全文获取类型
收费全文 | 279篇 |
免费 | 26篇 |
出版年
2022年 | 5篇 |
2021年 | 6篇 |
2020年 | 4篇 |
2019年 | 3篇 |
2018年 | 6篇 |
2017年 | 2篇 |
2016年 | 4篇 |
2015年 | 13篇 |
2014年 | 17篇 |
2013年 | 16篇 |
2012年 | 30篇 |
2011年 | 20篇 |
2010年 | 15篇 |
2009年 | 18篇 |
2008年 | 22篇 |
2007年 | 16篇 |
2006年 | 12篇 |
2005年 | 11篇 |
2004年 | 20篇 |
2003年 | 9篇 |
2002年 | 11篇 |
2001年 | 3篇 |
2000年 | 3篇 |
1999年 | 4篇 |
1998年 | 7篇 |
1997年 | 1篇 |
1996年 | 1篇 |
1995年 | 3篇 |
1994年 | 1篇 |
1993年 | 4篇 |
1992年 | 2篇 |
1991年 | 3篇 |
1989年 | 1篇 |
1987年 | 1篇 |
1986年 | 2篇 |
1985年 | 2篇 |
1984年 | 1篇 |
1983年 | 1篇 |
1982年 | 1篇 |
1981年 | 1篇 |
1979年 | 1篇 |
1977年 | 1篇 |
1976年 | 1篇 |
排序方式: 共有305条查询结果,搜索用时 78 毫秒
91.
Background
Uptake of health facilities for delivery care in Ethiopia has not been examined in the light of equality. We investigated differences in institutional deliveries by urbanity, administrative region, economic status and maternal education.Methods
This study was based on nation-wide repeated surveys undertaken in the years 2000, 2005, and 2011. The surveys used a cluster sampling design. Women of reproductive age were interviewed on the place of their last delivery. Data was analyzed using logistic regressions to estimate the weighted association between birth in a health facility and study''s predictors.Results
Utilization of health institutions for deliveries has improved throughout the study period, however, rates remain low (5.4%,2000 and 11.8%,2011). Compared with women from rural places, women from urban areas had independent OR of a health facility delivery of 4.9 (95% CI: 3.4, 7.0), 5.0 (95% CI: 3.6, 6.9), and 4.6 (95% CI: 3.5, 6.0) in 2000, 2005, and 2011, respectively. Women with secondary/higher education had more deliveries in a healthcare facility than women with no education, and these gaps widened over the years (OR: 35.1, 45.0 and 53.6 in 2000, 2005, and 2011, respectively). Women of the upper economic quintile had 3.0–7.2 times the odds of healthcare facility deliveries, compared with the lowest quintile, with no clear trend over the years. While Addis-Ababa and Dire Dawa remained with the highest OR for deliveries in a health facility compared with Amhara, other regions displayed shifts in their relative ranking with Oromiya, SNNPR, Afar, Harari, and Somali getting relatively worse over time.Conclusions
The disparity related to urbanity or education in the use of health facility for birth in Ethiopia is staggering. There is a small inequality between most regions except Addis Ababa/Dire Dawa and sign of abating inequity between economic strata except for the richest households. 相似文献92.
Andrew E. Fry Christopher Marra Anna V. Derrick William O. Pickrell Adam T. Higgins Johann te Water Naude Martin A. McClatchey Sally J. Davies Kay A. Metcalfe Hui Jeen Tan Rajiv Mohanraj Shivaram Avula Denise Williams Lauren I. Brady Ronit Mesterman Mark A. Tarnopolsky Yuehua Zhang Ying Yang Seo-Kyung Chung 《American journal of human genetics》2021,108(1):176-185
93.
Brie A. Stotler Ronit Reich-Slotky Joseph Schwartz William B. Inabnet James Lee Fann Wu Phyllis Della-Latta Jeffrey S. Jhang 《Cell and tissue banking》2011,12(2):111-116
Cryopreservation of parathyroid tissue (PT) provides patients undergoing parathyroidectomy with an option for delayed autologous
heterotopic parathyroid transplantation. A standard protocol for quality monitoring of PT has not been established. This article
describes a method for detecting the presence of bacterial contamination in PT tissue intended for autologous transplantation.
