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101.
诊断幽门螺杆菌感染的新进展 总被引:1,自引:1,他引:0
目前幽门螺杆菌感染的检测方法分为侵性检查和非侵入性检查,前者包括:培养,组织学检查,快速尿素酶试验,PCR;后者包括:^13C/^14C-尿素呼吸试验及^15N尿氨排泄试验,血清学,尽管检测方法较多,但在临床和科研中,由于使用目的的不同,选择的检测方法有区别。 相似文献
102.
幽门螺杆菌空泡毒作用-一种新发现的致病因素 总被引:1,自引:1,他引:0
目的用细胞毒实验对幽门螺杆菌(Helicobacterpylori,HP)致病机制作进一步研究。方法62株临床分离的幽门螺杆菌,43株的肉汤培养滤液(0.22um微孔滤膜)作用于体外培养的Vero细胞,能使其产生胞浆空泡样变。随着作用时间延长,空泡数目逐渐增多,体积逐渐增大,4天后细胞逐渐死亡。据此将HP分为有空泡毒作用的HP(Toxin+)及没有空泡毒作用的HP(Toxin-)。二类HP肉汤培养滤液的尿素酶活性无明显差异(P>0.05)。结果HP的这种空泡毒作用不同于已知的HP的致病因素,而是一种新近发现的致病因素。HP相关消化性溃疡、十二指肠球部溃疡、胃炎患者,HP(Toxin+)分别占其HP感染总数78.26%、84.38%、42.86%。结论HP相关消化性溃疡与HP(Toxin+)感染密切相关 相似文献
103.
104.
对31 例Du 患者及31 例慢性胃炎患者进行HP 检测及血清胃泌素测定,并对其中23 例HP阳性Du 患者抗HP 治疗后的血清胃泌素及HP 进行测定。结果显示HP 检出率Du 组为74 .19 % (23/31) ,较慢性胃炎组48 .39 % (15/31) 高( P< 0 .05) ;DuHP 阳性组的血清胃泌素较DuHP 阴性组、慢性胃炎HP 阳性组及慢性胃炎HP 阴性组明显增高( P 均< 0 .05) ,而DuHP 阴性组的血清胃泌素与慢性胃炎HP 阳性组及慢性胃炎HP 阴性组比较差异无显著性( P> 0 .05) ,23 例DuHP 阳性者抗HP 治疗后,HP转阴者的血清胃泌素较治疗前明显下降(P< 0 .05) ,HP 未转阴者的血清胃泌素前后差异无显著性( P>0.5) 。提示Du 血清胃泌素与幽门螺杆菌感染有一定相关性。 相似文献
105.
Lee CT Kuo BI Chen CY Chang FY Lee SD 《European journal of clinical pharmacology》1999,54(11):817-820
Objective: To determine which demographic factors may influence serum gastrin and pepsinogen I (PGI) levels in duodenal ulcer patients
undergoing omeprazole treatment.
Methods: We conducted an outpatient-based prospective study in the Veterans General Hospital, Taipei, to investigate the pharmacological
effects on patients with duodenal ulcers receiving omeprazole treatment for 4 weeks. Sixty-eight patients (61 males/7 females,
aged 25–73 years) with endoscopically confirmed duodenal ulcer were included. Gastrin and pepsinogen I levels were measured
before and after treatment. Demographic factors including age, sex, smoking, ulcer healing and antral Helicobacter pylori colonization/clearance were analyzed, in order to measure their probable influences on serum gastrin and pepsinogen I levels.
