Abernathywelsh2321

lncRNA MALAT1 was a "molecular sponge" of miR-503, regulating the expression of TLR4 and the proliferation, migration, and apoptosis of hPASMCs through miR-503. CONCLUSIONS lncRNA MALAT1 promotes the proliferation and migration of hPASMCs and inhibits their apoptosis by inhibiting the miR-503/TLR4 signal axis.BACKGROUND Pulmonary vein thrombosis (PVT) is a rare clinical entity. Etiologies include malignancy, hyper-viscosity syndromes, and other etiologies. Patients may present with dyspnea, cough, or hemoptysis. CASE REPORT We present a case of a 64-year-old man with a history of metastatic lung cancer diagnosed with PVT through transesophageal echocardiography (TEE) and complicated by 2 cerebrovascular accidents. The patient had a complicated hospital course and died later due to his malignancy burden and overall condition, despite anticoagulation therapy. CONCLUSIONS Patients with PVT are often asymptomatic or may have a nonspecific clinical presentation. Anticoagulation should be considered in patients with PVT given the life-threatening complications such as peripheral embolization. More research is needed to address this potentially catastrophic finding.BACKGROUND Although advances have been achieved in the therapy of clear cell renal cell carcinoma (ccRCC), the pathogenesis of ccRCC is not yet fully understood. This study aimed to explore the critical genes and pathways associated with ccRCC by meta-analysis. MATERIAL AND METHODS We performed an integrated analysis of 3 publicly available microarray datasets developed from ccRCC tumor samples and normal tissues. A list of overlapped differentially expressed genes (DEGs) with the consistent expression trend in ccRCC tumor samples were identified, for which the protein-protein interaction (PPI) network was constructed, followed by topology structure and module analysis. The microRNA (miRNA) regulatory network and ccRCC associated pathway network were reconstructed. RESULTS A total of 504 genes were found to be consistently and differentially regulated based on 3 microarray datasets. The overrepresented pathways for DEGs included citric acid cycle (TCA cycle) and peroxisome proliferator-activated receptor (PPAR) signaling pathway and cell cycle. The PPI network was clustered into 6 modules that were closely related with the M phase, desmosome assembly, and response to hormone stimulus. The hsa04110 cell cycle and hsa04510 focal adhesion were the significant pathways associated with ccRCC overlapped with enrichment analysis. KDR and ITGB4 were focal-adhesion-associated genes, which were regulated by has-miR-424 and has-miR-204, respectively. CCND2 and CCNA2 were cell-cycle-associated genes, which were regulated by hsa-miR-324-3p, hsa-miR-146a and hsa-miR-145. CONCLUSIONS Cell cycle and focal adhesion were dysregulated in ccRCC, which were associated with the expression of CCND2, ITGB4, KDR, and CCNA2 genes. The deregulation of pathways and associated genes may provide insights to ccRCC research and therapy.

Kallistatin and ENOX1 are regulators of inflammation and oxidative stress which are typical pathological reactions in atherosclerosis. However, there is limited information of kallistatin and ENOX1 in CHD.

50 healthy controls, 56 SAP patients and 47 ACS patients were included in this study. Kallistatin and ENOX1 in serum were measured by ELISA. Chi-square test was performed to analyze categorical data. ANOVA, Pearson correlation analysis, and multiple linear regression were performed to analyze the numerical data. Finally, ROC curve was applied to assess the diagnostic value of kallistatin in CHD.

Among the 153 participants, 59.5% were male and the average age was 63.8±11.39 years. Compared with the control group, kallistatin expression was decreased in SAP group and ACS group while ENOX1 expression was increased in ACS group (P<0.05). Pearson correlation analysis showed that kallistatin level was negatively correlated with gensini score (r=-0.210, P<0.01), WBC (r=-0.283, P<0.001) and triglyceride (r=-0.242, P<0.01), and positively correlated with age (r=0.353, P<0.001), and HDL-C (r=0.310, P<0.001). ENOX1 expression was positively correlated with WBC (r=0.244, P<0.01), INR (r=0.177, P<0.05), and gensini score (r=0.201, P<0.05). Multiple linear regression showed that creatinine, ALT, glucose and kallistatin are independent predictors for gensini score. Kallistatin had the highest diagnostic significance (P=0.007) when the AUC was 0.636, with a sensitivity of 0.735 and a specificity of 0.495.

Expression of kallistatin was decreased in CHD patients and ENOX1 was increased in ACS patients. Kallistatin and ENOX1 were closely connected with the severity of CHD and kallistatin may be helpful in the diagnosis of CHD.

Expression of kallistatin was decreased in CHD patients and ENOX1 was increased in ACS patients. Kallistatin and ENOX1 were closely connected with the severity of CHD and kallistatin may be helpful in the diagnosis of CHD.

Functional hepatic reserve is important when considering sequential tyrosine kinase inhibitor (TKI) therapy for patients with advanced hepatocellular carcinoma (HCC). We assessed albumin-bilirubin (ALBI) score and Child-Pugh class as indices of liver function during sorafenib and lenvatinib treatment.

A total of 212 patients with advanced HCC and Child-Pugh class A status who initiated TKI treatment at our hospital were enrolled in this retrospective cohort study. A total of 74 of the 212 patients underwent blood testing before starting sorafenib treatment and every 2 months after treatment initiation.

