11 research outputs found

    Compartment-Specific Remodeling Of Splenic Micro-Architecture During Experimental Visceral Leishmaniasis

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    Progressive splenomegaly is a hallmark of visceral leishmaniasis in humans, canids, and rodents. In experimental murine visceral leishmaniasis, splenomegaly is accompanied by pronounced changes in microarchitecture, including expansion of the red pulp vascular system, neovascularization of the white pulp, and remodeling of the stromal cell populations that define the B-cell and T-cell compartments. Here, we show that Ly6C/G+ (Gr-1+) cells, including neutrophils and inflammatory monocytes, accumulate in the splenic red pulp during infection. Cell depletion using monoclonal antibody against either Ly6C/G+ (Gr-1; RB6) or Ly6G+ (1A8) cells increased parasite burden. In contrast, depletion of Ly6C/G+ cells, but not Ly6G+ cells, halted the progressive remodeling of Meca-32+ and CD31+ red pulp vasculature. Strikingly, neither treatment affected white pulp neovascularization or the remodeling of the fibroblastic reticular cell and follicular dendritic cell networks. These findings demonstrate a previously unrecognized compartment-dependent selectivity to the process of splenic vascular remodeling during experimental murine visceral leishmaniasis, attributable to Ly6C+ inflammatory monocytes.PubMedWoSScopu

    Patient and physician delay in the diagnosis and treatment of non-small cell lung cancer in Turkey

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    WOS: 000351233200014PubMed ID: 25670053Aim: The early diagnosis and treatment of lung cancer are important for the prognosis of patients with lung cancer. This study was undertaken to investigate patient and doctor delays in the diagnosis and treatment of NSCLC and the factors affecting these delays. Materials and methods: A total of 1016 patients, including 926 (91.1%) males and 90 (8.9%) females with a mean age of 61.5 +/- 10.1 years, were enrolled prospectively in this study between May 2010 and May 2011 from 17 sites in various Turkish provinces. Results: The patient delay was found to be 49.9 +/- 96.9 days, doctor delay was found to be 87.7 +/- 99.6 days, and total delay was found to be 131.3 +/- 135.2 days. The referral delay was found to be 61.6 +/- 127.2 days, diagnostic delay was found to be 20.4 +/- 44.5 days, and treatment delay was found to be 24.4 +/- 54.9 days. When the major factors responsible for these delays were examined, patient delay was found to be more frequent in workers, while referral delay was found to be more frequent in patients living in villages (p < 0.05). We determined that referral delay, doctor delay, and total delay increased as the number of doctors who were consulted by patients increased (p < 0.05). Additionally, we determined that diagnostic and treatment delays were more frequent at the early tumour stages in NSCLC patients (p < 0.05). Discussion: The extended length of patient delay underscores the necessity of educating people about lung cancer. To decrease doctor delay, education is a crucial first step. Additionally, to further reduce the diagnostic and treatment delays of chest specialists, multidisciplinary management and algorithms must be used regularly. (C) 2015 Elsevier Ltd. All rights reserved

    Sherris Tıbbi Mikrobiyoloji

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