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Institution

Istanbul University

EducationIstanbul, Turkey
About: Istanbul University is a education organization based out in Istanbul, Turkey. It is known for research contribution in the topics: Population & Medicine. The organization has 19050 authors who have published 38464 publications receiving 727640 citations. The organization is also known as: İstanbul Üniversitesi & University of Istanbul.


Papers
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Journal ArticleDOI
Sabri Arik1
TL;DR: A new sufficient condition is given for the uniqueness and global asymptotic stability of the equilibrium point for delayed cellular neural networks (DCNN) and imposes constraints on the feedback and delayed feedback matrices of a DCNN independently of the delay parameter.
Abstract: In this paper, a new sufficient condition is given for the uniqueness and global asymptotic stability of the equilibrium point for delayed cellular neural networks (DCNNs). This condition imposes constraints on the feedback and delayed feedback matrices of a DCNN independently of the delay parameter. This result is also compared with the previous results derived in the literature.

288 citations

Journal ArticleDOI
TL;DR: It is the opinion that the three therapeutic modalities must be considered separately, and this was done in the present paper, and the research on the mechanism of action and cost effectiveness of such treatments are reviewed.
Abstract: The use of water for medical treatment is probably as old as mankind. Until the middle of the last century, spa treatment, including hydrotherapy and balneotherapy, remained popular but went into decline especially in the Anglo-Saxon world with the development of effective analgesics. However, no analgesic, regardless of its potency, is capable of eliminating pain, and reports of life-threatening adverse reactions to the use of these drugs led to renewed interest in spa therapy. Because of methodologic difficulties and lack of research funding, the effects of 'water treatments' in the relief of pain have rarely been subjected to rigorous assessment by randomised, controlled trials. It is our opinion that the three therapeutic modalities must be considered separately, and this was done in the present paper. In addition, we review the research on the mechanism of action and cost effectiveness of such treatments and examine what research might be useful in the future.

288 citations

Journal ArticleDOI
TL;DR: In this paper, the authors reported homozygous missense mutations in both intracellular and extracellular domains of ROR2 in affected individuals from three unrelated consanguineous families, and a nonsense mutation that removes the tyrosine kinase domain and all subsequent 3' regions of the gene in 14 patients from 7 families from Oman.
Abstract: The autosomal recessive form of Robinow syndrome (RRS; MIM 268310) is a severe skeletal dysplasia with generalized limb bone shortening, segmental defects of the spine, brachydactyly and a dysmorphic facial appearance. We previously mapped the gene mutated in RRS to chromosome 9q22 (ref. 4), a region that overlaps the locus for autosomal dominant brachydactyly type B (refs 5,6). The recent identification of ROR2, encoding an orphan receptor tyrosine kinase, as the gene mutated in brachydactyly type B (BDB1; ref. 7) and the mesomelic dwarfing in mice homozygous for a lacZ and/or a neo insertion into Ror2 (refs 8,9) made this gene a candidate for RRS. Here we report homozygous missense mutations in both intracellular and extracellular domains of ROR2 in affected individuals from 3 unrelated consanguineous families, and a nonsense mutation that removes the tyrosine kinase domain and all subsequent 3' regions of the gene in 14 patients from 7 families from Oman. The nature of these mutations suggests that RRS is caused by loss of ROR2 activity. The identification of mutations in three distinct domains (containing Frizzled-like, kringle and tyrosine kinase motifs) indicates that these are all essential for ROR2 function.

287 citations

Journal ArticleDOI
TL;DR: In this paper, the authors describe the clinical, laboratory, and histopathologic features, current treatment, and outcome of patients with macrophage activation syndrome (MAS) complicating systemic juvenile idiopathic arthritis (JIA).
Abstract: Objective To describe the clinical, laboratory, and histopathologic features, current treatment, and outcome of patients with macrophage activation syndrome (MAS) complicating systemic juvenile idiopathic arthritis (JIA). Methods In this multinational, multicenter study, pediatric rheumatologists and hemato-oncologists entered patient data collected retrospectively into a web-based database. Results A total of 362 patients, 22% of whom had MAS at the onset of systemic JIA, were included in the study by 95 investigators from 33 countries. The most frequent clinical manifestations were fever (96%), hepatomegaly (70%), and splenomegaly (58%). Central nervous system dysfunction and hemorrhages were recorded in 35% and 20% of the patients, respectively. Platelet count and liver transaminase, ferritin, lactate dehydrogenase, triglyceride, and d-dimer levels were the sole laboratory biomarkers showing a percentage change of >50% between the pre-MAS visit and MAS onset. Evidence of macrophage hemophagocytosis was found in 60% of the patients who underwent bone marrow aspiration. MAS occurred most frequently in the setting of active underlying disease, in the absence of a specific trigger. Nearly all patients were given corticosteroids, and 61% received cyclosporine. Biologic medications and etoposide were given to 15% and 12% of the patients, respectively. Approximately one-third of the patients required admission to the intensive care unit (ICU), and the mortality rate was 8%. Conclusion This study provides information on the clinical spectrum and current management of systemic JIA–associated MAS through the analysis of a very large patient sample. MAS remains a serious condition, as a sizeable proportion of patients required admission to the ICU or died.

286 citations

Journal ArticleDOI
15 Sep 2007-Blood
TL;DR: It is shown that freshly isolated, resting natural killer (NK) cells and CD8(+) T cells express syntaxin-11, which could explain the less severe disease progression observed in FHL4 patients, compared with FHL2 and FHL3 patients.

284 citations


Authors

Showing all 19361 results

NameH-indexPapersCitations
Bobby Samir Acharya1331121100545
Serkant Ali Cetin129136985175
Alexander Nikitenko129115982102
Aytul Adiguzel12496471366
Neil Risch12238670042
Laurent Poirel11762153680
Andrei Starodumov11469757900
Suat Ozkorucuklu11069855607
Robert J. Desnick10269439698
Lars Berglund9764142300
Angel Carracedo8888538053
Peter A. Merkel8543034014
Thomas A. Pearson8434941573
Willy Malaisse80163531641
C. Pagliarone7979627164
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20242
202386
2022404
20213,031
20202,663
20192,380