Tumor biomarkers: help or mislead in the diagnosis of xanthogranulomatous cholecystitis?-analysis of serum CA 19-9, carcinoembryonic antigen, and CA 12-5 / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Xanthogranulomatous cholecystitis (XGC) is a rare type of gallbladder inflammation. Unlike other cholecystitis, it can be easily misdiagnosed as gallbladder cancer based on radiological images. In response to misdiagnosis, extended surgical treatments are inappropriately given to patients, which is not beneficial to their health and/or recovery. In this study, we set out to determine whether tumor biomarkers can help to avoid misdiagnosis in patients with XGC.</p><p><b>METHODS</b>Between January 2005 and January 2012, a total of 37 preoperative patients at Sir Run Run Shaw Hospital were suspicious of having gallbladder cancer and was pathologically confirmed to be XGC after surgical operations. Before operations, all patients received a tumor biomarker test to verify diagnosis, which included serum CA 19-9, carcinoembryonic antigen (CEA), and CA 12-5.</p><p><b>RESULTS</b>A measured amount (54.05%) of cases (20 in 37) had at least one elevation over the thresholds of CA 19-9 (37 IU/L), CEA (5 ng/ml), and CA 12-5 (35 IU/L), which increased the suspicion of malignancy and consequently enhanced the difficulty to make right diagnosis of XGC as benign. 45.95% of cases (17 in 37) had an elevation in CA 19-9. 2.70% of cases (one in 37) had an elevation in CEA and 24.32% of cases (nine in 37) had an elevation in CA 12-5. Analysis with Fisher's exact test discovered that the presence of common bile duct stone was a contributor to elevations of CA19-9 in patients with XGC. However, even in cases without common bile duct stones, 42.86% of patients (nine in 21) had elevations of at least one tumor biomarker. Among them, 26.09% of patients (six in 21) had elevations of CA 19-9, with the maximum of 536.29 IU/L.</p><p><b>CONCLUSIONS</b>The elevations of tumor biomarkers in XGC were frequent, suggesting their inabilities to clarify the disease's nature, especially when there was a suspicion of gallbladder cancer. Intraoperative frozen pathology of gallbladder might be a possible solution. However, it is against the en bloc surgical principle and has the potential to cause tumor cell spreading. More research should be conducted, such as the discovery of a novel biomarker, so that XGC can less likely be misdiagnosed as malignancy until the final pathological judgment.</p>

Role of mitochondrial calcium uniporter in cardioprotection induced by ischemic postconditioning in isolated rat heart / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the role of mitochondrial calcium uniporter in cardioprotection elicited by ischemic postconditioning (Postcond).</p><p><b>METHODS</b>Male Sprague-Dawley rats were used for Langendorff isolated heart perfusion. The hearts subjected to global ischemia for 30 min followed by 120 min of reperfusion. Left ventricular developed pressure (LVDP), maximal rise/fall rate of left ventricular pressure (± dP/dtmax) were measured. The level of lactate dehydrogenase (LDH) in the coronary effluent was measured spectrophotometrically, the content of formazan of myocardium was also measured at the end of reperfusion.</p><p><b>RESULT</b>Compared to I/R group, Postcond had an significant increase in the mechanical function of the left ventricle, with LDH release reduced and the content of formazan increased. Spermine, the opener of mitochondrial calcium uniporter, deteriorated the mechanical function of left ventricle and decreased the formazan content, and increased LDH release. Ruthenium red, the inhibitor of mitochondrial calcium uniporter, increased the mechanical function of the left ventricle, decreased the LDH release, but the content of formazan was not increased.</p><p><b>CONCLUSION</b>The inhibition of mitochondrial calcium uniporter is involved in the mechanisms of ischemic postconditioning.</p>

Effect of gap junction on the cardioprotection of ischemic postconditioning in rat heart / 中国应用生理学杂志

<p><b>AIM</b>To determine whether the cardioprotection of ischemic postconditioning and heptanol in ischemic heart against ischemia/reperfusion (I/R) is mediated by gap junction.</p><p><b>METHODS</b>The effect of ischemic postconditioning, heptanol at different doses (0.03, 0.06, 0.30, and 0.60 mg/kg) and AAP10 (10 mg/kg) on the intact rat heart during 30 min ischemia and 2 h of reperfusion was observed. Ischemic postconditioning was achieved by 3 cycles of 10 s reperfusion/10 s regional ischemia starting at the beginning of the reperfusion. The infarct size and the arrhythmia scores were measured. The effect of ischemic postconditioning, heptanol at different doses (0.05, 0.10, 0.50 and 1.00 mmol/L) and AAP10 (1 x 10(-7)mol/L) on the isolated heart during 30 min ischemia and 2 h of reperfusion was observed. Ischemic postconditioning was achieved by 6 cycles of 10 s reperfusion/10 s global ischemia starting at the beginning of the reperfusion. The arrhythmia scores and conduction velocity of ventricle muscle were measured.</p><p><b>RESULTS</b>In the intact rat heart model, ischemic postconditioning and heptanol reduced infarct size and arrhythmia scores. In the Langendorff perfused rat heart model, ischemic postconditioning and heptanol reduced arrhythmia scores and conduction velocity of ventricle muscle. Administration of AAP10, an opener of gap junction attenuated the cardioprotection of ischemic postconditioning and heptanol.</p><p><b>CONCLUSION</b>The cardioprotection of ischemic postconditioning and heptanol may be related to the attenuation of gap junction communication on myocardiac ischemia/reperfusion injury.</p>