全文获取类型
收费全文 | 605篇 |
免费 | 52篇 |
国内免费 | 13篇 |
专业分类
耳鼻咽喉 | 1篇 |
儿科学 | 32篇 |
妇产科学 | 8篇 |
基础医学 | 101篇 |
口腔科学 | 9篇 |
临床医学 | 35篇 |
内科学 | 158篇 |
皮肤病学 | 19篇 |
神经病学 | 15篇 |
特种医学 | 138篇 |
外科学 | 56篇 |
综合类 | 20篇 |
预防医学 | 22篇 |
眼科学 | 6篇 |
药学 | 22篇 |
肿瘤学 | 28篇 |
出版年
2022年 | 1篇 |
2021年 | 9篇 |
2020年 | 3篇 |
2019年 | 5篇 |
2018年 | 7篇 |
2017年 | 2篇 |
2016年 | 7篇 |
2015年 | 16篇 |
2014年 | 9篇 |
2013年 | 12篇 |
2012年 | 16篇 |
2011年 | 25篇 |
2010年 | 26篇 |
2009年 | 33篇 |
2008年 | 17篇 |
2007年 | 35篇 |
2006年 | 34篇 |
2005年 | 27篇 |
2004年 | 33篇 |
2003年 | 15篇 |
2002年 | 15篇 |
2001年 | 20篇 |
2000年 | 13篇 |
1999年 | 8篇 |
1998年 | 23篇 |
1997年 | 37篇 |
1996年 | 22篇 |
1995年 | 22篇 |
1994年 | 17篇 |
1993年 | 8篇 |
1992年 | 6篇 |
1991年 | 2篇 |
1990年 | 12篇 |
1989年 | 13篇 |
1988年 | 11篇 |
1987年 | 17篇 |
1986年 | 11篇 |
1985年 | 12篇 |
1984年 | 6篇 |
1983年 | 9篇 |
1982年 | 7篇 |
1981年 | 9篇 |
1980年 | 12篇 |
1979年 | 1篇 |
1978年 | 4篇 |
1977年 | 7篇 |
1976年 | 8篇 |
1975年 | 5篇 |
1974年 | 1篇 |
排序方式: 共有670条查询结果,搜索用时 31 毫秒
661.
Post-translational modifications of the major linear epitope 169-190aa of Ro60 kDa autoantigen alter the autoantibody binding
下载免费PDF全文
![点击此处可从《Clinical and experimental immunology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Terzoglou AG Routsias JG Moutsopoulos HM Tzioufas AG 《Clinical and experimental immunology》2006,146(1):60-65
Ro60 kDa is a member of the Ro/LaRNP ribonucleoprotein complex and its major linear B cell epitope, corresponding to the region 169–190aa, has been found to be the initial target of the autoimmune response in patients with systemic lupus erythematosus. This sequence contains one serine and two arginine amino acid residues, which can potentially be modified post‐translationally by phosphorylation or citrullination, respectively. The aim of this study was to develop an immunoassay for anti‐Ro60 kDa epitope antibody detection and to investigate the changes in the antigenicity of the Ro60 kDa epitope when it is post‐translationally modified, by either citrullination or phosphorylation. Peptide analogues corresponding to the unmodified form of the epitope, its phosphorylated form, and a form with both arginine residues citrullinated were synthesized. The peptide coating conditions were investigated and it was found that the use of highly hydrophilic surfaces increase the efficiency of the coating, as well as the sensitivity of the method for anti‐peptide antibody detection. All peptides were tested by the optimized enzyme‐linked immunosorbent assay (ELISA) against 119 sera from patients with primary Sjögren's syndrome, systemic lupus erythematosus and rheumatoid arthritis with anti‐Ro/SSA reactivity, 20 sera from patients with systemic diseases without anti‐Ro/SSA immune reactivity, as well as against 65 sera from normal individuals. A large proportion of the tested sera reacted against all three peptide analogues, although with a preference for the unmodified form of the epitope. In conclusion, post‐translational modifications of the major Ro60 kDa B cell epitope can alter the autoantibody binding. 相似文献
662.