Results: Ulcer healing was seen in 92.6% of patients while 48 (70.6%) antral clearances were seen in 66 H. pylori colonized patients at the end of trial. Omeprazole monotherapy led to a marked elevation of serum gastrin (85.8 pg · ml−1, SD 32.0 pg · ml−1 vs 133.9 pg · ml−1, SD 71.6 pg · ml−1, P < 0.01), and pepsinogen I (111.0 ng · ml−1, SD 36.7 ng · ml−1 vs 253.6 ng · ml−1, SD 64.8 ng · ml−1, P < 0.01) levels when measured on day 29. Only patients showing antral H. pylori clearance exhibited an influence on the magnitude of pepsinogen I elevation following omeprazole monotherapy (143.9%, SD
67.3% vs 78.6%, SD 51.2%, P < 0.01). Moreover, the sensitivity and specificity of serum pepsinogen I variations were plotted on a receiving operating
characteristic (ROC) curve. The 140% increased pepsinogen I level yielded a maximum accuracy of 80% specificity or 50% sensitivity
to predict antral H. pylori clearance.
Conclusion: Antral H. pylori clearance is at least partially responsible for the omeprzaole-induced hyperpepsinogenemia I. The magnitude of hyperpepsinogenemia
I probably provides a non-invasive alternative for predicting H. pylori clearance.
Received: 22 August 1996 / Accepted in revised form: 1 October 1998 相似文献
106.
Chia-Hung Kao Chih-Kua Huang Shyh-Jen Wang Chung-Yuan Hsu Wan-Yu Lin Gran-Hum Chen 《European journal of nuclear medicine and molecular imaging》1993,20(8):708-711
Urease in the human gastric mucosa is a marker for infection with Helicobacter pylori (HP), an organism which is associated with peptic ulcer disease. To detect gastric urease, we examined 184 patients (144 males, 40 females; mean age: 49.8±15.6 years) with suspected peptic ulcer disease. Fasting patients were given orally 5 Ci of carbon-14 labelled urea. From each patient only one breath sample was collected in hyamine at 10 min. The amount of 14C collected at 10 min was expressed as follows: [(DPM/mmol CO2 collected)/(DPM administered)] × 100 × body weight (kg). The presence of HP colonization was determined by examination of multiple endoscopic prepyloric antral biopsy specimens subjected to culture or a rapid urease test. For the purpose of this study, HP-positive patients were defined as those with characteristic bacteria as indicated by a positive result of either the culture or the rapid urease test; HP-negative patients were defined as those with negative findings on both the culture and the rapid urease test. Of the 184 cases, 99 (53.8%) were positive for HP infection, and 85 (46.2%), negative. The sensitivity and specificity of the rapid 10 min 14C-urea breath test for the diagnosis of HP-associated peptic ulcer disease were evaluated by a receiver operating characteristic (ROC) curve with a variable cut-off value from 1.5 to 4.5. When a cut-off value of 1.5 was selected, the sensitivity was 100% and the specificity, 83.5%; when a cut-off value of 4.5 was selected, the sensitivity was 54.5% and the specificity, 97.6%.
Correspondence to: Chia-Hung Kao 相似文献
107.
The pathogenesis of duodenal ulcer disease is multifactorial and the contribution ofHelicobacter pylori in relation to the other factors to the release of duodenal ulcer is unknown. To investigate this, we studied 147 patients with endoscopically proven healed ulcers. These patients were randomized to receive either placebo, misoprostol 200 g or misoprostol 300 g four times daily, and clinical, personal, physiological and endoscopic characteristics were obtained prospectively. Endoscopy was performed at the active phase of the ulcer and when the ulcer healed. Biopsies were taken from the antrum to assess histologically for: (1) the activity of gastritis as assessed by the degree of polymorph infiltration, (2) the degree of chronic inflammation by the degree of chronic inflammatory cells infiltration and degree of mucosal degeneration, and (3) bacteriologically for the presence ofH. pylori. The severity of the gastritis and the bacterial density were graded independently by two pathologists. The patients were assessed at two-month intervals for 12 months or until the ulcer relapsed. The results demonstrated that the relapse rates of duodenal ulcer were similar in the three treatment groups. The relapse rate was higher in the group with higher density of the bacteria (P<0.05). The degree of gastritis did not affect the relapse rate of duodenal ulcer in either the placebo or misoprostol group or in all patients combined. Stepwise logistic regression analysis identified that increased duodenal inflammation, male sex, early-onset disease, andH. pylori adversely affected relapse of the ulcer. We conclude that multiple factors affect the relapse of duodenal ulcer andH. pylori is one of them. 相似文献
108.
