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The aim of the present study was to search for predictive and prognostic factors in patients with metastatic renal cell carcinoma (mRCC) treated with everolimus among the components of the WNT/beta-catenin pathway.

Patients and Methods

In a prospective, single-arm, phase II study, patients with mRCC received everolimus (10 mg/d) in a 30-day cycle. We performed a prospectively planned evaluation of the potential biomarkers of the WNT/beta-catenin pathway.


The serum level of soluble E-cadherin (sE-cadherin) in patients with RCC was significantly greater than that in the controls (71.62±22.28 pg/mL vs. 54.26±10.317 pg/mL; P =.0069). After 2 cycles of everolimus therapy, we observed a significance increase in sE-cadherin (from 71.81±21.18 pg/mL to 77.50±28.212 pg/mL; P =.0151). The Dickkopf-1 protein levels in the study and control groups were not significantly different (P=.2135). The favorable independent predictors for everolimus therapy were normal lactate dehydrogenase level before treatment (hazard ratio [HR], 0.52; 95% confidence interval [CI], 0.28-0.98; P =.0443) and low sE-cadherin level (HR, 0.54; 95% CI, 0.29-0.98; P =.0422). On multivariate analysis, we observed that worse overall survival was seen in patients with a lower regression coefficient of sE-cadherin after 2 cycles of treatment (HR, 2.60; 95% CI, 1.23-5.52; P =.0128), an increased corrected calcium level (HR, 3.09; 95% CI, 1.21-7.88; P = .0180), and an increased lactate dehydrogenase level before treatment (HR, 1.98; 95% CI, 1.02-3.83; P = .0426).


WNT/beta-catenin component expression in patients with mRCC had no effect on progression-free survival or overall survival. However, we found that the sE-cadherin level might interact with response to everolimus therapy, although confirmation in future studies is needed.


Even though cilostazol was assessed before in several models of atherosclerosis, so far its full systematic effect as a natural anti-inflammatory and anti-apoptotic mediator in the protection of liver damage and complication has not been fully clarified, which is the target of this study. For that purpose, we examined the protective effect of cilostazol (10 and 5 mg/kg, p.o. b.wt.) in an acute hepatic injury model by orally injecting it for 3 weeks prior to a single dose of TAA (300 mg/kg, i.p) injection. Ursodeoxycholic acid was used as a standard drug (50 mg/kg, p.o. b.wt.). After injection of thioacetamide by 48hr, rats were sacrificed. On the serum biochemical level, cilostazol ameliorated the thioacetamide consequence, where it presented a significant enhancement in the liver enzymes activities [Aspartate aminotransferase (AST) & Alanine aminotransferase (ALT)]. On the other hand, at the tissue level (Liver), it revealed a significant improvement in pro-inflammatory cytokines [Tumor necrosis factor alpha (TNF-alpha), Interleukin 1 beta (IL-1beta), Nuclear factor kappa B (NF-kB), NF-kB (P65/P50 nucleus translocation), caspase-3, cleaved caspase-3 & C-reactive protein (CRP)], redox level [Reduced glutathione (GSH) & Malondialdehyde (MDA)], histopathological findings, Reverse transcription polymerase chain reaction (RT-PCR) analysis (expression of TNF-alpha and NF-kB mRNA levels), and immunohistochemical reaction (caspase-3 & TNF-alpha). Obviously, the high dose of cilostazol (10 mg/kg, p.o. b.wt.) displayed a more pronounced effect than its lower one and nearly equal to ursodeoxycholic acid in the most of the parameters. These results give a new awareness into the hopeful molecular mechanisms by which cilostazol attenuates several factors participated in the progression of liver damage.