Terzoglou AG Routsias JG Avrameas S Moutsopoulos HM Tzioufas AG 《Clinical and experimental immunology》2006,144(3):432-439
Sera from patients with primary Sjögren Syndrome (pSS) or Systemic Lupus Erythematosus (SLE) often contain autoantibodies directed against La/SSB. The sequence 349–368aa represents the major B‐cell epitope of La/SSB, also it contains, at position 366, a serine aminoacid residue which constitutes the main phosphorylation site of the protein. In this study we investigated the differential recognition of the 349–368aa epitope and its phosphorylated form by antibodies found in sera from patients with systemic autoimmune diseases. Peptides corresponding to the sequence of the unphosphorylated (pep349–368aa) and the phosphorylated form (pep349–368aaPh) of the La/SSB epitope 349–368aa, as well as to a truncated form spanning the sequence 349–364aa and lacking the phosphorylation site (pep349–364aa), were synthesized. Sera from 53 patients with pSS and SLE with anti‐La/SSB specificity, 30 patients with pSS and SLE without anti‐La/SSB antibodies, 25 patients with rheumatoid arthritis and 32 healthy individuals were investigated by ELISA experiments. Autoantibodies to pep349–368aaPh were detected in sera of anti‐La/SSB positive patients with a higher prevalence compared to the pep349–368aa (66%versus 45%). Pep349–368aaPh inhibited the antibody binding almost completely (92%), while pep349–368aa inhibited the binding only partially (45%). Anti‐La/SSB antibodies presented a higher relative avidity for the phosphorylated than the unphosphorylated peptide. Immunoadsorbent experiments using the truncated peptide pep349–364aa indicated that the flowthrough showed a selective specificity for pep349–368aaPh, while the eluted antibodies reacted with both peptide analogues of the La/SSB epitope. These data suggest that sera from pSS and SLE patients with anti‐La/SSB reactivity possess autoantibodies that bind more frequently and with a higher avidity to the phosphorylated major B‐cell epitope of the molecule. 相似文献
663.
Background and purpose:
It is postulated that nitrite requires reduction to nitric oxide in order to exert its relaxant effect upon isolated hypoxic vessels. Herein, we evaluate the relative contribution of nitric oxide and characterize the downstream mechanisms of nitrite-induced vasorelaxation.Experimental approach:
Aortic rings were treated with pharmacological agents and exposed to hypoxia (<1% O2). Following pre-constriction, nitrite (10 µM final) was added to appropriate baths; isometric tension was recorded throughout.Key results:
Nitrite (under hypoxic conditions at physiological pH) is capable of exerting physiological effects that cannot be completely inhibited by the inhibitor of soluble guanylate cyclase (sGC), 1H [1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one or a nitric oxide scavenger (carboxy-2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide). Simultaneous blockade of both sGC and cyclooxygenase (COX) completely inhibited the response to nitrite. With regard to the nitric oxide-dependent component, we confirm that aldehyde oxidase, but not xanthine oxidase or endothelial nitric oxide synthase, was important for the actions of nitrite in our model.Conclusions and implications:
Nitric oxide generated from nitrite is not exclusively responsible for the physiological actions observed in isolated hypoxic vessels. Nitrite operates via different pathways dependent on the presence or absence of endothelium to produce vasorelaxation. In intact vessels, both sGC and COX enzymes appear to be important. Irrespective of this difference in relaxation mechanism, nitrite is capable of producing the same maximum relaxation, regardless of the presence of endothelium. Having investigated possible nitrite reduction sites, we confirm that aldehyde oxidase is important for the actions of nitrite. 相似文献664.
665.
Maegele M Lefering R Yucel N Tjardes T Rixen D Paffrath T Simanski C Neugebauer E Bouillon B;AG Polytrauma of the German Trauma Society 《Injury》2007,38(3):298-304
BACKGROUND: There is increasing evidence for acute traumatic coagulopathy occurring prior to emergency room (ER) admission but detailed information is lacking. PATIENTS AND METHODS: A retrospective analysis using the German Trauma Registry database including 17,200 multiple injured patients was conducted to determine (a) to what extent clinically relevant coagulopathy has already been established upon ER admission, and whether its presence was associated (b) with the amount of intravenous fluids (i.v.) administered pre-clinically, (c) with the magnitude of injury, and (d) with impaired outcome and mortality. Eight thousand seven hundred and twenty-four patients with complete data sets were screened. RESULTS: Coagulopathy upon ER admission as defined by prothrombin time test (Quick's value) <70% and/or platelets <100,000 microl(-1), was present in 34.2% of all patients. There was an increasing incidence for coagulopathy with increasing amounts of i.v. fluids administered pre-clinically. Coagulopathy was observed in >40% of patients with >2000 ml, in >50% with >3000 ml, and in >70% with >4000 ml administered. Ten percentage of patients presented with clotting disorders although pre-clinical resuscitation was limited to 500 ml of i.v. fluids maximum. The mean ISS score in the coagulopathy group was 30 (S.D. 15) versus 21 (S.D. 12) (p<0.001). Twenty-nine percentage of patients with coagulopathy developed multi organ failure (p<0.001). Early in-hospital mortality (<24h) was 13% in patients with coagulopathy (p<0.001) and overall in-hospital mortality totalled 28% (p<0.001). CONCLUSION: There is a high frequency of established coagulopathy in multiple injury upon ER admission. The presence of early traumatic coagulopathy was associated with the amount of intravenous fluids administered pre-clinically, magnitude of injury, and impaired outcome. 相似文献
666.
