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排序方式: 共有473条查询结果,搜索用时 0 毫秒
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Rakhshanda Layeequr Rahman Eric Siegel Cristiano Boneti Malene Ingram Julie Kepple Ronda S. Henry-Tillman V. Suzanne Klimberg 《American journal of surgery》2009,197(4):491-496
Background
Axillary staging provides the single most important piece of prognostic information in breast cancer patients. This retrospective study was performed to document the phenomenon of stage migration.Methods
Of 392 patients, 5 (1%) failed identification of sentinel lymph nodes (SLNs) and therefore underwent axillary lymph node dissection (ALND). Four patients (80%) had metastatic lymph nodes, 302 (77%) patients had negative SLNs, 47 (15%) underwent ALND, 85 (22%) had positive SLNs, 11 (13%) received adjuvant radiation treatment to the axilla, and 74 (87%) underwent completion ALND.Results
The median (quartiles) follow-up period was 29 months (19-46 mo). Twenty of 392 (5%) patients had disease relapse; 2 of which were local (.5%) and the rest were systemic. Earlier relapse was related significantly to lymph node status, tumor grade, and tumor size. SLN-negative patients who did not receive ALND had a relapse rate of 2.3% (6 of 256) compared with 0% in those who were truly negative based on confirmatory ALND. SLN-positive patients who did not receive ALND had a 9% (1 of 11) relapse rate.Discussion
The stage-matched pattern of relapse between SLN biopsy and ALND patients revealed lower relapse rates in SLN biopsy-staged patients, documenting the stage migration phenomenon. 相似文献54.
Donohue TM Curry-McCoy TV Todero SL White RL Kharbanda KK Nanji AA Osna NA 《Alcoholism, clinical and experimental research》2007,31(6):1053-1060
BACKGROUND: L-Buthionine (S,R) sulfoximine (BSO) is an inhibitor of glutathione biosynthesis and has been used as an effective means of depleting glutathione from cells and tissues. Here we investigated whether treatment with BSO enhanced ethanol-induced liver injury in mice. METHODS: Female C57Bl/6 mice were pair fed with control and ethanol-containing liquid diets in which ethanol was 29.2% of total calories. During the final 7 days of pair feeding, groups of control-fed and ethanol-fed mice were given 0, 5 or 7.6 mM BSO in the liquid diets. RESULTS: Compared with controls, ethanol given alone decreased total liver glutathione. This effect was exacerbated in mice given ethanol with 7.6 mM BSO, causing a 72% decline in hepatic glutathione. While ethanol alone caused no decrease in mitochondrial glutathione, inclusion of 7.6 mM BSO caused a 2-fold decline compared with untreated controls. L-Buthionine (S,R) sulfoximine did not affect ethanol consumption, but serum ethanol levels in BSO-treated mice were nearly 6-fold lower than in mice given ethanol alone. The latter decline in serum ethanol was associated with a significant elevation in the specific activities of cytochrome P450 2E1 and alcohol dehydrogenase in livers of BSO-treated animals. Ethanol consumption caused a 3.5-fold elevation in serum alanine aminotransferase levels but the enzyme fell to control levels when BSO was included in the diet. L-Buthionine (S,R) sulfoximine administration also attenuated ethanol-induced steatosis, prevented the leakage of lysosomal cathepsins into the cytosol, and prevented the ethanol-elicited decline in proteasome activity. CONCLUSIONS: L-Buthionine (S,R) sulfoximine, administered with ethanol, significantly depleted hepatic glutathione, compared with controls. However, despite the decrease in hepatic antioxidant levels, liver injury by ethanol was alleviated, due, in part, to a BSO-elicited acceleration of ethanol metabolism. 相似文献
55.
