Genome-wide analysis to predict protein sequence variations that change phosphorylation sites or their corresponding kinases

We define phosphovariants as genetic variations that change phosphorylation sites or their interacting kinases. Considering the essential role of phosphorylation in protein functions, it is highly likely that phosphovariants change protein functions and may constitute a proportion of the mechanisms by which genetic variations cause individual differences or diseases. We categorized phosphovariants into three subtypes and developed a system that predicts them. Our method can be used to screen important polymorphisms and help to identify the mechanisms of genetic diseases

Acute Cerebral Infarction Following Intravenous Glycoprotein IIb/IIIa Inhibitor for Acute Myocardial Infarction

Stroke is a rare but serious complication of acute myocardial infarction (AMI). Currently, glycoprotein (GP) IIb/IIIa inhibitor is used in clinical practice for acute coronary syndromes and percutaneous coronary interventions (PCIs). The incidence of stroke in patients receiving GP IIb/IIIa inhibitor during PCIs is very low. We report the case of a 47-year-old man who presented with AMI and suffered an acute cerebral infarction after infusion of a GP IIb/IIIa inhibitor following primary PCI

Idiopathic erythrocytosis in a patient on chronic hemodialysis

AbstractA 78-year-old man on hemodialysis presented to our hospital with erythrocytosis. He had started hemodialysis 4 years previously, with a hemoglobin level of 9.8g/dL, and was administered erythropoiesis stimulating agents and ferrous sulfate. Two years previously, his hemoglobin level increased to 14.5g/dL and the treatment for anemia was discontinued. He continued hemodialysis thrice weekly; however, the hemoglobin level had increased to 17.0g/dL at the time of presenting to our hospital. His serum erythropoietin level was 31.4mIU/mL (range, 3.7–31.5mIU/mL), carboxyhemoglobin level was 0.6% (range, 0–1.5%), and oxygen saturation in ambient air was 95.4%. The JAK2 V617F mutation was not observed and other bone marrow abnormalities were not identified. The patient was diagnosed with bladder cancer and a transurethral resection was performed. Eight months after the treatment of bladder cancer, his hemoglobin level was 15.1g/dL, and he was diagnosed with idiopathic erythrocytosis

Tissue Plasminogen Activator and Plasminogen Activator Inhibitor-1 Levels in Patients with Acute Paraquat Intoxication

To investigate the effects of reactive oxygen species (ROS) on tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) plasma levels, and their possible implications on clinical outcome, we measured tPA and PAI-1 levels in 101 patients with acute paraquat (PQ) intoxication. The control group consisted of patients who ingested non-PQ pesticides during the same period. tPA and PAI-1 levels were higher in the PQ group than in the controls. PQ levels were significantly correlated with ingested amount, timelag to hospital, tPA level, and hospitalization duration. tPA levels were correlated with PAI-1, fibrin degradation product (FDP), and D-dimer. D-dimer levels were lower in the PQ group than in the controls. Univariate analysis indicated the following significant determinants of death: age, ingested amount, PQ level, timelag to hospital, serum creatinine, lipase, pH, pCO2, HCO3-, WBC, FDP, PAI-1, and tPA. However, multivariate analysis indicated that only PQ level was significant independent factor predicting death. In conclusion, tPA and PAI-1 levels were higher, while D-dimer levels were lower in the PQ group than in the controls, implying that ROS stimulate tPA and PAI-1, but PAI-1 activity overrides tPA activity in this setting. Decreased fibrinolytic activity appears to be one of the clinical characteristics of acute PQ intoxication

Usefulness of fusion images of unenhanced and contrast-enhanced arterial phase cone-beam CT in the detection of viable hepatocellular carcinoma during transarterial chemoembolization

PURPOSE:We aimed to evaluate the diagnostic efficacy of fusion imaging of unenhanced and arterial phase contrast-enhanced cone-beam computed tomography (CBCT) by comparing with multidetector computed tomography (MDCT) in detection of viable hepatocellular carcinoma (HCC) in patients who have been previously treated with transarterial chemoembolization (TACE).METHODS:In this retrospective study, a total of 173 tumors in 33 known HCC patients (21 men, 12 women; mean age, 64±7.6 years; mean tumor size, 2.15±1.70 cm) who had been previously treated with TACE and underwent additional session of TACE were included. The sensitivity and positive predictive values of preprocedural MDCT and fusion CBCT for detection of viable tumor were analyzed with follow-up MDCT images performed 3-4 weeks after TACE, as reference standard.RESULTS:A total of 141 remote and 32 marginal viable tumors were included. The sensitivities for detection of remote, marginal, and total viable tumors were 80.9%, 68.8%, and 78.6% for MDCT and 96.5%, 96.9%, and 96.5% for fusion CBCT, respectively. The positive predictive values for detection of remote, marginal, and total viable tumors were 95.0%, 78.6%, and 95.8% for MDCT, and 97.1%, 88.6%, and 97.7% for fusion CBCT, respectively. Fusion CBCT showed statistically higher sensitivity and positive predictive value for detection of viable tumors (P < 0.001).CONCLUSION:The diagnostic performance of fusion imaging of unenhanced and contrast-enhanced arterial phase CBCT was superior to MDCT for detection of viable HCCs

Deficiency of peroxiredoxin 2 exacerbates angiotensin II-induced abdominal aortic aneurysm

Abdominal aortic aneurysm: Potential enzyme biomarker identified An enzyme with antioxidant properties may provide a biomarker and therapeutic agent to help treat abdominal aortic aneurysm (AAA). AAA involves the structural deterioration of the aorta through chronic inflammation and oxidative stress, and can trigger life-threatening artery rupture. An antioxidant enzyme called peroxiredoxin 2 (PRDX2) is increased in patients with ruptures, but whether its role in AAA is beneficial or detrimental is unclear. Goo Taeg Oh at the Ewha Womans University in Seoul, Jong-Gil Park at the Korea Research Institute of Bioscience and Biotechnology, Daejeon, South Korea, and co-workers examined the effect of PRDX2 on AAA progression. PRDX2 suppressed structural damage in mice, limiting artery dilation and protein degradation. Loss of PRDX2 accelerated AAA development. Measuring levels of PRDX2 may indicate AAA severity in patients, while boosting the enzyme could repair aortic damage