Athanasios G. Tzioufas MD Associate Professor Michael Voulgarelis MD Assistant Professor 《Best Practice & Research: Clinical Rheumatology》2007,21(6):989
Sjögren's syndrome is a chronic autoimmune disease that affects not only the exocrine glands but also various extraglandular sites. The syndrome can be found alone (primary) or in association with other autoimmune rheumatic diseases (secondary). The diagnosis is based on a combination of subjective and objective criteria, proposed by the American–European Study Group; the differential diagnosis includes diseases producing dry mouth, KCS, and major salivary gland enlargement. The initial clinical picture determines the outcome of patients Thus the periepithelial extraglandular manifestations are the result of lymphocytic invasion in epithelial tissues of lungs, kidneys, and liver; they appear early in the disease and have a benign course. The extraepithelial manifestations, such as skin vasculitis, peripheral neuropathy, and glomerulonephritis, with low C4 levels, are associated with increased morbidity and high risk for lymphoma. A strong predisposition seems to exist in these patients for the development of lymphoproliferation, especially for low-grade salivary gland MZ lymphomas. Therefore, the clinical follow-up of Sjögren's syndrome patients should include routine complement determination and serum immunoelectrophoresis to detect the possible emergence of a monoclonal B-cell population, susceptible to lymphoma development.
- • Sjögren's syndrome is a chronic and, in the majority of patients, is a disease with benign course.
- • Sjögren's syndrome can occur alone or in association with other autoimmune diseases.
- • Characteristic autoantibodies are anti-Ro/SSA and La/SSB.
- • The differential diagnosis includes all disease presenting with dry mouth, dry eye, or major salivary gland enlargement.
- • The clinical picture at the presentation of the patient determines the outcome. Thus, periepithelial extraglandular manifestations appear early in the disease and have a benign course. Extraepithelial manifestations, with low C4 levels, are associated with increased morbidity and high risk of lymphoma.
- • A physician examining a patient with Sjögren's syndrome for the first time should consider the presence of NHL if the patient displays clinical signs such as significant enlargement of the salivary glands, lymphadenopathy, splenomegaly, skin vasculitis, and peripheral neuropathy.
- • NHLs in Sjögren's syndrome fall into two main categories: the first relates to the majority of patients who develop an indolent extranodal MZ lymphomas; the second relates to those developing high-grade aggressive lymphomas, such as de novo or secondary DLBCLs, which are only occasionally encountered in Sjögren's syndrome.
- • Patients with Sjögren's syndrome with indolent salivary MALT lymphomas usually have a quite uncomplicated clinical course with a median overall survival of 6.4 years. The combination of rituximab plus CHOP has a significant clinical effect in DLBCL.
- • At the initial presentation, it is important to identify clinical features that possibly predispose to histologic progression and parameters that address the efficacy of treatment in presenting high-grade transformation.
References
1 U. Dafni, A.G. Tzioufas and P. Staikos et al., The prevalence of Sjögren's syndrome in a close rural community, Annals of the Rheumatic Diseases 56 (1997), pp. 521–525. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (88)
2 L. Jacobsson, T.E. Axell and B. Hansen et al., Dry eyes or mouth – an epidemiological study in Swedish adults with special reference to primary Sjögren's syndrome, Journal of Autoimmunity 2 (1989), pp. 521–527. Abstract | PDF (486 K)
| View Record in Scopus | Cited By in Scopus (92)
3 H.M. Moutsopoulos, Sjögren's syndrome autoimmune epithelitis, Clinical Immunology and Immunopathology 72 (1994), pp. 162–165. Abstract | PDF (250 K)
| View Record in Scopus | Cited By in Scopus (150)
4 D.I. Mitsias, E.K. Kapsogeorgou and H.M. Moutsopoulos, Sjögren's syndrome: why autoimmune epithelitis?, Oral Diseases 12 (2006), pp. 523–532. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (14)
5 T.E. Daniels and J.P. Whitcher, Association of patterns of labial salivary gland inflammation with keratoconjunctivitis sicca. Analysis of 618 patients with suspected Sjögren's syndrome, Arthritis & Rheumatism 37 (1994), pp. 869–877. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (92)
6 S. Salomonsson, M.V. Jonsson and K. Skarstein et al., Cellular basis of ectopic germinal center formation and autoantibody production in the target organ of patients with Sjögren's syndrome, Arthritis & Rheumatism 48 (2003), pp. 3187–3201. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (99)
7 N.A. Pavlidis, J. Karsh and H.M. Moutsopoulos, The clinical picture of primary Sjögren's syndrome: a retrospective study, The Journal of Rheumatology 9 (1982), pp. 685–690. View Record in Scopus | Cited By in Scopus (41)
8 I. Al-Hashimi, S. Khuder, N. Haghighat and M. Zipp, Frequency and predictive value of the clinical manifestations in Sjögren's syndrome, Journal of Oral Pathology & Medicine 30 (2001), pp. 1–6. View Record in Scopus | Cited By in Scopus (22)
9 E.A. Boutsi, S. Paikos and U.G. Dafni et al., Dental and periodontal status of Sjögren's syndrome, Journal of Clinical Periodontology 27 (2000), pp. 231–235. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (15)
10 T.E. Daniels and P.C. Fox, Salivary and oral components of Sjögren's syndrome, Rheumatic Diseases Clinics of North America 18 (1992), pp. 571–589. View Record in Scopus | Cited By in Scopus (97)
11 R.K. Niemela, R. Takalo and E. Paakko et al., Ultrasonography of salivary glands in primary Sjögren's syndrome. A comparison with magnetic resonance imaging and magnetic resonance sialography of parotid glands, Rheumatology (Oxford) 43 (2004), pp. 875–879. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (32)
12 Y. Morimoto, M. Habu and T. Tomoyose et al., Dynamic magnetic resonance sialography as a new diagnostic technique for patients with Sjögren's syndrome, Oral Diseases 12 (2006), pp. 408–414. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (10)
13 M. Samarkos and H.M. Moutsopoulos, Recent advances in the management of ocular complications of Sjögren's syndrome, Current Allergy and Asthma Reports 5 (2005), pp. 327–332. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (9)
*14 S.S. Kassan and H.M. Moutsopoulos, Clinical manifestations and early diagnosis of Sjögren syndrome, Archives of Internal Medicine 164 (12) (2004 Jun 28), pp. 1275–1284.
