-coloboma syndrome and results
in developmental defects of the brain, ear, eye, and kidney 下载免费PDF全文
Jack Favor Rodica Sandulache Angelika Neuhuser-Klaus Walter Pretsch Bimal Chatterjee Elfriede Senft Wolfgang Wurst Vronique Blanquet Patricia Grimes Ralf Sprle Klaus Schughart 《Proceedings of the National Academy of Sciences of the United States of America》1996,93(24):13870-13875
We describe a new mouse frameshift mutation (Pax21Neu) with a 1-bp insertion in the Pax2 gene. This mutation is identical to a previously described mutation in a human family with renal-coloboma syndrome [Sanyanusin, P., McNoe, L. A., Sullivan, M. J., Weaver, R. G. & Eccles, M. R. (1995) Hum. Mol. Genet. 4, 2183–2184]. Heterozygous mutant mice exhibit defects in the kidney, the optic nerve, and retinal layer of the eye, and in homozygous mutant embryos, development of the optic nerve, metanephric kidney, and ventral regions of the inner ear is severely affected. In addition, we observe a deletion of the cerebellum and the posterior mesencephalon in homozygous mutant embryos demonstrating that, in contrast to mutations in Pax5, which is also expressed early in the mid-hindbrain region, loss of Pax2 gene function alone results in the early loss of the mid-hindbrain region. The mid-hindbrain phenotype is similar to Wnt1 and En1 mutant phenotypes, suggesting the conservation of gene regulatory networks between vertebrates and Drosophila. 相似文献
59.
V K Chatterjee J A Ball C Proby J M Burrin S R Bloom 《The Journal of endocrinology》1988,116(2):R1-R2
In five healthy normal male volunteers, pretreatment with the cholinergic muscarinic antagonist pirenzepine (30 mg i.v.) almost abolished the growth hormone (GH) response to a maximal dose (120 micrograms i.v.) of growth hormone-releasing hormone (GHRH) (GH response at 40 min 5.6 + 1.3 mU/l with GHRH and pirenzepine vs 40.8 +/- 5.3 mU/l with GHRH alone, P less than 0.02). Concomitant i.v. infusion of galanin (40 pmol/kg/min) with pirenzepine not only restored but significantly potentiated the GH response to GHRH (GH at 40 min 72.2 +/- 10.5 mU/l, P less than 0.001 vs GHRH and pirenzepine, P less than 0.02 vs GHRH alone). Previous studies have proposed that cholinergic pathways control GH release via somatostatin and this study suggests that galanin may act by modulating hypothalamic somatostatinergic tone either directly or, possibly, by facilitating cholinergic neurotransmission. 相似文献