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排序方式: 共有104条查询结果,搜索用时 15 毫秒
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Zipora Weinbaum Steven J. Samuels Marc B. Schenker 《Archives of environmental & occupational health》2013,68(5):341-348
This study was conducted to identify risk factors for paraquat-related occupational illnesses. Pesticide-related illness is a reportable disease in California. A total of 231 skin (26.0%), eye (32.0%), local respiratory (3.5%), and systemic (38.5%) paraquat-related cases were reported to the Worker Health and Safety Branch, California Department of Food and Agriculture, during 1971 through 1985. Following paraquat exposure, we found no cases of pulmonary fibrosis. Annual numbers of cases ranged between 1 and 33 (median = 14 cases/y). Information on illnesses reported during 1981 through 1985 (n = 62) was merged with detailed information on paraquat use in agricultural settings (111 716 applications) for the same years. We found that crop treated, method of application, and season of application all contributed independently to the risk of reported illness. Hand application was associated with a higher risk of illness, compared with air application (RR = 99.1, 95% CI = 22.16–443.47); summer application was associated with a higher risk of illness than was winter application (RR = 4.1, 95% CI = 1.91–8.61); and fruit trees were associated with higher risk of illness than were other crops (mainly cotton) (RR = 3.6, 95% CI = 1.18–11.21). 相似文献
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The Ca(2+)-activated K+ channels of human red blood cells (RBCs) (Gardos channels, hIK1, hSK4) can mediate rapid cell dehydration, of particular relevance to the pathophysiology of sickle cell disease. Previous investigations gave widely discrepant estimates of the number of Gardos channels per RBC, from as few as 1 to 3 to as many as 300, with large cell-to-cell differences, suggesting that RBCs could differ extensively in their susceptibility to dehydration by elevated Ca2+. Here we investigated the distribution of dehydration rates induced by maximal and uniform Ca2+ loads in normal (AA) and sickle (SS) RBCs by measuring the time-dependent changes in osmotic fragility and RBC volume distributions. We found a remarkable conservation of osmotic lysis and volume distribution profiles during Ca(2+)-induced dehydration, indicating overall uniformity of dehydration rates among AA and SS RBCs. In light of these results, alternative interpretations were suggested for the previously proposed low estimates and heterogeneity of channel numbers per cell. The results support the view that stochastic Ca2+ permeabilization rather than Gardos-channel variation is the main determinant selecting which SS cells dehydrate through Gardos channels in each sickling episode. 相似文献
4.
Inhibition of concanavalin A-induced acute T cell dependent hepatic damage in mice by hypothyroidism
Haim Shirin Iris Dotan Moshe Papa Yoram Maaravi Husein Aeet Lillian Zaidel Zipora Matas Rafael Bruck Steven F Moss Zamir Halpern Ran Oren 《Liver international》1999,19(3):206-211
Abstract: Aims/Background: Concanavalin A (Con A) activates T lymphocytes and causes acute T-cell-mediated hepatic injury in mice. Decreased thyroid hormonal production is associated with a variety of immunological manifestations, including inactivation of macrophages with reduced TNF production and reduced soluble IL-2 receptors in the serum. We have recently shown that hypothyroidism prevents the development of cirrhosis and also minimizes hepatic damage in rats with fulminant hepatic failure. In the present study we examined the effects of hypothyroidism on a mouse model of Con A induced T cell-mediated acute hepatitis. Methods: Hypothyroidism was induced both medically (MMI, PTU) and surgically. Eight groups of 10 mice each were studied: euthyroid controls (2 groups: water, Con A) and hypothyroid (6 groups: MMI, PTU, Surgical, MMI-Con A, PTU-Con A, Surgical-Con A). Results: Hepatic inflammation was significantly decreased in each of the Con A treated hypothyroid groups of mice. The serum transaminases, TNF-α and IL-6 levels were significantly elevated in the Con A treated group while near normal levels were found in the hypothyroid Con A treated groups (mean±SE AST: 1499±18 vs 78±10 IU/1, p<0.001; TNF: 2500±250 vs 135± 15 pg/ml. p<0.001, IL-6: 12,200±300 vs 1260±140 pg/ml, p<0.001, respectively). Conclusions: Hypothyroidism, independent of the mode of induction, can effectively inhibit the development of acute T cell-mediated liver damage in mice. These results suggest that some decrease in thyroid function might have a role in the prevention of immune mediated liver diseases. 相似文献
5.
