Institution
Uludağ University
Education•Bursa, Turkey•
About: Uludağ University is a education organization based out in Bursa, Turkey. It is known for research contribution in the topics: Population & Turkish. The organization has 5301 authors who have published 9676 publications receiving 151126 citations.
Topics: Population, Turkish, Poison control, Cancer, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: The high prevalence of depression, anxiety and stress symptoms among university students is alarming and shows the need for primary and secondary prevention measures, with the development of adequate and appropriate support services for this group.
Abstract: Background
The mental health of university students is an area of increasing concern worldwide. The objective of this study is to examine the prevalence of depression, anxiety and stress among a group of Turkish university students.
1,035 citations
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TL;DR: A deviation towards a regulatory/suppressor T cell response during SIT and in normal immunity as a key event for the healthy immune response to mucosal antigens is demonstrated.
Abstract: The regulation of normal and allergic immune responses to airborne allergens in the mucosa is still poorly understood, and the mechanism of specific immunotherapy (SIT) in normalizing the allergic response to such allergens is currently not clear. Accordingly, we have investigated the immunoregulatory mechanism of both normal and allergic responses to the major house-dust mite (HDM) and birch pollen allergens — Dermatophagoides pteroynyssinus (Der p)1 and Bet v 1, respectively — as well as the immunologic basis of SIT to HDM in rhinitis and asthma patients. In normal immunity to HDM and birch pollen, an allergen-specific peripheral T cell suppression to Der p 1 and Bet v 1 was observed. The deviated immune response was characterized by suppressed proliferative T celland Th1 (IFN-γ) and Th2 (IL-5, IL-13) cytokine responses, and increased IL-10 and TGF-β secretion by allergen-specific T cells. Neutralization of cytokine activity showed that T cell suppression was induced by IL-10 and TGF-β during SIT and in normal immunity to the mucosal allergens. In addition, SIT induced an antigen-specific suppressive activity in CD4+ CD25+ T cells of allergic individuals. Together, these results demonstrate a deviation towards a regulatory/suppressor T cell response during SIT and in normal immunity as a key event for the healthy immune response to mucosal antigens.
900 citations
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TL;DR: Findings implicate Neurokinin B as a critical central regulator of human gonadal function and suggest new approaches to the pharmacological control of human reproduction and sex hormone-related diseases.
Abstract: The timely secretion of gonadal sex steroids is essential for the initiation of puberty, the postpubertal maintenance of secondary sexual characteristics and the normal perinatal development of male external genitalia. Normal gonadal steroid production requires the actions of the pituitary-derived gonadotropins, luteinizing hormone and follicle-stimulating hormone. We report four human pedigrees with severe congenital gonadotropin deficiency and pubertal failure in which all affected individuals are homozygous for loss-of-function mutations in TAC3 (encoding Neurokinin B) or its receptor TACR3 (encoding NK3R). Neurokinin B, a member of the substance P-related tachykinin family, is known to be highly expressed in hypothalamic neurons that also express kisspeptin, a recently identified regulator of gonadotropin-releasing hormone secretion. These findings implicate Neurokinin B as a critical central regulator of human gonadal function and suggest new approaches to the pharmacological control of human reproduction and sex hormone-related diseases.
819 citations
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French Institute of Health and Medical Research1, Rockefeller University2, Paris Descartes University3, University of Debrecen4, Academy of Medical Sciences, United Kingdom5, Charité6, University of Zurich7, Ludwig Maximilian University of Munich8, Rappaport Faculty of Medicine9, Hiroshima University10, Uludağ University11, Boston Children's Hospital12
TL;DR: Whole-exome sequencing reveals activating STAT1 mutations in some patients with autosomal dominant chronic mucocutaneous candidiasis disease.
Abstract: Chronic mucocutaneous candidiasis disease (CMCD) may be caused by autosomal dominant (AD) IL-17F deficiency or autosomal recessive (AR) IL-17RA deficiency. Here, using whole-exome sequencing, we identified heterozygous germline mutations in STAT1 in 47 patients from 20 kindreds with AD CMCD. Previously described heterozygous STAT1 mutant alleles are loss-of-function and cause AD predisposition to mycobacterial disease caused by impaired STAT1-dependent cellular responses to IFN-γ. Other loss-of-function STAT1 alleles cause AR predisposition to intracellular bacterial and viral diseases, caused by impaired STAT1-dependent responses to IFN-α/β, IFN-γ, IFN-λ, and IL-27. In contrast, the 12 AD CMCD-inducing STAT1 mutant alleles described here are gain-of-function and increase STAT1-dependent cellular responses to these cytokines, and to cytokines that predominantly activate STAT3, such as IL-6 and IL-21. All of these mutations affect the coiled-coil domain and impair the nuclear dephosphorylation of activated STAT1, accounting for their gain-of-function and dominance. Stronger cellular responses to the STAT1-dependent IL-17 inhibitors IFN-α/β, IFN-γ, and IL-27, and stronger STAT1 activation in response to the STAT3-dependent IL-17 inducers IL-6 and IL-21, hinder the development of T cells producing IL-17A, IL-17F, and IL-22. Gain-of-function STAT1 alleles therefore cause AD CMCD by impairing IL-17 immunity.
699 citations
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TL;DR: In this article, the process e(+)e(-) -> pi(+)pi(-) J/psi at a center-of-mass energy of 4.260 GeV using a 525 pb(-1) data sample collected with the BESIII detector operating at the Beijing Electron Positron Collider was studied.
Abstract: We study the process e(+)e(-) -> pi(+)pi(-) J/psi at a center-of-mass energy of 4.260 GeV using a 525 pb(-1) data sample collected with the BESIII detector operating at the Beijing Electron Positron Collider. The Born cross section is measured to be (62.9 +/- 1.9 +/- 3.7) pb, consistent with the production of the Y(4260). We observe a structure at around 3.9 GeV/c(2) in the pi(+/-) J/psi mass spectrum, which we refer to as the Z(c)(3900). If interpreted as a new particle, it is unusual in that it carries an electric charge and couples to charmonium. A fit to the pi(+/-) J/psi invariant mass spectrum, neglecting interference, results in a mass of (3899.0 +/- 3.6 +/- 4.9) MeV/c(2) and a width of (46 +/- 10 +/- 20) MeV. Its production ratio is measured to be R = (sigma(e(+)e(-) -> pi(+/-) Z(c)(3900)(-/+) -> pi(+)pi(-) J/psi)/sigma(e(+)e(-) -> pi(+)pi(-) J/psi)) = (21.5 +/- 3.3 +/- 7.5)%. In all measurements the first errors are statistical and the second are systematic.
677 citations
Authors
Showing all 5449 results
Name | H-index | Papers | Citations |
---|---|---|---|
Serkant Ali Cetin | 129 | 1369 | 85175 |
Zhiqing Zhang | 120 | 1046 | 56554 |
S. J. Chen | 116 | 1559 | 62804 |
L. Sun | 115 | 1355 | 89319 |
L. L. Ma | 114 | 899 | 62778 |
X. Y. Zhang | 106 | 1130 | 66432 |
Xingguo Li | 104 | 761 | 55475 |
Y. Ban | 104 | 1346 | 49897 |
Yi Zhang | 102 | 1817 | 53417 |
S. Malde | 91 | 1064 | 37904 |
G. Wilkinson | 89 | 1016 | 35424 |
Z. P. Zhang | 84 | 888 | 29402 |
Shan Jin | 83 | 365 | 37419 |
H. J. Yang | 81 | 612 | 24756 |
Y. J. Mao | 81 | 829 | 29089 |