Intra-Abdominal Hypertension and Abdominal Compartment Syndrome in Liver Diseases

Intra-abdominal hypertension (IAH) is defined as an intra-abdominal pressure (IAP) above 12 mmHg. Abdominal compartment syndrome (ACS) is defined as an IAP above 20 mmHg with evidence of organ failure. Moreover, IAH/ACS is a condition that can cause acute renal failure, respiratory failure, circulatory disease, gastrointestinal dysfunction, and liver failure due to elevated IAP. The incidence of IAH/ACS increases in the more critically ill patient and is associated with significantly increased morbidity and mortality. Ascites, blood, or tumors increase IAP. In liver cirrhosis, massive ascites is often encountered. Hence, preventing IAH/ACS conditions may improve outcomes of patients with liver disease

Involvement of DNA Damage Response via the Ccndbp1–Atm–Chk2 Pathway in Mice with Dextran-Sodium-Sulfate-Induced Colitis

The dextran sodium sulfate (DSS)-induced colitis mouse model has been widely utilized for human colitis research. While its mechanism involves a response to double-strand deoxyribonucleic acid (DNA) damage, ataxia telangiectasia mutated (Atm)–checkpoint kinase 2 (Chk2) pathway activation related to such response remains unreported. Recently, we reported that cyclin D1-binding protein 1 (Ccndbp1) activates the pathway reflecting DNA damage in its knockout mice. Thus, this study aimed to examine the contribution of Ccndbp1 and the Atm–Chk2 pathway in DSS-induced colitis. We assessed the effect of DSS-induced colitis on colon length, disease activity index, and histological score and on the Atm–Chk2 pathway and the subsequent apoptosis in Ccndbp1-knockout mice. DSS-induced colitis showed distal colon-dominant Atm and Chk2 phosphorylation, increase in TdT-mediated dUTP-biotin nick end labeling and cleaved caspase 3-positive cells, and histological score increase, causing disease activity index elevation and colon length shortening. These changes were significantly ameliorated in Ccndbp1-knockout mice. In conclusion, Ccndbp1 contributed to Atm–Chk2 pathway activation in the DSS-induced colitis mouse model, causing inflammation and apoptosis of mucosal cells in the colon

Incidental detection of localized prostate cancer with low PSA by computed tomography scan: A report of two cases

Abstract Serum prostate‐specific antigen (PSA) levels play an important role in the screening and diagnosis of prostate cancer (PCa). The recommended PSA cut‐off in PCa screening is 4 ng/ml. We report two cases of localized PCa with low PSA levels that were incidentally found by computed tomography (CT) performed for another disease

Cyclin D1 Binding Protein 1 Responds to DNA Damage through the ATM–CHK2 Pathway

Cyclin D1 binding protein 1 (CCNDBP1) is considered a tumor suppressor, and when expressed in tumor cells, CCNDBP1 can contribute to the viability of cancer cells by rescuing these cells from chemotherapy-induced DNA damage. Therefore, this study focused on investigating the function of CCNDBP1, which is directly related to the survival of cancer cells by escaping DNA damage and chemoresistance. Hepatocellular carcinoma (HCC) cells and tissues obtained from Ccndbp1 knockout mice were used for the in vitro and in vivo examination of the molecular mechanisms of CCNDBP1 associated with the recovery of cells from DNA damage. Subsequently, gene and protein expression changes associated with the upregulation, downregulation, and irradiation of CCNDBP1 were assessed. The overexpression of CCNDBP1 in HCC cells stimulated cell growth and showed resistance to X-ray-induced DNA damage. Gene expression analysis of CCNDBP1-overexpressed cells and Ccndbp1 knockout mice revealed that Ccndbp1 activated the Atm–Chk2 pathway through the inhibition of Ezh2 expression, accounting for resistance to DNA damage. Our study demonstrated that by inhibiting EZH2, CCNDBP1 contributed to the activation of the ATM–CHK2 pathway to alleviate DNA damage, leading to chemoresistance