PT was received in the tissue bank, processed under aseptic conditions, and placed into cryopreservation medium. Sterility
testing was performed at 2 time points prior to cryopreservation. From January 2005 to October 2008, 47 PT samples were cryopreserved.
The following bacteria were isolated from 11 PT specimens: Staphylococcus epidermidis, Staphylococcus capitis subspecies ureolyticus, Staphylococcus lugdunensis, Bacillus pumilus, and corynebacteria (diphtheroids). 23% of PTs were contaminated at the time of collection, predominantly with indigenous bacteria. Quality monitoring using
this protocol is a useful tool to identify tissues contaminated with bacteria. 相似文献
94.
Biallelic SZT2 Mutations Cause Infantile Encephalopathy with Epilepsy and Dysmorphic Corpus Callosum
Lina Basel-Vanagaite Tova Hershkovitz Eli Heyman Miquel Raspall-Chaure Naseebullah Kakar Pola Smirin-Yosef Marta Vila-Pueyo Liora Kornreich Holger Thiele Harald Bode Irina Lagovsky Dvir Dahary Ami Haviv Monika Weisz Hubshman Metsada Pasmanik-Chor Peter Nürnberg Doron Gothelf Christian Kubisch Mordechai Shohat Alfons Macaya Guntram Borck 《American journal of human genetics》2013
95.
Ronit Shaltiel-Karyo Moran Frenkel-Pinter Edward Rockenstein Christina Patrick Michal Levy-Sakin Abigail Schiller Nirit Egoz-Matia Eliezer Masliah Daniel Segal Ehud Gazit 《The Journal of biological chemistry》2013,288(24):17579-17588
The development of disease-modifying therapy for Parkinson disease has been a main drug development challenge, including the need to deliver the therapeutic agents to the brain. Here, we examined the ability of mannitol to interfere with the aggregation process of α-synuclein in vitro and in vivo in addition to its blood-brain barrier-disrupting properties. Using in vitro studies, we demonstrated the effect of mannitol on α-synuclein aggregation. Although low concentration of mannitol inhibited the formation of fibrils, high concentration significantly decreased the formation of tetramers and high molecular weight oligomers and shifted the secondary structure of α-synuclein from α-helical to a different structure, suggesting alternative potential pathways for aggregation. When administered to a Parkinson Drosophila model, mannitol dramatically corrected its behavioral defects and reduced the amount of α-synuclein aggregates in the brains of treated flies. In the mThy1-human α-synuclein transgenic mouse model, a decrease in α-synuclein accumulation was detected in several brain regions following treatment, suggesting that mannitol promotes α-synuclein clearance in the cell bodies. It appears that mannitol has a general neuroprotective effect in the transgenic treated mice, which includes the dopaminergic system. We therefore suggest mannitol as a basis for a dual mechanism therapeutic agent for the treatment of Parkinson disease. 相似文献
96.