15 A. Castro-Poltronieri and D. Alarcon-Segovia, Articular manifestations of primary Sjögren's syndrome, The Journal of Rheumatology 10 (1983), pp. 485–488. View Record in Scopus | Cited By in Scopus (12)
16 F.N. Skopouli, A. Talal and V. Galanopoulou et al., Raynaud's phenomenon in primary Sjögren's syndrome, The Journal of Rheumatology 17 (1990), pp. 618–620. View Record in Scopus | Cited By in Scopus (24)
17 R.I. Fox and A.Y. Liu, Sjögren's syndrome in dermatology, Clinics in Dermatology 24 (2006), pp. 393–413. Article | PDF (674 K)
| View Record in Scopus | Cited By in Scopus (8)
18 S.A. Papiris, M. Maniati and S.H. Constantopoulos et al., Lung involvement in primary Sjögren's syndrome is mainly related to the small airway disease, Annals of the Rheumatic Diseases 58 (1999), pp. 61–64. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (54)
19 I. Ito, S. Nagai and M. Kitaichi et al., Kitaichi M,et al Pulmonary manifestations of primary Sjögren's syndrome: a clinical, radiologic, and pathologic study, American Journal of Respiratory and Critical Care Medicine 15 (171) (2005), pp. 632–638. View Record in Scopus | Cited By in Scopus (47)
20 H. Trevino, E.B. Tsianos and S. Schenker, Gastrointestinal and hepatobiliary features in Sjögren's syndrome. In: N. Talal, H.M. Moutsopoulos and S.S. Kassan, Editors, Sjögren's syndrome: clinical and immunological aspects, Springer-Verlag, Berlin (1987), pp. 89–95.
21 F.N. Skopouli, C. Barbatis and H.M. Moutsopoulos, Liver involvement in primary Sjögren's syndrome, British Journal of Rheumatology 33 (1994), pp. 745–748. View Record in Scopus | Cited By in Scopus (56)
22 A. Goules, S. Masouridi and A.G. Tzioufas et al., Clinically significant and biopsy-documented renal involvement in primary Sjögren syndrome, Medicine (Baltimore) 79 (2000), pp. 241–249. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (60)
23 M. Pertovaara, M. Korpela, T. Kouri and A. Pasternack, The occurrence of renal involvement in primary Sjögren's syndrome: a study of 78 patients, Rheumatology (Oxford) 38 (1999), pp. 1113–1120. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (43)
24 H.M. Moutsopoulos, J.E. Balow and T.J. Lawley et al., Immune complex glomerulonephritis in sicca syndrome, American Journal of Medicine 64 (1978), pp. 955–960. Abstract | PDF (3175 K)
| View Record in Scopus | Cited By in Scopus (45)
25 M. Tsokos, S.A. Lazarou and H.M. Moutsopoulos, Vasculitis in primary Sjögren's syndrome: histologic classification and clinical presentation, American Journal of Clinical Pathology 88 (1987), pp. 26–31. View Record in Scopus | Cited By in Scopus (32)
26 E.L. Alexander, F.C. Arnett, T.T. Provost and M.B. Stevens, Sjögren's syndrome: association of anti-Ro(SS-A) antibodies with vasculitis, hematologic abnormalities, and serologic hyperreactivity, Annals of Internal Medicine 98 (1983), pp. 155–159. View Record in Scopus | Cited By in Scopus (85)
27 F. Gemignani, A. Marbini and G. Pavesi et al., Peripheral neuropathy associated with primary Sjögren's syndrome, Journal of Neurology, Neurosurgery, and Psychiatry 57 (1994), pp. 983–986. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (76)
28 P. Kanellopoulos, C. Baltoyiannis and A.G. Tzioufas, Primary Sjögren's syndrome associated with inclusion body myositis, Rheumatology (Oxford) 41 (2002), pp. 440–444. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (12)
29 G.E. Alexander, T.T. Provost, M.B. Stevens and E.L. Alexander, Sjögren's syndrome: central nervous system manifestations, Neurology 31 (1981), pp. 1391–1396. View Record in Scopus | Cited By in Scopus (89)
30 J.P. Ioannidis and H.M. Moutsopoulos, Sjögren's syndrome: too many associations, too limited evidence. The enigmatic example of CNS involvement, Seminars in Arthritis and Rheumatism 29 (1999), pp. 1–3. Abstract | PDF (304 K)
| View Record in Scopus | Cited By in Scopus (14)
31 J. Karsh, N. Pavlidis, B.D. Weintraub and H.M. Moutsopoulos, Thyroid disease in Sjögren's syndrome, Arthritis & Rheumatism 23 (1980), pp. 1326–1329. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (43)