In 74 patients, the median ALBI score before TKI treatment was -2.53, and after 2, 4, and 6 months it was -2.45, -2.44, and -2.36, respectively. ALBI scores tended to increase during TKI therapy. Among patients who experienced a time to progression ≤3.8 months, ALBI scores had increased 2 months after treatment initiation, and at 4 and 6 months, significant differences were observed (p < 0.01). In all 212 patients, during first-line TKI treatment, the Child-Pugh class deteriorated to B or C in 72.2% of the patients, and the median time to deterioration was 3.9 months. The factors in hepatic reserve deterioration were serum albumin ≤3.8 g/dL and the presence of macroscopic vascular invasion. The hepatic reserve of 68.0% of the patients with deterioration of liver function recovered to Child-Pugh class A following dose reduction, drug withdrawal, or treatment intended for recovery of liver function.

ALBI scores deteriorate in patients treated with TKIs, suggesting that tumor progression induces these changes.

ALBI scores deteriorate in patients treated with TKIs, suggesting that tumor progression induces these changes.

The aim of this study was to characterize clinical features, etiologies, and mechanisms of strokes due to bilateral middle cerebellar peduncle infarction (BMCPI).

Cases diagnosed as BMCPI in our hospital were retrieved, and a literature review was performed. Data on clinical features and brain MRI were obtained. Extracranial and intracranial segments of the vertebrobasilar artery were assessed by using digital subtraction angiography, magnetic resonance angiography, or computed tomography angiography.

Thirteen cases (11 men and 2 women) of BMCPI were identified. A high-intensity signal of diffusion-weighted imaging sequence involving the bilateral middle cerebellar peduncle was observed in all patients. Most patients experienced vertigo, dysarthria, ataxia, and hearing disorders. Eleven of these cases were classified as large artery atherosclerosis, one as traumatic vertebral artery (VA) dissection, and one as giant cell arteritis.

BMCPI is a rare cerebrovascular disease characterized by vertigo, ataxia, and dysarthria, which may also be accompanied by a hearing deficit or clinical signs of brainstem damage. BMCPI may be associated with hypoperfusion secondary to occlusive disease of the bilateral VA or proximal basilar artery.

BMCPI is a rare cerebrovascular disease characterized by vertigo, ataxia, and dysarthria, which may also be accompanied by a hearing deficit or clinical signs of brainstem damage. BMCPI may be associated with hypoperfusion secondary to occlusive disease of the bilateral VA or proximal basilar artery.

Calcium loading has been associated with cardiovascular risk in hemodialysis (HD) patients. However, it remains to be elucidated whether alterations of intradialytic calcium buffering add to the increased cardiovascular disease burden in this high-risk population.

Intradialytic calcium kinetics was evaluated in a cross-sectional observational study by measuring dialysate-sided ionized calcium mass balance (iCaMB), calcium buffer capacity, and change in serum calcium levels in 40 chronic HD patients during a routine HD session. A dialysate calcium of 3.5 mEq/L was used to adequately challenge calcium buffer mechanisms. Aortic pulse wave velocity and serum osteocalcin levels were measured prior to the HD session. Presence of cardiovascular disease and diabetes was assessed.

The mean dialysate-sided iCaMB, extracellular fluid ionized calcium mass gain, and buffered ionized calcium mass were 469 (±154), 111 (±49), and 358 (±145) mg/HD, respectively. The mean ionized serum calcium increase (∆iCa) was 0.42 (±e for evaluating the prognostic potential of intradialytic calcium kinetics in prospective clinical trials.

Glycogen storage disease Type III (GSD III) is an autosomal recessive disease caused by the deficiency of glycogen debranching enzyme, encoded by the AGL gene. Two clinical types of the disease are most prevalent GSD IIIa involves the liver and muscle, whereas IIIb affects only the liver. The classical dietetic management of GSD IIIa involves prevention of fasting, frequent feeds with high complex carbohydrates in small children, and a low-carb-high-protein diet in older children and adults. Recently, diets containing high amount of fat, including ketogenic and modified Atkins diet (MAD), have been suggested to have favorable outcome in GSD IIIa.

Six patients, aged 3-31 years, with GSD IIIa received MAD for a duration of 3-7 months. Serum glucose, transaminases, creatine kinase (CK) levels, capillary ketone levels, and cardiac parameters were followed-up.

In all patients, transaminase levels dropped in response to MAD. Decrease in CK levels were detected in 5 out of 6 patients. Hypoglycemia was evident in 2 patients but was resolved by adding uncooked cornstarch to diet.

Our study demonstrates that GSD IIIa may benefit from MAD both clinically and biochemically.

Our study demonstrates that GSD IIIa may benefit from MAD both clinically and biochemically.

To analyze decision-making in patients with male urinary incontinence (SUI) in centers of expertise. The artificial urinary sphincter (AUS) remains the gold standard for male patients with moderate to severe SUI but adjustable male slings are a minimally invasive treatment option with good results, hence without a high level of evidence regarding the optimal patient selection.

In total, 220 patients (88 AUS; 132 adjustable slings) were investigated from the DOMINO database that underwent surgery between 2010 and 2012 in 5 urological departments that offer adjustable sling systems as well as AUS systems for patients with moderate to severe urinary incontinence. For statistical analysis, the Mann-Whitney U test was used to identify differences between both groups.

Patients selected for an adjustable male sling were less likely to have a neurological disease (5.3 vs. 9.1%; p = 0.030), a prior urethral stricture (22.7 vs. 50.0%; p = 0.001), a prior incontinence surgery (24.4 vs. 45.5%; p = 0.01), or a prior radiation therapy (26.