The serum CA125 levels were significantly related with cardiac function in CHD patients. Serum CA125 levels that remain elevated after CHD onset could be helpful for predicting the short-term risk of heart failure events in CHD patients.

Abstract. Squamous cell lung cancer is a major histotype of non-small cell lung cancer (NSCLC) that is distinct from lung adenocarcinoma. We used whole-exome sequencing to identify novel non-synonymous somatic mutations in squamous cell lung cancer. We identified 101 single-nucleotide variants (SNVs) including 77 non-synonymous SNVs (67 missense and 10 nonsense mutations) and 11 INDELs causing frameshifts. We also found four SNVs located within splicing sites. We verified 62 of the SNVs (51 missense, 10 nonsense and 1 splicing-site mutation) and 10 of the INDELs as somatic mutations in lung cancer tissue. Sixteen of the mutated genes were also mutated in at least one patient with a different type of lung cancer in the Catalogue of Somatic Mutation in Cancer (COSMIC) database. Four genes (LPHN2, TP53, MYH2 and TGM2) were mutated in approximately 10% of the samples in the COSMIC database. We identified two missense mutations in C10orf137 and MS4A3 that also occurred in other solid-tumor tissues in the COSMIC database. We found another somatic mutation in EP300 that was mutated in 4.2% of the 2,020 solid-tumor samples in the COSMIC database. Taken together, our results implicate TP53, EP300, LPHN2, C10orf137, MYH2, TGM2 and MS4A3 as potential driver genes of squamous cell lung cancer. IntroductionLung cancer is the leading cause of cancer-related death worldwide and accounts for one quarter of all cancer mortalities in the US (1). Non-small cell lung cancer (NSCLC) accounts for approximately 80% of all lung cancer cases and can be classified by histotypes as adenocarcinoma (AC), squamous cell carcinoma (SCC), and large-cell lung cancer (LCLC). The high mortality rate of lung cancer is mainly attributed to the disease not being diagnosed until it is in advanced stages. Chemotherapy with platinum-based drugs in combination with taxanes, camptothecins, or vinca alkaloids, the first-line treatment for patients with NSCLC, has made little progress in improving prognoses in recent decades (1).Similar to other malignancies, tumorigenesis in NSCLC depends on the clustering of gene dysfunction as a result of genetic susceptibility and/or the accumulation of noxious environmental factors. The discoveries of recurrent mutations in the epidermal growth-factor receptor (EGFR) kinase and fusions, such as EML4-ALK, involving anaplastic lymphoma kinase (ALK) led to a dramatic change in the treatment of lung AC (2,3). Recent data suggest that substance CI1040 can bind to MEK and mutated BRAF, resulting in the shrinkage of lung ACs that harbor mutated KRAS and BRAF, respectively (4). Other recent data show that targeting mutations in AKT1, ERBB2 and PIK3CA and fusions involving ROS1 and RET may also be successful (5). Unfortunately, activating mutations in EGFR, EML4-ALK fusions, and mutations in KRAS are only detected in lung AC, and are not present in the second most-common type of lung cancer, SCC (6). Thus, targeted agents developed for lung AC are largely ineffective against lung SCC (7).Lung SCC accounts for 45% of NSCLC, and ...

The serum albumin (25.60 ± 5.31 vs 34.00 ± 6.90; P < 0.05) and CD4 cell count (28.5 ± 30.5 vs 229.50 ± 229.45; P < 0.05) of group A were much lower than those of group B. The serum albumin and CD4 cell count negatively correlated with the incidence of CAP. The CD4 cell count (24.15 ± 25.1 vs 47.85 ± 132.5; P < 0.05) and partial pressure of oxygen (7.86 ± 1.43 vs 9.41 ± 2.15; P < 0.05) of group A1 were significantly lower than those of group A2 . Low serum albumin levels and high blood urea nitrogen levels were the risk factors of hypoxaemia in group A. Early screening and diagnosis of AIDS, as well as nutritional support, would prevent AIDS patients from developing CAP or progressing to severe pneumonia or respiratory failure.