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22 ["EGFR gene copy number as a predictive/biomarker for patients with non-small-cell lung cancer receiving tyrosine kinase inhibitor treatment: a systematic review and meta-analysis"] 10.1136/jim-2016-000252 2016-09-24T02:48:22Z [] 41 6 ["1081-5589", "1708-8267"] Journal of Investigative Medicine <jats:p>Epidermal growth factor receptor (<jats:italic>EGFR</jats:italic>) gene copy number has been proposed as a candidate biomarker for predicting treatment response to EGFR tyrosine kinase inhibitors (EGFR-TKIs) in patients with advanced non-small-cell lung cancer (NSCLC). MEDLINE, PubMed, Cochrane, and Google Scholar databases were searched until October 21, 2015 using the following search terms: lung neoplasms/lung cancer/non-small cell lung cancer/NSCLC, EGFR, gene amplification, copy number, erlotinib, gefitinib, tyrosine-kinase inhibitor/TKI, predictor. 17 studies were included in the analysis with a total of 2047 patients. The overall analysis found that increased <jats:italic>EGFR</jats:italic> gene copy number was associated with higher overall response rate (ORR), overall survival (OS) and progression-free survival (PFS; p values ≤0.008) compared with patients without a high <jats:italic>EGFR</jats:italic> gene copy number. Subgroup analysis found that in a population of patients who were primarily Caucasian, a higher <jats:italic>EGFR</jats:italic> gene copy number was also associated with increased ORR, OS, and PFS (p values ≤0.018). The results were similar in a population of Asian patients, except that a higher <jats:italic>EGFR</jats:italic> gene copy number was not associated with improved OS (p=0.248). Sensitivity analysis indicated that no one study overly influenced the results and that the findings are robust. The result of the analysis found that <jats:italic>EGFR</jats:italic> gene copy number was associated with increased OS and PFS, supporting the idea that <jats:italic>EGFR</jats:italic> gene copy number is a biomarker for response to EGFR-TKI therapy in patients with advanced NSCLC.</jats:p> 4 [] ["Xin Zhang", "Yiwen Zhang", "Hailing Tang", "Jianxing He"] [""] [""] [""]
77 ["Metabolic and cardiovascular effects of chronic mild hyperuricemia in rodents"] 10.1136/jim-2018-000729 2018-07-24T17:51:06Z ["General Biochemistry, Genetics and Molecular Biology", "General Medicine"] 33 0 ["1081-5589", "1708-8267"] Journal of Investigative Medicine <jats:p>Mildly elevated serum uric acid levels are common in people with metabolic syndrome and type 2 diabetes mellitus (T2DM), but whether elevated uric acid has a causal role in the pathogenesis of diabetes remains uncertain. We tested whether chronic mild hyperuricemia in rodents under controlled laboratory conditions can cause glucose intolerance in otherwise healthy animals, or whether it can worsen glucometabolic control in animals that are genetically predisposed to T2DM. We used an established model of experimental hyperuricemia in rodents with potassium oxonate dietary supplementation, which led to sustained, approximately two-fold elevation of uric acid compared with control animals. We also reversed the hyperuricemic effect of oxonate in some animals by treatment with a xanthine oxidase inhibitor. Manipulation of serum uric acid levels in Sprague-Dawley rats for up to 18 weeks did not affect fasting glucose and glucose tolerance. Blood pressure was also not affected by hyperuricemia in rats fed a Western-type diet. We next sought to determine whether uric acid may aggravate or accelerate the onset of glucometabolic abnormalities in rats already predisposed to T2DM. Chronic oxonate treatment in Zucker diabetic fatty (ZDF) and lean control rats for up to 6 weeks did not affect fasting glucose, insulin, and glucose tolerance in ZDF rats. Taken together, these findings indicate that elevated uric acid does not directly contribute to the pathogenesis of glucose intolerance and T2DM in rodents.</jats:p> 7 [] ["Sun K Park", "Tara R Rosenthal", "Jessica S Williams", "John M Shelton", "Masaya Takahashi", "Shanrong Zhang", "Ion Alexandru Bobulescu"] [] ["National Institutes of Health", "Takeda Pharmaceuticals U.S.A."] ["10.13039/100000002", "10.13039/100007723"]
85 ["ID: 129: PARTICULATE MATTER DISRUPTS ENDOTHELIAL CELL PERMEABILITY VIA GAP JUNCTION PROTEIN"] 10.1136/jim-2016-000120.124 2016-05-10T23:43:02Z [] 0 0 ["1081-5589", "1708-8267"] Journal of Investigative Medicine <jats:sec><jats:title>Introduction</jats:title><jats:p>Particulate matter (PM) is significantly associated with cardiopulmonary morbidity and mortality. We previously demonstrated that PM induces endothelial barrier disruption via reactive oxygen species (ROS)-dependent mechanisms. This study is focused on characterization of PM-regulated endothelial dysfunction via connexin43 (Cx43), a Gap junction protein. Gap junction is designated as intercellular channel which allows cells to communicate with each other, share nutrients, and transfer chemical or electrical signals, in turn, enables cells in a tissue to function in a coordinated manner.</jats:p></jats:sec><jats:sec><jats:title>Methods and Results</jats:title><jats:p>Cx43 protein levels were evaluated by western blotting, and band density quantified using MyImageAnalysis. Real-time PCR was conducted to determine Cx43 mRNA levels. Human pulmonary artery endothelial cell (EC) barrier function was measured using the electrical cell-substrate impedance sensing (ECIS) system (Applied Biophysics) that provides a readout of transendothelial electrical resistance (TER). PM sample (0.1–0.3 µm of aerodynamic diameter) was collected (April of 2005) from the Ft. McHenry Tunnel, Baltimore, MD using a high-volume cyclone collector. PM (100 µg/ml) induced time-dependent increases in EC Cx43 mRNA levels (∼5 fold increase at 4 hr) and protein expression which was attenuated by N-acetyl-cysteine (NAC, 5 mM, 1 hr pretreatment), an ROS scavenger. Unlike Cx43, Cx37, another connexin expressed in ECs, remained unaltered by PM challenge. In addition, EC pretreatment with a Cx43 inhibitor, connexin-mimetic peptide Gap27 (500 µM, 2 hr pretreatment), significantly attenuated PM-reduced TER reduction by 45%, suggesting a central role of Cx43 in PM-induced lung EC barrier integrity disruption and signal transduction.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Our results suggest Cx43 as a key and novel participant in PM-mediated signal transduction that results in loss of vascular barrier integrity. Cx43 may serve as a therapeutic target in PM-induced cardiopulmonary toxicities.</jats:p></jats:sec> 4 [] ["X Wu", "X Xu", "JG Garcia", "T Wang"] [""] [""] [""]