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Li X.,Tianjin Institute of Respiratory Diseases | Brownlee N.A.,Pathology Assoc.of Greenville | Sporn T.A.,Duke University | Mahar A.,Royal Prince Alfred Hospital | Roggli V.L.,Duke University
Archives of Pathology and Laboratory Medicine | Year: 2015

Context. - Ionizing radiation has a role in the development of malignant mesothelioma, in several epidemiologic studies, including patients with hematologic malignancies. Objective. - To study the clinicopathologic characteristics of patients with malignant mesothelioma and hematologic malignancies with and without a history of radiotherapy. Design. - From a database of approximately 3600 patients with malignant mesothelioma, we identified 45 patients (1%) who also had hematologic malignancies. We examined clinicopathologic features and noted whether the patient had received radiotherapy for malignancy, comparing those with and those without such exposure. Results. - Among the 45 cases, 18 (40%) had Hodgkin lymphoma, 15 (33%) had non-Hodgkin lymphoma, 10 (4%) had chronic lymphocytic leukemia, and 2 (22%) had chronic myelogenous leukemia; 20 patients (44%) had a history of radiotherapy, and 23 (51%) did not. Most patients with Hodgkin lymphoma (16 of 18; 90.0%) received radiation, whereas none of the patients with leukemia (0 of 12) and only 20% (3 of 15) of the patients with non-Hodgkin lymphoma did so. Patients without radiation were older than patients who received radiotherapy (median, 73 versus 54 years, respectively; P < .001), had a shorter interval from diagnosis of hematologic malignancy to that of mesothelioma (median, 2 versus 24 years, respectively; P < .001), and had a shorter survival period (median, 6.0 versus 14.0 months, respectively; P = .02). Epithelial mesotheliomas were proportionately more common in patients with a history of radiotherapy. Conclusions. - Patients with mesothelioma and hematologic malignancies with a history of radiation tended to be younger, had a longer interval from diagnosis of hematologic malignancy to that of mesothelioma, had a longer survival period, and were more likely to have the epithelial variant compared with patients without radiotherapy.

Ma S.,CAS Shanghai Institutes for Biological Sciences | Fang Z.,CAS Shanghai Institutes for Biological Sciences | Luo W.,CAS Shanghai Institutes for Biological Sciences | Yang Y.,CAS Shanghai Institutes for Biological Sciences | And 7 more authors.
Oxidative Medicine and Cellular Longevity | Year: 2016

Excessive reactive oxygen species/reactive nitrogen species (ROS/RNS) produced as a result of ageing causes damage to macromolecules and organelles or leads to interference of cell signalling pathways, which in turn results in oxidative stress. Oxidative stress occurs in many neurodegenerative diseases (e.g., Parkinson's disease) and contributes to progressive neuronal loss. In this study, we show that cell apoptosis is induced by oxidative stress and that lysosomes play an important role in cell survival under oxidative stress. As a compensatory response to this stress, lysosomal genes were upregulated via induction of transcription factor EB (TFEB). In addition, localization of TFEB to the nucleus was increased by oxidative stress. We also confirmed that TFEB protects cells from oxidative stress both in vitro and in vivo. Finally, we found that C-ETS2 senses oxidative stress, activates TFEB transcription, and mediates the upregulation of lysosomal genes. Our results demonstrate a mechanistic pathway for inducing lysosomal activity during ageing and neurodegeneration. © 2016 Shumin Ma et al.

Yin Q.,Tianjin Medical University | Zhou Y.-Y.,Tianjin Institute of Respiratory Diseases | Wang P.,Tianjin Medical University | Ma L.,Tianjin Medical University | And 4 more authors.
Oncology Letters | Year: 2016

