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91.
干扰素诱导淋巴瘤细胞凋亡实验及临床研究 总被引:2,自引:0,他引:2
目的:分析梯度浓度的干扰素(IFN-α)对Burkitt淋巴瘤细胞株Daudi和T细胞淋巴瘤细胞株Jurkut及15例难治性淋巴瘤患者的直接作用。方法:以MTT法测定梯度浓度的IFN-α对两种淋巴瘤细胞株Daudi、Jurkat增殖作用的影响,以DNA末端标记法,流式细胞术,电镜观察测定IFN-α对淋巴瘤细胞的凋亡诱导作用,并采用瘤内注射IFN-α联合化疗治疗15例耐药的难治性淋巴瘤。结果:低浓度亚IFN-α对DaudiJurkat细胞增殖无明显抑制作用,高浓度IFN(10000U/ml)可显著抑制两种细胞增殖,且有时间相关性。高浓度的IFN-α可诱导淋巴瘤细胞凋亡。15例患者CR5例,PR7例,有效率80%,无明显毒副作用。结论:IFN-α可抑制淋巴瘤细胞增殖,诱导凋亡,有显著时间,剂量依赖性。局部应用IFN-α联合化疗是治疗难治性淋巴瘤的有效方法之一。 相似文献
92.
JJ Favre Ph Chaffanjon JG Passagia JP Chirossel 《Surgical and radiologic anatomy : SRA》1995,17(2):133-138
Summary The authors report the results of a series of dissections and anatomic sections of the fronto-basal region of the brain and of the anterior cranial fossa in human cadavers. The constant presence of an arachnoidal cistern above the olfactory nerve was verified. The arachnoid separates from the pial membrane and forms a bridge with the ventral part of the olfactory bulb and tract, from the lateral edge of the olfactory sulcus to the medial edge of the gyrus rectus. The cistern is wide in its anterior portion, between the gyrus rectus and the olfactory bulb, and is reduced to a virtual slit in its posterior portion where the tract is lodged in the olfactory sulcus. The olfactory nerve can be separated without damaging fronto-basal arachnoidial adhesions over several centimeters. Dissection of this region after intravascular injection of colored media shows the constant presence of an artery destined to the olfactory bulb and tract. It originates either from the lateral surface of the anterior cerebral a. (segment A2), or from the medial fronto-basal a., and consistently provides terminal branches in front of the olfactory trigone in the medial olfactory sulcus. At their ventral extremity, the olfactory structures are therefore vascularised independently for several centimeters, from the lower face of the frontal lobe. The independent vascularisation of the olfactory nerve, the tenuous and easily detachable adhesions, and the actual presence of a true arachnoidal cistern all contribute to enabling surgical techniques which conserve olfactory function during anterior approaches.
Vascularisation du nerf olfactif. Rapports méningés et applications chirurgicales
Résumé Les auteurs rapportent les résultats d'une série de dissections et de coupes de la région fronto-basale de l'encéphale et de la fosse crânienne antérieure sur sujets cadavériques. La présence constante d'une citerne arachnoïdienne au dessus du n. olfactif a été vérifiée. L'arachnoïde se sépare du feuillet pial et passe en pont à la partie ventrale du bulbe et du tractus olfactifs, du bord latéral du sillon olfactif au bord médial du gyrus rectus. La citerne est large dans sa portion antérieure, entre le gyrus rectus et le bulbe olfactif, se réduit à une fente virtuelle postérieure lorsque le tractus se loge dans le sillon olfactif. Le n. olfactif peut être séparé sans dommage des adhérences arachnoïdiennes fronto-basales sur quelques centimètres. La dissection de cette région, après injection intravasculaire de masses colorées montre, de façon originale, la présence constante d'une artère destinée au tractus et au bulbe olfactifs. Elle naît soit de la face latérale de l'a. cérébrale antérieure (segment A2), soit de l'a. fronto-basale médiale, pour donner ses branches terminales toujours en avant du trigone olfactif dans le sillon orbitaire médial. Sur quelques centimètres à leur extrémité ventrale, les structures olfactives ont donc une vascularisation indépendante de la face inférieure du lobe frontal. L'indépendance vasculaire du n. olfactif, des adhérences ténues, facilement détachables, et la réalité vérifiée d'une véritable citerne arachnoïdienne permettent d'imaginer des techniques conservatrices de la fonction olfactive utilisées dans plusieurs indications de la chirurgie de la fosse crânienne antérieure.相似文献
93.