32 M. Ramos-Casals, M. Garcia-Carrasco and R. Cervera et al., Thyroid disease in primary Sjögren syndrome. Study in a series of 160 patients, Medicine (Baltimore) 79 (2000), pp. 103–108. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (41)
33 N.I. Tapinos, M. Polihronis, A.G. Tzioufas and H.M. Moutsopoulos, Sjögren's syndrome. Autoimune epithelitis, Advances In Experimental Medicine and Biology 455 (1999), pp. 127–134. View Record in Scopus | Cited By in Scopus (31)
34 N. Haneji, T. Nakamura and K. Takio et al., Identification of alpha-fodrin as a candidate autoantigen in primary Sjögren's syndrome, Science 276 (1997), pp. 604–607. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (242)
35 M. Kuwana, T. Okano and Y. Ogawa et al., Autoantibodies to the amino-terminal fragment of beta-fodrin expressed in glandular epithelial cells in patients with Sjögren's syndrome, Journal of Immunology 167 (2001), pp. 5449–5456. View Record in Scopus | Cited By in Scopus (23)
36 S. Bacman, C. Perez Leiros and L. Sterin-Borda et al., Autoantibodies against lacrimal gland M3 muscarinic acetylcholine receptors in patients with primary Sjögren's syndrome, Investigative Ophthalmology & Visual Science 39 (1998), pp. 151–156. View Record in Scopus | Cited By in Scopus (110)
37 E. Feist, U. Kuckelkorn and T. Dorner et al., Autoantibodies in primary Sjögren's syndrome are directed against proteasomal subunits of the alpha and beta type, Arthritis & Rheumatism 42 (1999), pp. 697–702. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (36)
38 C.P. Mavragani, A.G. Tzioufas and H.M. Moutsopoulos, Sjögren's syndrome: autoantibodies to cellular antigens. Clinical and molecular aspects, International Archives of Allergy and Applied Immunology 123 (2000), pp. 46–57. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (17)
39 M.N. Manoussakis, A.G. Tzioufas, P.J. Pange and H.M. Moutsopoulos, Serological profiles in subgroups of patients with Sjögren's syndrome, Scandinavian Journal of Rheumatology Supplement 61 (1986), pp. 89–92. View Record in Scopus | Cited By in Scopus (35)
40 H.M. Moutsopoulos, B.L. Webber and T.P. Vlagopoulos et al., Differences in the clinical manifestations of sicca syndrome in the presence and absence of rheumatoid arthritis, American Journal of Medicine 66 (1979), pp. 733–736. Abstract | PDF (505 K)
| View Record in Scopus | Cited By in Scopus (50)
41 M.N. Manoussakis, C. Georgopoulou and E. Zintzaras et al., Sjögren's syndrome associated with systemic lupus erythematosus: clinical and laboratory profiles and comparison with primary Sjögren's syndrome, Arthritis & Rheumatism 50 (2004), pp. 882–891. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (41)
42 A.P. Andonopoulos, A.A. Drosos, F.N. Skopouli and H.M. Moutsopoulos, Sjögren's syndrome in rheumatoid arthritis and progressive systemic sclerosis. A comparative study, Clinical and Experimental Rheumatology 7 (1989), pp. 203–205. View Record in Scopus | Cited By in Scopus (17)
43 C.P. Mavragani, N.M. Moutsopoulos and H.M. Moutsopoulos, The management of Sjögren's syndrome, Nature Clinical Practice. Rheumatology 2 (2006), pp. 252–261. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (32)
44 J.F. Fries, M.C. Hochberg and T.A. Medsger et al., Criteria for rheumatic diseases. Different types and functions, Arthritis & Rheumatism 37 (1994), pp. 454–462. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (65)
45 C. Vitali and S. Bombardieri, Diagnostic criteria for Sjögren's syndrome: the state of the art, Clinical and Experimental Rheumatology 8 (supplement 5) (1990), pp. 13–16. View Record in Scopus | Cited By in Scopus (8)
46 C. Vitali, S. Bombardieri and H.M. Moutsopoulos et al., Preliminary criteria for the classification of Sjögren's syndrome. Results of a prospective concerted action supported by the European Community, Arthritis & Rheumatism 36 (1992), pp. 340–348.