Donohue TM Curry-McCoy TV Nanji AA Kharbanda KK Osna NA Radio SJ Todero SL White RL Casey CA 《Alcoholism, clinical and experimental research》2007,31(11):1944-1952
BACKGROUND: Women exhibit greater liver damage than men after chronic alcohol consumption. Similar findings are reported in animal models. Here, we determined whether differential liver injury occurred in male and female rats after feeding these animals liquid diets containing either ethanol or isocaloric dextrose with fish oil as the sole source of lipid. METHODS: Control and ethanol liquid diets containing fish oil were pair-fed to male and female rats for 8 weeks. Liver damage was evaluated by triglyceride accumulation, lipid peroxide formation, serum transaminases, histological evaluation, and the activities of selected lysosomal and hepatoprotective enzymes. RESULTS: Fatty liver was detected after ethanol feeding in both genders, but in female rats, triglyceride levels were 60% higher, lipid peroxides were 2-fold higher, and inflammatory cells were more evident than in males. A 2-fold elevation of cathepsin B in hepatic cytosol fractions, indicating lysosomal leakage, was detected in ethanol-fed female rats but no such elevation was observed in males. The basal activity of the hepatoprotective enzyme, betaine-homocysteine methyltransferase was 4-fold higher in livers of control male rats than females, and the enzyme activity was further elevated in ethanol-fed male rats but not in females. CONCLUSIONS: Thus, female rats given ethanol in a diet containing fish oil exhibited more severe liver damage than males. We propose that this difference results, in part, from a greater tendency by females to accumulate hepatic fat, thereby enhancing the potential for oxidative stress, which in turn leads to hepatic inflammation. In addition, our findings indicate that female rats have a higher susceptibility to liver damage because of a reduced capacity for hepatoprotection. 相似文献
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Chu Xiao-Yan Liang Yuexia Cai Xiaoxin Cuevas-Licea Karla Rippley Ronda K. Kassahun Kelem Shou Magang Braun Matthew P. Doss George A. Anari M. Reza Evers Raymond 《Pharmaceutical research》2009,26(2):459-468
Purpose Gaboxadol, a selective extrasynaptic agonist of the delta-containing γ-aminobutyric acid type A (GABAA) receptor, is excreted in humans into the urine as parent drug and glucuronide conjugate. The goal of this study was to identify
the UDP-Glucuronosyltransferase (UGT) enzymes and the transporters involved in the metabolism and active renal secretion of
gaboxadol and its metabolite in humans.Methods. The structure of the glucuronide conjugate of gaboxadol in human urine was identified by LC/MS/MS. Human recombinant UGT
isoforms were used to identify the enzymes responsible for the glucuronidation of gaboxadol. Transport of gaboxadol and its
glucuronide was evaluated using cell lines and membrane vesicles expressing human organic anion transporters hOAT1 and hOAT3,
organic cation transporter hOCT2, and the multidrug resistance proteins MRP2 and MRP4.Results. Our study indicated that the gaboxadol-O-glucuronide was the major metabolite excreted in human urine. UGT1A9, and to a lesser extent UGT1A6, UGT1A7 and UGT1A8, catalyzed
the O-glucuronidation of gaboxadol in vitro. Gaboxadol was transported by hOAT1, but not by hOCT2, hOAT3, MRP2, and MRP4. Gaboxadol-O-glucuronide was transported by MRP4, but not MRP2.Conlusion. Gaboxadol could be taken up into the kidney by hOAT1 followed by glucuronidation and efflux of the conjugate into urine via
MRP4. 相似文献
58.
59.
Miranda E Arroyo A Ronda JM Muñoz JL Alonso C Martínez-Peñuelas F Martí-Viaño JL 《Revista espa?ola de anestesiología y reanimación》2007,54(6):381-383
Blunt abdominal trauma can damage the intestinal vasculature and may occasionally lead to delayed intestinal perforation, associated with a combined rate of morbidity and mortality of 25%. The diagnosis of such complications is hindered by sedation in critical patients, however, and morbimortality in this population is therefore higher. We report the case of a man with multiple injuries admitted to the intensive care unit, where delayed perforations of the sigmoid colon and cecum were diagnosed. The management of blunt abdominal trauma is reviewed and the possible causes, diagnostic approaches, and treatment options for colon injuries are discussed. 相似文献
60.
Mintz-Binder R 《Nurse educator》2008,33(6):233-4; author reply 234