Morphological detection and quantification of lipoprotein(a) deposition in atheromatous lesions of human aorta and coronary arteries 总被引:8,自引:0,他引:8
Axel Niendorf Matthias Rath Katrin Wolf Susanne Peters Hartmut Arps Ulrike Beisiegel Manfred Dietel 《Virchows Archiv : an international journal of pathology》1990,417(2):105-111
Summary Lipoprotein(a), as an atherogenic particle, represents an independent risk factor for coronary heart disease. In the present
study the morphological distribution of apoprotein (a) and apoprotein B within the arterial wall is described. Apoprotein
B, a constituent of very low-density lipoprotein, low-density lipoprotein and lipoprotein(a) has previously been demonstrated
in atheromatous lesions. Lipoprotein(a) possesses an additional protein, designated apoprotein (a). Autopsy material (n=74) from the left coronary artery and from the thoracic aorta has been examined by means of immunohistochemistry and both
apoprotein (a) and apoprotein B were detected, primarily associated with the extracellular matrix and accumulating in lesions
in the arterial wall. The staining pattern for both antigens was almost always found to be congruent, suggesting that the
detection of (a)-antigen has to be attributed at least in part to the presence of lipoprotein(a). It is concluded that both
low-density lipoprotein and lipoprotein(a) have an important role in the pathogenesis of atherosclerosis. 相似文献
94.
用BA-ELISA斑点法检测痢疾杆菌免疫小鼠GALT中的特异性抗体分泌细胞(ASC) 总被引:1,自引:0,他引:1
改进的BA-ELISPOT法使免疫酶斑更为清晰,保存时间延长。用此法检测了痢疾杆菌福氏2a经口及腹腔免疫后,小鼠派伊尔氏(PP)淋巴结、肠系膜淋巴结(MLN)及脾脏(SPL)中特异性IgA、IgG、IgM抗体分泌细胞(AntibodySecretingcell,ASC)的动态变化,得到有规律的结果:两种免疫途径均能在PP及MLN中诱导出3类特异ASC的显著升高,但口服导致的升高其持续时间较腹腔途径为短。此外,腹腔途径还能诱导SPL中3种ASC升高。 相似文献
95.
AIMS: To elucidate the mechanism of marked stromal fibrosis in strictured colorectal carcinomas (SC) that cause complete ileus. METHODS AND RESULTS: Sixteen cases of SC and 29 cases of non-strictured colorectal carcinoma (NSC) were studied. These carcinomas showed similar clinicopathological features except for bowel stricture. The stricture index (SI) showing the degree of bowel stricture was 59.8 +/- 12.1% in SC versus 20.8 +/- 24.6% in NSC (P < 0.001). The fibrosis index (FI), defined to reflect the extent of stromal fibrosis, was 56.3 +/- 8.8% in SC versus 21.9 +/- 10.6% in NSC (P < 0.001). COX-2+ myofibroblasts were detected in 13 cases (81.3%) in SC versus eight cases (27.6%) in NSC (P < 0.01). The COX-2+ myofibroblast density was 276.7 +/- 181.1 cells/mm(2) in SC versus 26.6 +/- 52.7 cells/mm(2) in NSC (P < 0.001). When all cases were divided into two groups with and without COX-2+ myofibroblasts, the SI was 48.8 +/- 19.1% in those with COX-2+ myofibroblasts versus 24.8 +/- 29.3% in those with COX-2- myofibroblasts (P < 0.001). CONCLUSION: COX-2+ myofibroblasts may play an important role in extensive bowel stricture in colorectal carcinomas. 相似文献
96.
