全文获取类型
收费全文 | 690篇 |
免费 | 34篇 |
国内免费 | 18篇 |
专业分类
耳鼻咽喉 | 5篇 |
儿科学 | 36篇 |
妇产科学 | 6篇 |
基础医学 | 64篇 |
口腔科学 | 19篇 |
临床医学 | 67篇 |
内科学 | 124篇 |
皮肤病学 | 6篇 |
神经病学 | 42篇 |
特种医学 | 143篇 |
外国民族医学 | 1篇 |
外科学 | 101篇 |
综合类 | 8篇 |
预防医学 | 44篇 |
眼科学 | 3篇 |
药学 | 45篇 |
肿瘤学 | 28篇 |
出版年
2021年 | 4篇 |
2020年 | 2篇 |
2019年 | 6篇 |
2018年 | 7篇 |
2017年 | 9篇 |
2016年 | 12篇 |
2015年 | 5篇 |
2014年 | 12篇 |
2013年 | 17篇 |
2012年 | 16篇 |
2011年 | 16篇 |
2010年 | 20篇 |
2009年 | 17篇 |
2008年 | 11篇 |
2007年 | 29篇 |
2006年 | 24篇 |
2005年 | 28篇 |
2004年 | 12篇 |
2003年 | 12篇 |
2002年 | 16篇 |
2001年 | 16篇 |
2000年 | 12篇 |
1999年 | 20篇 |
1998年 | 34篇 |
1997年 | 21篇 |
1996年 | 28篇 |
1995年 | 21篇 |
1994年 | 23篇 |
1993年 | 14篇 |
1992年 | 21篇 |
1991年 | 14篇 |
1990年 | 15篇 |
1989年 | 26篇 |
1988年 | 34篇 |
1987年 | 18篇 |
1986年 | 23篇 |
1985年 | 17篇 |
1984年 | 13篇 |
1983年 | 8篇 |
1982年 | 10篇 |
1981年 | 6篇 |
1980年 | 12篇 |
1979年 | 4篇 |
1978年 | 6篇 |
1977年 | 11篇 |
1976年 | 11篇 |
1973年 | 7篇 |
1972年 | 3篇 |
1971年 | 5篇 |
1969年 | 5篇 |
排序方式: 共有742条查询结果,搜索用时 15 毫秒
1.
R K Beals 《Journal of pediatric orthopedics》1990,10(6):717-720
Three patients who experienced premature complete physeal closure of the ipsilateral limb following diaphyseal fractures are reported. The diagnosis was recognized because of unexpected progressive limb length discrepancy following fracture healing. The cause is unknown. This phenomenon should be recognized by those treating fractures in children. 相似文献
2.
Barry J. Cusack Stephan P. Young Vicki L. Loseke Michelle R. Hurty Loring Beals Richard D. Olson 《Cancer chemotherapy and pharmacology》1992,30(2):145-148
Summary Malnutrition involving protein deficiency, which commonly occurs in cancer patients receiving anthracycline treatment, is considered to be a risk factor for the development of cardiotoxicity. Protein deficiency has been shown to impair the metabolism of drugs such as theophylline and acetaminophen. If protein deficiency also impairs anthracycline metabolism, it could explain at least in part the enchanced anthracycline toxicity associated with malnutrition. We tested this idea by determining the effect of a low- protein, isocaloric diet on doxorubicin pharmacokinetics in rabbits. The animals were randomized into two groups for 8–12 weeks. Rabbits in group 1 received a low-protein (5%), isocaloric diet, whereas those in group 2 received a normal-protein (15%) diet. Both groups (group 1,n=15; group 2,n=14) were given 5 mg/kg doxorubicin by i.v. bolus. After doxorubicin injection, blood samples were obtained over the next 52 h for the measurement of doxorubicin and doxorubicinol plasma concentrations by high-performance liquid chromatography (HPLC) with fluorometric detection. The low-protein diet significantly decreased doxorubicin clearance (48±3 vs 59±4 ml min–1 kg–1;P<0.05), prolonged the terminal climination half-life (28±2 vs 22±2 h;P<0.05), and increased the area under the plasma concentration/time curve extrapolated to infinity (1722±122 vs 1405±71 ng h ml–1;P<0.05) as compared with the values determined for rabbits fed the standard rabbit chow (15% protein). The volume of distribution for doxorubicin was not altered by the low-protein diet. In addition, in rabbits fed the the low-portein diet, the terminal elimination half-life of the alcohol metabolite, doxorubicinol was prolonged (52±5 vs 40±2 h;P<0.05). Thus, a low-protein diet causes a reduction in the ability of rabbits to eliminate doxorubicin and possibly its alcohol metabolite doxorubicinol. If a similar alteration in anthracycline pharmacokinetics occurs in malnourished cancer patients, this phenomenon may contribute to their increased risk of developing cardiotoxicity associated with anthracycline therapy.Supported by the Department of Veterans Affairs and the American Heart Foundation 相似文献
3.