Haim Haviv Michael Habeck Ryuta Kanai Chikashi Toyoshima Steven J. D. Karlish 《The Journal of biological chemistry》2013,288(14):10073-10081
Membrane proteins interact with phospholipids either via an annular layer surrounding the transmembrane segments or by specific lipid-protein interactions. Although specifically bound phospholipids are observed in many crystal structures of membrane proteins, their roles are not well understood. Na,K-ATPase is highly dependent on acid phospholipids, especially phosphatidylserine, and previous work on purified detergent-soluble recombinant Na,K-ATPase showed that phosphatidylserine stabilizes and specifically interacts with the protein. Most recently the phosphatidylserine binding site has been located between transmembrane segments of αTM8–10 and the FXYD protein. This paper describes stimulation of Na,K-ATPase activity of the purified human α1β1 or α1β1FXYD1 complexes by neutral phospholipids, phosphatidylcholine, or phosphatidylethanolamine. In the presence of phosphatidylserine, soy phosphatidylcholine increases the Na,K-ATPase turnover rate from 5483 ± 144 to 7552 ± 105 (p < 0.0001). Analysis of α1β1FXYD1 complexes prepared with native or synthetic phospholipids shows that the stimulatory effect is structurally selective for neutral phospholipids with polyunsaturated fatty acyl chains, especially dilinoleoyl phosphatidylcholine or phosphatidylethanolamine. By contrast to phosphatidylserine, phosphatidylcholine or phosphatidylethanolamine destabilizes the Na,K-ATPase. Structural selectivity for stimulation of Na,K-ATPase activity and destabilization by neutral phospholipids distinguish these effects from the stabilizing effects of phosphatidylserine and imply that the phospholipids bind at distinct sites. A re-examination of electron densities of shark Na,K-ATPase is consistent with two bound phospholipids located between transmembrane segments αTM8–10 and TMFXYD (site A) and between TM2, -4, -6, -and 9 (site B). Comparison of the phospholipid binding pockets in E2 and E1 conformations suggests a possible mechanism of stimulation of Na,K-ATPase activity by the neutral phospholipid. 相似文献
97.
Jogchum Plat Tim Hendrikx Veerle Bieghs Mike L. J. Jeurissen Sofie M. A. Walenbergh Patrick J. van Gorp Els De Smet Maurice Konings Anita C. E. Vreugdenhil Yasmin Dias Guichot Sander S. Rensen Wim A. Buurman Jan Willem M. Greve Dieter Lütjohann Ronald P. Mensink Ronit Shiri-Sverdlov 《PloS one》2014,9(10)
The inflammatory component of non–alcoholic steatohepatitis (NASH) can lead to irreversible liver damage. Therefore there is an urgent need to identify novel interventions to combat hepatic inflammation. In mice, omitting cholesterol from the diet reduced hepatic inflammation. Considering the effects of plant sterol/stanol esters on cholesterol metabolism, we hypothesized that plant sterol/stanol esters reduces hepatic inflammation. Indeed, adding plant sterol/stanol esters to a high-fat-diet reduced hepatic inflammation as indicated by immunohistochemical stainings and gene expression for inflammatory markers. Finally, adding sterol/stanol esters lowered hepatic concentrations of cholesterol precursors lathosterol and desmosterol in mice, which were highly elevated in the HFD group similarly as observed in severely obese patients with NASH. In vitro, in isolated LPS stimulated bone marrow derived macrophages desmosterol activated cholesterol efflux whereas sitostanol reduced inflammation. This highly interesting observation that plant sterol/stanol ester consumption leads to complete inhibition of HFD-induced liver inflammation opens new venues in the treatment and prevention of hepatic inflammation. 相似文献
98.
Syed Nuruddin Gry Helen Enger Syverstad Sveinung Lillehaug Trygve B. Leergaard Lars N. G. Nilsson Erik Ropstad Anette Krogen?s Ira Ronit Hebold Haraldsen Reidun Torp 《PloS one》2014,9(8)
Research on Alzheimer''s disease (AD) has indicated an association between hormones of the hypothalamic–pituitary–gonadal (HPG) axis and cognitive senescence, indicating that post meno-/andropausal changes in HPG axis hormones are implicated in the neuropathology of AD. Studies of transgenic mice with AD pathologies have led to improved understanding of the pathophysiological processes underlying AD. The aims of this study were to explore whether mRNA-levels of gonadotropin-releasing hormone (Gnrh) and its receptor (Gnrhr) were changed in plaque-bearing Alzheimer''s disease transgenic mice and to investigate whether these levels and amyloid plaque deposition were downregulated by treatment with a gonadotropin-releasing hormone analog (Gnrh-a; Leuprorelin acetate). The study was performed on mice carrying the Arctic and Swedish amyloid-β precursor protein (AβPP) mutations (tgArcSwe). At 12 months of age, female tgArcSwe mice showed a twofold higher level of Gnrh mRNA and more than 1.5 higher level of Gnrhr mRNA than age matched controls. Male tgArcSwe mice showed the same pattern of changes, albeit more pronounced. In both sexes, Gnrh-a treatment caused significant down-regulation of Gnrh and Gnrhr mRNA expression. Immunohistochemistry combined with quantitative image analysis revealed no significant changes in the plaque load after Gnrh-a treatment in hippocampus and thalamus. However, plaque load in the cerebral cortex of treated females tended to be lower than in female vehicle-treated mice. The present study points to the involvement of hormonal changes in AD mice models and demonstrates that these changes can be effectively counteracted by pharmacological treatment. Although known to increase in normal aging, our study shows that Gnrh/Gnrhr mRNA expression increases much more dramatically in tgArcSwe mice. Treatment with Leuprorelin acetate successfully abolished the transgene specific effects on Gnrh/Gnrhr mRNA expression. The present experimental approach should serve as a platform for further studies on the usefulness of Gnrh-a treatment in suppressing plaque development in AD. 相似文献
99.