47 C. Vitali, H.M. Moutsopoulos and S. Bombardieri, The European Community Study Group on diagnostic criteria for Sjögren's syndrome. Sensitivity and specificity of tests for ocular and oral involvement in Sjögren's syndrome, Annals of the Rheumatic Diseases 53 (1994), pp. 637–647. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (181)
48 C. Vitali, S. Bombardieri and H.M. Moutsopoulos et al., Assessment of the European classification criteria for Sjögren's syndrome in a series of clinically defined cases: results of a prospective multicentre study. The European Study Group on Diagnostic Criteria for Sjögren's Syndrome, Annals of the Rheumatic Diseases 55 (1996), pp. 116–121. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (336)
49 C. Vitali, S. Bombardieri and R. Jonsson et al., Classification criteria for Sjögren's syndrome: a revised version of the European criteria proposed by the American-European Consensus Group, Annals of the Rheumatic Diseases 61 (2002), pp. 554–558. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (976)
50 H. Rubin and M. Holt, Secretory sialography in diseases of the major salivary glands, AJR American Journal of Roentgenology 77 (1957), pp. 575–598.
51 G.L. Shall, L.G. Anderson and R.O. Wolf et al., Xerostomia in Sjögren's syndrome: evaluation by sequential scintigraphy, Journal of the American Medical Association 216 (1971), pp. 2109–2116.
52 A.A. Drosos, S.H. Constantopoulos and D. Psychos et al., The forgotten cause of sicca complex; sarcoidosis, The Journal of Rheumatology 16 (1989), pp. 1548–1551. View Record in Scopus | Cited By in Scopus (23)
53 S. Itescu, L.J. Braneato and J. Buxbaum et al., A diffuse infiltrative CD8 lymphocytosis syndrome in human immunodeficiency virus (HIV) infection: a host immune response associated with HLA-DR5, Annals of Internal Medicine 112 (1990), pp. 3–10. View Record in Scopus | Cited By in Scopus (121)
54 J. Haddad, P. Deny and C. Munz-Gothiel et al., Lymphocytic sialadenitis of Sjögren's syndrome associated with chronic hepatitis C virus liver disease, Lancet 339 (1992), pp. 321–323. Abstract | Article | PDF (455 K)
| View Record in Scopus | Cited By in Scopus (338)
55 C. Vitali, M. Sciuto and R. Neri et al., Anti hepatitis C virus antibodies in primary Sjögren's syndrome: false positive results are related to hyper-g-globulinemia, Clinical and Experimental Rheumatology 10 (1992), pp. 103–104. View Record in Scopus | Cited By in Scopus (26)
56 M. Ramos-Casals, V. Loustaud-Ratti and S. De Vita et al., Sjögren syndrome associated with hepatitis C virus: a multicenter analysis of 137 cases, Medicine (Baltimore) 84 (2005), pp. 81–89. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (46)
57 I.R. Mackay and N.R. Rose, Autoimmunity and lymphoma: tribulations of B cells, Nature Immunology 2 (2001), pp. 793–795. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (37)
*58 E. Zintzaras, M. Voulgarelis and H.M. Moutsopoulos, The risk of lymphoma development in autoimmune diseases: a meta-analysis, Archives of Internal Medicine 165 (2005), pp. 2337–2344. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (97)
59 S.S. Kassan, T.L. Thomas and H.M. Moutsopoulos et al., Increased risk of lymphoma in sicca syndrome, Annals of Internal Medicine 89 (1978), pp. 888–892. View Record in Scopus | Cited By in Scopus (397)
*60 M. Voulgarelis, U.G. Dafni, D.A. Isenberg and H.M. Moutsopoulos, Malignant lymphoma in primary Sjögren's syndrome: a multicenter, retrospective, clinical study by the European Concerted Action on Sjögren's Syndrome, Arthritis & Rheumatism 42 (1999), pp. 1765–1772. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (177)
*61 B. Royer, D. Cazals-Hatem and J. Sibilia et al., Lymphomas in patients with Sjögren's syndrome are marginal zone B-cell neoplasms, arise in diverse extranodal and nolal sites and are not associated with viruses, Blood 90 (1997), pp. 766–775. View Record in Scopus | Cited By in Scopus (151)
62 X. Mariette, Lymphomas in patients with Sjögren's syndrome: review of the literature and physiopathologic hypothesis, Leukemia & Lymphoma 33 (1–2) (1999), pp. 93–99. View Record in Scopus | Cited By in Scopus (55)
*63 E. Theander, G. Henriksson and O. Ljungberg et al., Lymphoma and other malignancies in primary Sjögren's syndrome: a cohort study on cancer incidence and lymphoma predictors, Annals of the Rheumatic Diseases 65 (2006), pp. 796–803. View Record in Scopus | Cited By in Scopus (67)
64 K.E. Smedby, H. Hjalgrim and J. Askling et al., Autoimmune and chronic inflammatory disorders and risk of non-Hodgkin lymphoma by subtype, Journal of the National Cancer Institute 98 (2006), pp. 51–60. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (96)
65 R.J. Pelstring, J.H. Essell and P.J. Kurtin et al., Diversity of organ site involvement among malignant lymphomas of mucosa-associated tissues, American Journal of Clinical Pathology 96 (1991), pp. 738–745. View Record in Scopus | Cited By in Scopus (95)