Release of soluble transferrin receptor from the surface of human leukemic HL60 cells 总被引:2,自引:0,他引:2
Information regarding transferrin (Tf) receptor degradation is largely incomplete. HL60 cells were shown to release to their growth medium a Tf-binding protein which could be immunoprecipitated by anti-Tf receptor monoclonal antibodies (MoAbs) B3/25 and OKT9. Soluble Tf receptor was detected in the medium within one hour of replating of cells, and its release was inhibited at 4 degrees C. The affinity of Tf for the soluble receptor released by cells (kd = 2.3 x 10(-10) mol/L) was slightly lower than its affinity for the detergent-solubilized cellular receptor (kd = 1.2 x 10(-10) mol/L). 125I-Tf internalized and released by cells subsequently bound to Tf receptor released by the same cells, and soluble Tf receptor in the conditioned medium (CM) inhibited 125I-Tf binding to intact cells. The soluble Tf receptor isolated from the CM was smaller (78,000 daltons) than the cell surface receptor (94,000 daltons) when analyzed by gel electrophoresis under reducing conditions. Isolated cell membranes readily released soluble receptor; however, this release could be blocked by protease inhibitors. The soluble Tf receptor may represent the extracytoplasmic domain of the cellular Tf receptor released from the surface of HL60 cells through proteolytic cleavage by a membrane-based protease. 相似文献
4.
5.
Dodd Steven W. Havel Henry A. Kovach Paul M. Lakshminarayan Chitra Redmon Martin P. Sargeant Charlene M. Sullivan Gary R. Beals John M. 《Pharmaceutical research》1995,12(1):60-68
Mixing pharmaceutical preparations of soluble neutral regular insulin solution (NRI) and neutral protamine Hagedorn (NPH) crystalline insulin suspension leads to a reduction in the measurable amount of soluble insulin in the formulation supernatant. However in spite of the loss in soluble insulin, the time-actions of these components have been shown, in clinical trials, to be unaffected. The interaction between these different physical forms of insulin has been studied using reversed-phase HPLC, isothermal titrating calorimetry, and Doppler electrophoretic light scattering analysis. Sorbent surface and solution perturbation studies revealed that the NRI adsorbs to the surface of the NPH crystal with an equilibrium constant ranging from 104 M–1 to 107 M–!, depending on the protamine concentration, pH, ionic strength, and temperature. This adsorption behavior suggests that the binding is mediated by electrostatic interactions arising between the positively-charged NPH crystal and the negatively-charged NRI hexamer. Doppler electrophoretic light scattering results, used to probe the pH-dependent surface charge of NPH and soluble insulin hexamer, support the conclusion that electrostatic interactions mediate the adsorption process. Adsorption studies under physiological conditions indicate that the elevated temperature and ionic strength, in a subcutaneous depot, are sufficient to lead to the dissociation of the NRI/NPH complex that exists in these NPH mixture formulations. 相似文献
6.
7.
Sanjana VM; Johnston PA; Robertson CR; Jamison RL 《The American journal of physiology》1976,231(2):313-318
8.
Localization of a gene for otosclerosis to chromosome 15q25-q26 总被引:5,自引:0,他引:5
Tomek MS; Brown MR; Mani SR; Ramesh A; Srisailapathy CR; Coucke P; Zbar RI; Bell AM; McGuirt WT; Fukushima K; Willems PJ; Van Camp G; Smith RJ 《Human molecular genetics》1998,7(2):285-290
Among white adults otosclerosis is the single most common cause of hearing
impairment. Although the genetics of this disease are controversial, the
majority of studies indicate autosomal dominant inheritance with reduced
penetrance. We studied a large multi- generational family in which
otosclerosis has been inherited in an autosomal dominant pattern. Five of16
affected persons have surgically confirmed otosclerosis; the remaining nine
have a conductive hearing loss but have not undergone corrective surgery.