Filip M. Segers Froukje J. Verdam Charlotte de Jonge Bas Boonen Ann Driessen Ronit Shiri-Sverdlov Nicole D. Bouvy Jan Willem M. Greve Wim A. Buurman Sander S. Rensen 《PloS one》2014,9(10)
The innate immune system plays a major role in the pathogenesis of nonalcoholic steatohepatitis (NASH). Recently we reported complement activation in human NASH. However, it remained unclear whether the alternative pathway of complement, which amplifies C3 activation and which is frequently associated with pathological complement activation leading to disease, was involved. Here, alternative pathway components were investigated in liver biopsies of obese subjects with healthy livers (n = 10) or with NASH (n = 12) using quantitative PCR, Western blotting, and immunofluorescence staining. Properdin accumulated in areas where neutrophils surrounded steatotic hepatocytes, and colocalized with the C3 activation product C3c. C3 activation status as expressed by the C3c/native C3 ratio was 2.6-fold higher (p<0.01) in subjects with NASH despite reduced native C3 concentrations (0.94±0.12 vs. 0.57±0.09; p<0.01). Hepatic properdin levels positively correlated with levels of C3c (rs = 0.69; p<0.05) and C3c/C3 activation ratio (rs = 0.59; p<0.05). C3c, C3 activation status (C3c/C3 ratio) and properdin levels increased with higher lobular inflammation scores as determined according to the Kleiner classification (C3c: p<0.01, C3c/C3 ratio: p<0.05, properdin: p<0.05). Hepatic mRNA expression of factor B and factor D did not differ between subjects with healthy livers and subjects with NASH (factor B: 1.00±0.19 vs. 0.71±0.07, p = 0.26; factor D: 1.00±0.21 vs. 0.66±0.14, p = 0.29;). Hepatic mRNA and protein levels of Decay Accelerating Factor tended to be increased in subjects with NASH (mRNA: 1.00±0.14 vs. 2.37±0.72; p = 0.22; protein: 0.51±0.11 vs. 1.97±0.67; p = 0.28). In contrast, factor H mRNA was downregulated in patients with NASH (1.00±0.09 vs. 0.71±0.06; p<0.05) and a similar trend was observed with hepatic protein levels (1.12±0.16 vs. 0.78±0.07; p = 0.08). Collectively, these data suggest a role for alternative pathway activation in driving hepatic inflammation in NASH. Therefore, alternative pathway factors may be considered attractive targets for treating NASH by inhibiting complement activation. 相似文献
100.
Dimitrios Karussis Hagai Shor Julia Yachnin Naama Lanxner Merav Amiel Keren Baruch Yael Keren-Zur Ofra Haviv Massimo Filippi Panayiota Petrou Shalom Hajag Urania Vourka-Karussis Adi Vaknin-Dembinsky Salim Khoury Oded Abramsky Henri Atlan Irun R. Cohen Rivka Abulafia-Lapid 《PloS one》2012,7(12)