为了探讨中药治疗幽门螺旋杆菌的方法和疗效,综述了1997年至2002年近6年的文献资料。结果表明,中医药治疗幽门螺旋杆菌相关性胃病,无论采用主方加减、单方治疗或中西药合用均疗效显著,愈后复发率低,副作用少.长期应用无耐药性。 相似文献
109.
心理因素、幽门螺杆菌与消化性溃疡的关系 总被引:12,自引:2,他引:12
目的:探讨心理因索和幽门螺扦菌(HP)对消化性溃疡的发生、愈合、复发的影响。方法:以HAMD、I-lAMA、SDS量表检测正常人和消化性溃疡(PU)患者心理异常率;分别以奥美拉唑(奥)抑酸、羟基苄青霉素和甲硝唑根除HP(抗HP)、心理行为疗法治疗等方式治疗不同组PU患者。以胃镜检查PU愈合、复发状态;以尿素酶试验等检测HP感染率、复发率。结果:(1)心理异常率:正常人组:22.9%,PU组76.1%。(2)HP感染率:正常人组:51.4%,PU组86.4%。(3)HP根除率:A组(奥 抗HP 心理治疗):92.3%,B组(奥 抗HP):88.9%,C组(奥):38.5%。(4)2年累积HP复发率:A组19.2%,B组22.2%,c组61.5%。(5)溃疡治愈率:A组96.2%,B组85.2%,c组84.6%。(6)2年累积溃疡复发率:A组3.9%,B组25.9%,C组42.3%。结论:心理因素和HP感染皆参与了PU的发病:在予以抗HP和心理行为治疗后,PU复发率降低。 相似文献
110.
儿童消化性溃疡与幽门螺杆菌感染临床治疗探讨 总被引:8,自引:0,他引:8
为探讨儿童消化性溃疡(PU)与幽门螺杆菌(H.pylori)感染的关系,观察274例(4~14岁)有上消化道症状的儿童,男174例,女100例,电子胃镜证实PU。病理及H.pylori检测后,随机分为7组根除H.pylori。A、B组应用枸橼酸铋钾(CBS)和克拉霉素(CLA),A组加甲硝唑(MET)、B组加呋喃唑酮(FUR),疗程7d。D组标准三联疗程14d。A、D两组再加泰胃美6周。质子泵抑制剂(PPI)组洛赛克和CLA,加另一抗生素AMO(C组)、MET(E组)、FUR(F组)疗程7d。G组Smecta、AMO和MET疗程14d。停药4周以上复查胃镜和/或~(13)C-尿素呼气试验(~(13)C-UBT)。结果:①274例患儿H.pylori检出率79.93%,胃镜见十二指肠溃疡95.26%,慢性浅表性胃炎(CSG)89.42%,胃粘膜炎症和溃疡活动度与H.pylori感染有显著相关(P<0.01)。②治疗后1周内PPI组和铋剂A、B两组腹痛缓解均≥90%,各组腹痛消退时问比较差异有显著性(P<0.01);停药4周以上复胃镜53例,溃疡愈合和消失88.68%。③随访210例,H.pylori转阴81.43%、耐药14.29%,复燃2.86%,再感染1.43%,各组转归之间差异无显著性(P>0.05)。用胃镜复查H.pylori转阴75.76%;用~(13)C-UBT检测H.pylori转阴82.17%;胃镜联合~(13)C-UBT检查20例,H.pylori转阴90%,随访方式与转归之间有显著相关(P<0.01)。表明H.pylori是小儿PU的 相似文献