To locate the disease- causing gene we completed genetic linkage analysis
using short tandem repeat polymorphisms (STRPs) distributed over the entire
genome. Multipoint linkage analysis showed that only one genomic region, on
chromosome 15q, generated a lod score >2.0. Additional STRPs were typed
in this area, resulting in a lod score of 3.4. STRPs FES (centromeric) and
D15S657 (telomeric) flank the 14. 5 cM region that contains an otosclerosis
gene.
相似文献
9.
Peritoneal fluid concentrations of interleukin-8 in women with endometriosis: relationship to stage of disease 总被引:7,自引:10,他引:7
Gazvani MR; Christmas S; Quenby S; Kirwan J; Johnson PM; Kingsland CR 《Human reproduction (Oxford, England)》1998,13(7):1957-1961
There is increasing evidence that immunological mechanisms play a role in
the pathogenesis and pathophysiology of endometriosis. It was therefore of
interest to study interleukin-8 (IL-8), a chemokine, in the peritoneal
fluid and peripheral blood of women undergoing laparoscopic procedures. The
presence and concentrations of IL-8 in relation to endometriosis,
infertility and abdominal pain were evaluated. Samples of peritoneal fluid
(n = 49) and peripheral blood (n = 50) were obtained from 50 consecutive
patients undergoing laparoscopic surgery for various gynaecological
indications (abdominal pain, infertility, sterilization). IL-8 was present
in the peritoneal fluid of most women (87%). The concentration of IL-8 in
the peritoneal fluid was higher in women with endometriosis compared to
women without (P = 0.02). This difference was more pronounced in early
(stage 1) endometriosis (P = 0.001). IL-8 concentrations in the peritoneal
fluid were also higher in women with early endometriosis compared to women
with later stages of the disease (P = 0.003). Peripheral blood
concentrations did not correlate with peritoneal fluid concentrations of
IL-8 and/or the presence of endometriosis. We conclude that IL-8 is an
important factor that may contribute to the pathogenesis of endometriosis
possibly by promoting neovascularization. This information can be a guide
in the development of new therapeutic approaches for the treatment of
endometriosis.
相似文献
10.
Prolonged exposure to inhalational anesthetic nitrous oxide kills neurons in adult rat brain 总被引:3,自引:0,他引:3
Short-term exposure of adult rats to nitrous oxide (N2O), an inhalational anesthetic and NMDA (N-methyl-D-aspartate) antagonist, causes a reversible neurotoxic vacuole reaction in neurons of the posterior cingulate/retrosplenial cortex (PC/RSC) which resembles that caused by low doses of other NMDA antagonists. Since high doses or prolonged exposure to other NMDA antagonists can cause neurons to die, we assessed whether prolonged N2O exposure might also cause neuronal cell death. Adult female Sprague-Dawley rats were exposed to 150-vol% N2O (approximately EC50 for N2O anesthesia in rats) for various durations from 1 to 16 h. The time course for onset and disappearance of the reversible vacuole reaction was studied, as was the time course and dose requirement for triggering cell death. A maximum vacuole reaction was observed in PC/RSC neurons in brains examined immediately after 3 h of 150-vol% N2O exposure and the same magnitude of vacuole reaction was observed when brains were examined immediately after a longer period of N2O exposure. When N2O was terminated at 3 h and the rats were killed 1 h later, the vacuole reaction was markedly diminished and if the rats were killed 3 h later the vacuole reaction had completely disappeared. Prolonged exposure to 150-vol% N2O (for 8 h or more) caused neuronal cell death which was detectable by silver staining 32 h later. Concurrently administered GABAergic agents, diazepam (an i.v. anesthetic), or isoflurane (an inhalational anesthetic), prevented this cell death reaction.Our findings demonstrate that short-term exposure of adult rats to N2O causes injury to PC/RSC neurons that is rapidly reversible, and prolonged N2O exposure causes neuronal cell death. These neurotoxic effects, including the cell death reaction, can be prevented by coadministration of GABAmimetic anesthetic agents. Duration of NMDA receptor blockade appears to be an important determinant of whether neurons are reversibly injured or are driven to cell death by an NMDA antagonist drug. 相似文献