Sawyer EJ Hanby AM Poulsom R Jeffery R Gillett CE Ellis IO Ellis P Tomlinson IP 《The Journal of pathology》2003,200(5):627-632
The aim of this study was to assess the expression of IGF-I and IGF-II in phyllodes tumours and fibroadenomas and to see if there is any correlation between nuclear beta-catenin expression and IGF-I and IGF-II expression in these tumours. In a previous study, it has been shown that Wnt signalling is important in the pathogenesis of phyllodes tumours of the breast. Epithelial Wnt5a overexpression and stromal Wnt2 overexpression were associated with abnormal, nuclear localization of beta-catenin in the stromal cells of these tumours. However, not all tumours with beta-catenin accumulation showed Wnt overexpression. One other possible cause of beta-catenin accumulation is overexpression of insulin-like growth factors (IGFs), as both IGF-I and IGF-II have been shown to stabilize beta-catenin. In this study, 30 fibroadenomas of the breast were assessed for beta-catenin expression using immunohistochemistry and the results were compared with previous data from 119 phyllodes tumours. In situ hybridization was used to assess IGF-I and IGF-II expression in 23 phyllodes tumours and 16 fibroadenomas. Nineteen phyllodes tumours (83%) showed widespread overexpression of IGF-II and 5/23 (22%) showed widespread overexpression of IGF-I. IGF-I expression correlated with nuclear beta-catenin staining in phyllodes tumours. Malignant phyllodes tumours showed no or little IGF-I expression. There was a degree of nuclear beta-catenin expression in the stroma (weak in 33%, moderate in 27%, and strong in 40%) in all fibroadenomas and nuclear beta-catenin staining correlated with IGF-I overexpression. Extensive IGF-II overexpression was also found in the majority of fibroadenomas (12/16). These results support the hypothesis that IGF-I and IGF-II overexpression may be important in the pathogenesis of fibroepithelial neoplasms of the breast and that IGF-I overexpression is likely to be contributing to the nuclear beta-catenin localization observed in the tumours. 相似文献
97.
Correlation of P-selectin and lipoprotein(a), and other lipid parameters in preeclampsia 总被引:1,自引:0,他引:1
Preeclampsia is a pregnancy specific disorder and is thought to be associated with generalized endothelial dysfunction. P-selectin,
an adhesion molecule, mediates the interaction of monocytes, platelets, and endothelial cells. Increased P-selectin levels
and altered lipid and lipoprotein metabolism were reported in preeclampsia and during pregnancy. In order to investigate
the relationship between serum P-selectin and lipoprotein(a), and other lipid parameters, 28 preeclampsia [13 severe (group
I) and 15 mild preeclampsia (group II), 15 healthy pregnant (group III) and 20 non-pregnant (group IV)] women were investigated.
Serum P-selectin, lipoprotein(a), total cholesterol, triglyceride, and high density lipoprotein cholesterol were measured
and low-density lipoprotein cholesterol was derived. Serum P-selectin concentrations were consistently and significantly higher
in the severe preeclampsia group than in the mild preeclampsia, healthy pregnancy, and non-pregnant control groups (P<0.0001, for all). The mild preeclampsia group also had increased serum P-selectin concentrations compared with the healthy
pregnancy group and non-pregnant controls (P<0.05 and P<0.0001, respectively). Serum P-selectin and lipoprotein(a) levels revealed a significant and linear increase with the severity
of preeclampsia. There were also significant (in groups I and II) and borderline (in groups III and IV) correlations between
P-selectin and total cholesterol. The present study suggests that P-selectin may be an additional risk marker for preeclampsia,
and may be useful in distinguishing women with mild and severe preeclampsia and normal pregnancy.
Received: 9 November 2001 / Accepted: 6 February 2002 相似文献
98.