Diabetic nephropathy is the most common microvascular complications of diabetes. Berberine is the main active ingredient of Coptis chinensis and previous studies have been showed that berberine could delay the progression of diabetic nephropathy by regulating related cytokines and signaling pathways. Glomerular mesangial cells and podocytes are two vital indigenous cells of kidney and interaction between these two cellular components via exosomes might affect function of glomerulus in diabetic nephropathy condition. On the basis of our previous studies, transwell systems were used to demonstrate that the exosomes released by glomerular mesangial cells induced by the high glucose were involved in podocytes injury. The current study demonstrates that berberine can reduce TGFbeta1 in exosomes released by high glucose-induced glomerular mesangial cells. Berberine-treated high glucose-induced exosomes which are secreted by glomerular mesangial cells can protect damage of podocytes by reducing apoptosis and increasing adhesion. These results suggest that berberine could protect the function of podocytes through inhibiting the transfer of TGFbeta1 from the glomerular mesangial cells to the podocytes, which is one of the potential mechanisms of protective effect of berberine on diabetic nephropathy.


Perfluorododecanoic acid (PFDoA), a kind of perfluorinated carboxylic acid (PFCA) with 12 carbon atoms, has an extensive industrial utilization and is widespread in both wildlife and the water environment, and was reported to have the potential to cause a disruption in the thyroid hormone system homeostasis. In this study, zebrafish embryos/larvae were exposed to different concentrations of PFDoA (0, 0.24, 1.2, 6?mg/L) for 96?h post-fertilization (hpf). PFDoA exposure caused obvious growth restriction connected with the reduced thyroid hormones (THs) contents in zebrafish larvae, strengthening the interference effect on the growth of fish larvae. The transcriptional level of genes within the hypothalamic-pituitary-thyroid (HPT) axis was analyzed. The gene expression levels of thyrotropin-releasing hormone (trh) and corticotrophin-releasing hormone (crh) were upregulated upon exposure to 6?mg/L of PFDoA, and iodothyronine deiodinases (dio2) was upregulated in the 1.2?mg/L PFDoA group. The transcription of thyroglobulin (tg) and thyroid receptor (trβ) were significantly downregulated upon exposure to 1.2?mg/L and 6?mg/L of PFDoA. PFDoA could also decrease the levels of sodium/iodide symporter (nis) and transthyretin (ttr) gene expression in a concentration-dependent manner after exposure. A significant decrease in thyroid-stimulating hormone betA (tsh beta), uridinediphosphate-glucuronosyltransferase (ugt1ab) and thyroid receptor (tralpha) gene expression were observed at 6?mg/L PFDoA exposure. Upregulation and downregulation of iodothyronine deiodinases (dio1) gene expression were observed upon the treatment of 1.2?mg/L and 6?mg/L PFDoA, respectively. All the data demonstrated that gene expression in the HPT axis altered after different PFDoA treatment and the potential mechanisms of the disruption of thyroid status could occur at several steps in the process of synthesis, regulation, and action of thyroid hormones.



The hemostatic system cooperates with proteolytic degradation in processes allowing abdominal aortic aneurysm (AAA) formation. In previous studies, it has been suggested that aneurysm rupture depends on intraluminal thrombus (ILT) thickness, which varies across each individual aneurysm. We hypothesized that hemostatic components differentially accumulate in AAA tissue in relation to ILT thickness. Thick (A1) and thin (B1) segments of ILTs and aneurysm wall sections A (adjacent to A1) and B (adjacent to B1) from one aneurysm sac were taken from 35 patients undergoing elective repair.


Factor levels were measured using enzyme-linked immunosorbent assay of protein extract.


Tissue factor (TF) activities were significantly higher in thinner segments of AAA (B1 vs A1, P = .003; B vs A, P < .001; B vs A1, P < .001; B vs B1, P = .001). Significantly higher tissue plasminogen activator was found in thick thrombus-covered wall segments (A) than in B, A1, and B1 (P = .015, P < .001, and P < .001, respectively). Plasminogen concentrations were highest in ILT. Concentrations of α2-antiplasmin in thin ILT adjacent walls (B) were higher compared with wall (A) adjacent to thick ILT (P = .021) and thick ILT (A1; P < .001). Significant correlations between levels of different factors were mostly found in thick ILT (A1). However, no correlations were found at B sites, except for a correlation between plasmin and TF activities (r = 0.55; P = .004).


These results suggest that higher TF activities are present in thinner AAA regions. These parameters and local fibrinolysis may be part of the processes leading to destruction of the aneurysm wall.

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