66 A. Dogan, M. Du and A. Koulis et al., Expression of lymphocyte homing receptors and vascular addressins in low-grade gastric B-cell lymphomas of mucosa-associated lymphoid tissue, American Journal of Pathology 151 (1997), pp. 1361–1369. View Record in Scopus | Cited By in Scopus (64)
67 N.L. Harris and P.G. Isaacson, What are the criteria for distinguishing MALT from non-MALT lymphoma at extranodal sites?, American Journal of Clinical Pathology 111 (1 Suppl 1) (1999), pp. S126–S132. View Record in Scopus | Cited By in Scopus (64)
68 E.S. Jaffe, Lymphoid lesions of the head and neck: a model of lymphocyte homing and lymphomagenesis, Modern Pathology 15 (2002), pp. 255–263. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (24)
69 D. Rossi and G. Gaidano, Molecular heterogeneity of diffuse large B-cell lymphoma: implications for disease management and prognosis, Hematology 7 (2002), pp. 239–252. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (16)
70 L.G. Anderson and N. Talal, The spectrum of benign to malignant lymphoproliferation in Sjögren's syndrome, Clinical and Experimental Immunology 10 (1972), pp. 199–221. View Record in Scopus | Cited By in Scopus (29)
*71 A.G. Tzioufas, D.S. Boumba, F.N. Skopouli and H.M. Moutsopoulos, Mixed monoclonal cryoglobulinemia and monoclonal rheumatoid factor cross-reactive idiotypes as predictive factors for the development of lymphoma in primary Sjögren's syndrome, Arthritis & Rheumatism 39 (1996), pp. 767–772. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (111)
72 M.T. Walters, F.K. Stevenson and A. Herbert et al., Urinary monoclonal free light chains in the primary Sjögren's syndrome: an aid to the diagnosis of malignant lymphoma, Annals of the Rheumatic Diseases 45 (1986), pp. 210–219. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (19)
73 F.N. Skopouli, U. Dafni, J.P. Ioannidis and H.M. Moutsopoulos, Clinical evolution, and morbidity and mortality of primary Sjögren's syndrome, Seminars in Arthritis and Rheumatism 29 (2000), pp. 296–304. Abstract | PDF (847 K)
| View Record in Scopus | Cited By in Scopus (121)
74 J.P. Ioannidis, V.A. Vassiliou and H.M. Moutsopoulos, Long-term risk of mortality and lymphoproliferative disease and predictive classification of primary Sjögren's syndrome, Arthritis & Rheumatism 46 (2002), pp. 741–747. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (126)
75 M. Ramos-Casals, P. Brito-Zeron and J. Yague et al., Hypocomplementaemia as an immunological marker of morbidity and mortality in patients with primary Sjögren's syndrome, Rheumatology (Oxford) 44 (2005), pp. 89–94. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (36)
76 N. Sutcliffe, M. Inanc, P. Speight and D. Isenberg, Predictors of lymphoma development of primary Sjögren's syndrome, Seminars in Arthritis and Rheumatism 28 (1998), pp. 80–87. Abstract | PDF (664 K)
| View Record in Scopus | Cited By in Scopus (47)
77 J.M. Anaya, H.S. McGuff, P.M. Banks and N. Talal, Clinicopathological factors relating malignant lymphoma with Sjögren's syndrome, Seminars in Arthritis and Rheumatism 25 (1996), pp. 337–346. Abstract | PDF (2646 K)
| View Record in Scopus | Cited By in Scopus (65)
*78 G.S. Cheema, V. Roschke, D.M. Hilbert and W. Stohl, Elevated serum B lymphocyte stimulator levels in patients with systemic immune-based rheumatic diseases, Arthritis & Rheumatism 44 (2001), pp. 1313–1319. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (275)
*79 J. Groom, S.L. Kalled and A.H. Cutler et al., Association of BAFF/BLyS overexpression and altered B cell differentiation with Sjögren's syndrome, The Journal of Clinical Investigation 109 (2002), pp. 59–68. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (347)
80 A.M. Jacobi, M. Odendahl and K. Reiter et al., Correlation between circulating CD27high plasma cells and disease activity in patients with systemic lupus erythematosus, Arthritis & Rheumatism 48 (2003), pp. 1332–1342. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (85)
81 J.O. Bohnhorst, J.E. Thoen, J.B. Natvig and K.M. Thompson, Significantly depressed percentage of CD27+ (memory) B cells among peripheral blood B cells in patients with primary Sjögren's syndrome, Scandinavian Journal of Immunology 54 (2001), pp. 421–427. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (29)
82 A. Hansen, M. Odendahl and K. Reiter et al., Diminished peripheral blood memory B cells and accumulation of memory B cells in the salivary glands of patients with Sjögren's syndrome, Arthritis & Rheumatism 46 (2002), pp. 2160–2171. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (66)
83 J. Zulman, R. Jaffe and N. Talal, Evidence that the malignant lymphoma of Sjögren's syndrome is a monoclonal B-cell neoplasm, The New England Journal of Medicine 299 (1978), pp. 1215–1220. View Record in Scopus | Cited By in Scopus (73)
84 E. Theander, R. Manthorpe and L.T. Jacobsson, Mortality and causes of death in primary Sjögren's syndrome: a prospective cohort study, Arthritis & Rheumatism 50 (2004), pp. 1262–1269. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (60)