Previous in vivo and in vitro studies have shown that human mesenchymal stem cells (MSCs) exhibit tropism for gliomas. However, the mechanism underlying this directed migration remains unclear. The aim of the present study was to investigate the possible mechanism underlying platelet-derived growth factor-BB (PDGF-BB)-induced chemotactic migration of bone marrow-derived MSCs (BMSCs) toward glioma. Rat glioma C6 cell-conditioned medium was utilized to evaluate the chemotactic response of BMSCs toward glioma using an in vitro migration assay. Recombinant rat PDGF-BB was added to C6 cell-conditioned medium to assess its effect on the tropism of BMSCs. The effect of PDGF-BB on the expression levels of cluster of differentiation (CD)44 in BMSCs was evaluated by reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence assays. The results revealed that chemotactic migration was induced in BMSCs by rat glioma C6 cell-conditioned medium, which was enhanced by PDGF-BB treatment in a dose-dependent manner. Furthermore, RT-PCR and immunofluorescence assays showed that CD44 expression was upregulated in BMSCs following treatment with 40 ng/ml PDGF-BB for 12 h. Additionally, 3-h pretreatment with the anti-CD44 neutralizing antibody OX-50 was observed to attenuate the tropism of BMSCs toward glioma in the presence or absence of PDGF-BB. The results of the present study indicate that CD44 mediates the tropism of BMSCs toward glioma, and PDGF-BB promotes the migration of BMSCs toward glioma via the upregulation of CD44 expression in BMSCs. These findings suggest CD44 inhibition may be a potential therapeutic target for the treatment of glioma. © 2016, Spandidos Publications. All rights reserved.

Liu R.,Tianjin Institute of Respiratory Diseases
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases | Year: 2010

To study the clinical application and significance of the recently published expert consensus on endobronchial tuberculosis (EBTB). A retrospective analysis of 288 cases of EBTB hospitalized in Tianjin Haihe Hospital from May 2005 to April 2010 was carried out. The classification and typing of the disease were based on a consensus report recently published by Chinese Journal of Tuberculosis and Respiratory Diseases. Chi-square test was performed to analyze the differences between groups. Of the 288 cases of EBTB, 47.9% (138/288) was classified as Type I (Inflammatory infiltrative), 33.3% (96/288) as Type II (ulcerous necrotic), 5.2% (15/288) as Type III (granulomatous hyperplastic), 7.3% (21/288) as Type IV (scar stricture) and 0.4% (1/288) as Type V (Bronchomalacia), respectively. There were 17 cases (5.9%) classified as a mixed type with a combination of Type IV or Type V disease with 1 or more of the other types. 37.5% (108/288) of the patients were young females, while young and middle-aged patients with type I and type II diseases accounted for 74.7% (215/288) of the cases, much more than old aged patients (6.6%, 19/288). 97.2% (n=280) of the cases suffered from secondary pulmonary tuberculosis. In 107 cases, the disease was located in the left, 162 cases in the right, while in 109 cases the right upper lobe bronchus was involved, and right main bronchus in 36 cases, 3 cases and 58 cases in left upper lobe with and without lingular segment, 10 cases in lingular segment only. Chest CT showed that local mucosal thickening of the trachea or bronchus was evident in 40.3% (116/288); toothed or spike protuberance in 30.9% (89/288), bronchial obstruction in 11.1% (32/288), and bronchial stenosis in 87.9% (253/288). The negative rate of sputum in the first month after interventional therapy was 60.2% (56/93), significantly higher than that in non-interventional therapy group (23.1%, 18/78). The new consensus report on EBTB was clinically useful for classification and typing of the disease, and for the selection of treatment modalities.

Zhang D.,CAS Shanghai Institutes for Biological Sciences | Zhang D.,University of Chinese Academy of Sciences | Wang W.,CAS Shanghai Institutes for Biological Sciences | Wang W.,University of Chinese Academy of Sciences | And 17 more authors.
Autophagy | Year: 2016

Macroautophagy/autophagy is a conserved catabolic process that recycles cytoplasmic material during low energy conditions. BECN1/Beclin1 (Beclin 1, autophagy related) is an essential protein for function of the class 3 phosphatidylinositol 3-kinase (PtdIns3K) complexes that play a key role in autophagy nucleation and elongation. Here, we show that AMP-activated protein kinase (AMPK) regulates autophagy by phosphorylating BECN1 at Thr388. Phosphorylation of BECN1 is required for autophagy upon glucose withdrawal. BECN1T388A, a phosphorylation defective mutant, suppresses autophagy through decreasing the interaction between PIK3C3 (phosphatidylinositol 3-kinase catalytic subunit type 3) and ATG14 (autophagy-related 14). The BECN1T388A mutant has a higher affinity for BCL2 than its wild-type counterpart; the mutant is more prone to dimer formation. Conversely, a BECN1 phosphorylation mimic mutant, T388D, has stronger binding to PIK3C3 and ATG14, and promotes higher autophagy activity than the wild-type control. These findings uncover a novel mechanism of autophagy regulation. © 2016 Taylor & Francis

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