99.
Bin Yu Youming Ding Xiaofeng Liao Changhua Wang Bin Wang Xiaoyan Chen 《Pathology, research and practice》2019,215(5):939-945
Background
TONSL has been suggested to function as an oncogene in lung, esophageal and cervical cancer. This study was aimed to identify the expression of TONSL and its role in hepatocellular carcinoma (HCC).Methods
By data mining in the Cancer Genome Atlas (TCGA) and Human Protein Atlas (HPA) databases, the expression profile of TONSL, its clinical significance, the potential mechanisms of its dysregulation and its underlying biological function in HCC were investigated.Results
TONSL was significantly upregulated in HCC tissues relative to normal liver tissues (P?<?0.05). High TONSL expression was significantly correlated with advanced TNM stage, poorly differentiated tumors, vascular invasion, elevated serum alpha-fetoprotein expression and a worse prognosis (all P?<?0.05). Multivariate analysis further confirmed that TONSL overexpression was an independent risk factor for poor overall survival (OS) and recurrence-free survival (RFS) in HCC (all P?<?0.05). Additionally, 16% of HCC cases (n?=?370) had TONSL DNA amplification. The total methylation level of TONSL was moderately and negatively correlated with its mRNA expression (P?<?0.05). TONSL was predictively targeted by miR-133b, which was downregulated in HCC and negatively related to TONSL mRNA expression (all P?<?0.05). Kaplan-Meier analyses demonstrated that low miR-133b expression was significantly associated with poor OS and RFS (all P?<?0.05). Moreover, gene set enrichment analysis revealed that cases with TONSL overexpression were enriched in cell cycle regulation pathways (all P?<?0.05).Conclusions
TONSL holds promise for serving as a prognostic biomarker for HCC. DNA amplification, hypomethylation and miR-133b downregulation could be the mechanisms associated with TONSL upregulation in HCC. TONSL might function as an oncogene via cell cycle regulation pathways in HCC. 相似文献100.
Kawaguchi K Oda Y Saito T Yamamoto H Tamiya S Takahira T Miyajima K Iwamoto Y Tsuneyoshi M 《The Journal of pathology》2003,201(3):487-495
The p16INK4a tumour suppressor gene, encoding p16 protein, plays a crucial role in regulation of the G1 cell-cycle phase. To investigate the potential role of p16 in soft tissue leiomyosarcoma (LMS), an immunohistochemical analysis was performed of 77 LMSs for p16 expression. Decreased expression of the p16 protein was identified in 25 of 77 LMSs (32%). Decreased expression of p16 correlated significantly with large tumour size (p=0.0038). In a univariate analysis, large tumour size and decreased expression of p16 were statistically significant adverse prognostic factors (p=0.025 and p=0.0021, respectively). In a multivariate analysis including conventional clinicopathological parameters, decreased expression of p16 protein was revealed as the only independent unfavourable prognostic factor (p=0.012). To elucidate the mechanisms of inactivation of the p16INK4a gene, 49 LMSs for which genomic DNA was available were examined; analysis for homozygous deletion, mutation, and promoter hypermethylation was conducted using differential PCR, PCR-SSCP, and methylation-specific PCR, respectively. Promoter hypermethylation was detected in 11 of 49 LMS cases (22%); homozygous deletion was detected in 3 of 49 cases (6%); and mutation was not recognized in any of the cases studied. Eight of 15 cases (53%) with decreased expression of p16 protein revealed methylation of the p16INK4a gene promoter. Promoter hypermethylation correlated closely with decreased expression and poor prognosis (p=0.0014 and p=0.0088, respectively). These results suggest that decreased expression of p16 protein can be considered as an independent reliable prognostic parameter in patients with soft tissue LMS. Furthermore, promoter methylation was more frequent than either homozygous deletion or mutation in this tumour, and promoter methylation was also shown to have a strong association with inactivation of the p16INK4a gene. 相似文献