85 P.L. Zinzani, M. Magagnoli and P. Galieni et al., Nongastrointestinal low-grade mucosa-associated lymphoid tissue lymphoma: analysis of 75 patients, Journal of Clinical Oncology 17 (1999), pp. 1254–1258. View Record in Scopus | Cited By in Scopus (155)
86 E. Zucca, A. Conconi and E. Pedrinis et al., Nongastric marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue, Blood 101 (2003), pp. 2489–2495. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (124)
87 C. Thieblemont, F. Berger and C. Dumontet et al., Mucosa-associated lymphoid tissue lymphoma is a disseminated disease in one third of 158 patients analyzed, Blood 95 (3) (2000), pp. 802–806. View Record in Scopus | Cited By in Scopus (191)
88 M. Voulgarelis and H.M. Moutsopoulos, Malignant lymphoma in primary Sjögren's syndrome, The Israel Medical Association Journal 3 (2001), pp. 761–766. View Record in Scopus | Cited By in Scopus (15)
89 M. Voulgarelis, G. Petroutsos, H.M. Moutsopoulos and F.N. Skopouli, 2-chloro-2-deoxyadenosine in the treatment of Sjögren's syndrome-associated B cell lymphoproliferation, Arthritis & Rheumatism 46 (2002), pp. 2248–2249. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (9)
*90 J. Pijpe, G.W. van Imhoff and F.K. Spijkervet et al., Rituximab treatment in patients with primary Sjögren's syndrome: an open-label phase II study, Arthritis & Rheumatism 52 (2005), pp. 2740–2750. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (143)
91 J. Pijpe, G.W. van Imhoff and A. Vissink et al., Changes in salivary gland immunohistology and function after rituximab monotherapy in a patient with Sjögren's syndrome and associated MALT lymphoma, Annals of the Rheumatic Diseases 64 (2005), pp. 958–960. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (36)
92 M. Voulgarelis, S. Giannouli, D. Anagnostou and A.G. Tzioufas, Combined therapy with rituximab plus cyclophosphamide/doxorubicin/vincristine/prednisone (CHOP) for Sjögren's syndrome-associated B-cell aggressive non-Hodgkin's lymphomas, Rheumatology (Oxford) 43 (2004), pp. 1050–1053. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (31)
*93 M. Voulgarelis, S. Giannouli, A.G. Tzioufas and H.M. Moutsopoulos, Long-term remission of Sjögren's syndrome-associated aggressive B-cell non-Hodgkin's lymphomas following administration of combined B-cell depletion therapy and CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone), Annals of the Rheumatic Diseases 65 (2006), pp. 1033–1037. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (24)
相似文献
667.
Interactions among the immune, nervous and endocrine systems, which are mediated by hormones, neuropeptides, neurotransmitters, cytokines and their receptors, appear to play an important role in modulating host susceptibility and resistance to inflammatory disease. The neuroendocrine system has two main components: the central and the peripheral. The central compartment is located in the locus ceruleus, the brainstem centers of the autonomic system and the paraventricular nucleus; the peripheral mainly consists of the sympathetic/adrenomedullary system, the hypothalamic-pituitary-adrenal axis (HPA), the hypothalamic-pituitary-gonadal (HPG) axis, and the neuroendocrine tissue located in several organs throughout the body. Hormones and neuropeptides may influence the activities of lymphoid organs and cells via endocrine and local autocrine/paracrine pathways or alter the function of different cell types in target organs. Recent studies highlighted alterations of the neuroendocrine system in systemic autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus and Sjogren's syndrome (SS). SS, a prototype autoimmune disorder, has a wide clinical spectrum, extending from organ involvement (autoimmune exocrinopathy) to systemic disease and B cell lymphoma. In SS, several functions of the neuroendocrine system are impaired. First, the HPA axis appears to be disturbed, since significantly lower basal ACTH and cortisol levels were found in patients with SS and were associated with a blunted pituitary and adrenal response to ovine corticotropin-releasing factor compared to normal controls. Second, HPG axis is also involved, since lack of estrogens is associated with human disease and the development of autoimmune exocrinopathy in several experimental models. Finally, exocrine glands are enriched with neuroendocrine-related molecules, adjacent to local autoimmune lesions. Certain clinical manifestations of the disease, including the sicca manifestations, easy fatigue, fibromyalgia and psychological disturbances can be very well explained by mechanisms directly related to disturbances of the neuroendocrine axis. On the other hand, the molecular and biochemical effects of the inflammatory molecules or cell-to-cell interaction, observed during the local or systemic autoimmune injury with cells and mediators of the neuroendocrine system, are largely unexplored. 相似文献
668.
669.
670.