Melatonin inhibits nuclear factor kappa B activation and oxidative stress and protects against thioacetamide induced liver damage in rats 总被引:10,自引:0,他引:10
Bruck R Aeed H Avni Y Shirin H Matas Z Shahmurov M Avinoach I Zozulya G Weizman N Hochman A 《Journal of hepatology》2004,40(1):86-93
BACKGROUND/AIMS: Free radical-mediated oxidative stress has been implicated in the pathogenesis of acute liver injury. The aim of our study was to investigate whether melatonin, a potent free radical scavenger could prevent fulminant hepatic failure in rats. METHODS: Liver damage was induced by two consecutive injections of thioacetamide (TAA, 300 mg/kg/i.p.) at 24 h intervals. Treatment with melatonin (3 mg/kg/daily, i.p) was initiated 24 h prior to TAA. RESULTS: Twenty-four h after the second TAA injection, serum liver enzymes and blood ammonia were lower in rats treated with TAA+melatonin compared to TAA (P<0.001). Liver histology was significantly improved and the mortality in the melatonin-treated rats was decreased (P<0.001). The increased nuclear binding of nuclear factor kappa B in the livers of the TAA-treated rats, was inhibited by melatonin. The hepatic levels of thiobarbituric acid reactive substances, protein carbonyls and inducible nitric oxide synthase were lower in the TAA+melatonin-treated group (P<0.01), indicating decreased oxidative stress and inflammation. CONCLUSIONS: In a rat model of TAA-induced fulminant hepatic failure, melatonin improves survival and reduces liver damage and oxidative stress. The results suggest a causative role of oxidative stress in TAA-induced hepatic damage and suggest that melatonin may be utilized to reduce liver injury associated with oxidative stress. 相似文献
6.
Neuhaus Zipora Feiga Gutvirtz Gil Pariente Gali Wainstock Tamar Landau Daniella Sheiner Eyal 《Archives of gynecology and obstetrics》2020,301(1):143-149
Archives of Gynecology and Obstetrics - To evaluate the long-term pediatric neuropsychiatric morbidity of children born to obese patients. A population-based cohort analysis was performed comparing... 相似文献
7.
Pyrrolidine dithiocarbamate protects against thioacetamide-induced fulminant hepatic failure in rats 总被引:3,自引:0,他引:3
Bruck R Aeed H Schey R Matas Z Reifen R Zaiger G Hochman A Avni Y 《Journal of hepatology》2002,36(3):370-377
BACKGROUND/AIMS: Reactive oxygen species and nuclear factor kappa B (NF-kappaB) activation have been implicated in the pathogenesis of cell injury in experimental models of liver damage. The aim of the present study was to examine whether pyrrolidine dithiocarbamate (PDTC), an anti oxidant and inhibitor of NF-kappaB activation, would prevent hepatic damage induced in a rat model of thioacetamide (TAA)-induced liver failure. METHODS: Fulminant hepatic failure was induced in the control and treatment groups by two intraperitoneal injections of TAA (either 300 or 400 mg/kg) at 24-h intervals. In the treatment groups, rats were treated also with PDTC (60 mg/kg/24 h, i.p.), initiated 24 h prior to TAA. RESULTS: Liver enzymes, blood ammonia, and hepatic levels of thiobarbituric acid reactive substances (P<0.001) and protein carbonyls (P<0.05) were significantly lower in rats treated with PDTC compared to TAA only. Liver histology and the survival rate in the PDTC-treated rats were also improved (P<0.01 compared to TAA only). NF-kappaB activation, 2 and 6 h after TAA administration, was inhibited by PDTC. CONCLUSIONS: In a rat model of fulminant hepatic failure, the administration of PDTC attenuated liver damage and improved survival. This effect may be due to decreased oxidative stress and inhibition of NF-kappaB activation. 相似文献
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Nuclear localization of androgen receptors (ARs) is essential for their activity. Melatonin induces AR nuclear exclusion via
increase in cGMP, calcium, and protein kinase C (PKC) activation, presumably through G-protein(s). The effects of regulators
of G-protein signaling (RGS) on AR localization were studied in AR-expressing PC3 cells. Gi-specific RGS10 inhibited melatonin
but not cGMP-induced AR nuclear exclusion, independent of androgen. No evidence for Gq activation by melatonin was found.
However, Gi/Gq-selective RGS4 inhibited AR nuclear exclusion downstream of PKC activation—an effect that was abrogated by
constitutively active Gq. RGS10 and RGS4, but not RGS2, ablated the inhibitory effects of melatonin on AR reporter gene activity.
For the first time, these data show regulation by Gi and Gi-specific RGS protein-mediated AR nuclear exclusion, which is potentially
important in the treatment of AR-dependent cancers and neurodegenerative disorders. They also reveal a role for a Gq protein
downstream of PKC activation in AR nuclear localization. 相似文献
10.