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Abstract
Introduction
Cadherin family proteins are involved in the tumorigenesis of several malignancies. However, their significance in renal cell carcinoma (RCC) has not been extensively investigated. The current study investigates the potential of several cadherins to perform as biomarkers for tumor detection and exert functional RCC activity.

Methods
Pre- and postoperative concentrations of sE-cadherin, cadherin-6, N-cadherin, cadherin-11, cadherin-17, and cadherin-5 were measured in serum of patients undergoing surgery for RCC and correlated to clinical and histopathological parameters. Control serum was obtained from healthy volunteers. A498 and Caki-1 cells were incubated with sE-cadherin and assessed for cell growth, adhesion, and chemotaxis.

Results
sE-cadherin was significantly upregulated in RCC patients, as compared to controls, and discriminated them with striking accuracy (area under the curve value 0.83). Serum levels remained stable several days after surgery. Treating A498 and Caki-1 cancer cells with various concentrations of sE-cadherin attenuated cell growth and adhesion, while chemotaxis was augmented.

Conclusions
sE-cadherin is overexpressed in serum of RCC patients and provides a functional cellular switch from sessility to aggressive dissemination. While sE-cadherin is not tumor-specific and thus inappropriate for population-based screening, further studies are warranted to investigate its role in monitoring RCC and employing it as a therapeutic target.

Abstract
The presence of trace levels of pharmaceuticals is an emerging issue impacting the aquatic ecosystem. Naproxen (NPX) is a nonsteroidal anti-inflammatory drug (NSAID) that has been frequently detected in aquatic environments worldwide. Recently, concerns regarding endocrine disruption by NSAIDs have increased; however, their effects on the thyroid system have yet to be understood. In this study, zebrafish were utilized to evaluate the thyroid-disrupting effects of NPX. After a 60-day exposure to various concentrations of NPX (0.1, 1, 10 and 100?μg/L), the body length and weight of the zebrafish were significantly decreased. The decrease of cytochrome P450 gene expression and enzyme activity might inhibit the metabolism of NPX, which might result in the significant bioconcentration in zebrafish. Thyroid hormone (TH) analysis showed that both triiodothyronine (T3) and thyroxine (T4) levels were substantially decreased. Gene transcription expressions along the hypothalamic-pituitary-thyroid (HPT) axis were also markedly affected. Significant downregulation of dio1, dio2, nis, nkx2.1, pax8, tg, tpo, trβ and ttr levels, along with the stimulation of the tshβ gene, were also observed in exposed fish compared to controls. Western blot analysis indicated that expression of the TTR protein was significantly decreased, which coincides with the results of the gene expression analysis. Collectively, our observations show that NPX increases the risk of bioconcentration and thyroid disruption in zebrafish. Given the continued increasing consumption and emission of pharmaceuticals, thyroid disruption should be considered when assessing the aquatic risk of long-term exposure to environmentally relevant concentrations of pharmaceuticals.

Tetramethylpyrazine (TMP) protects rats against acute pancreatitis through NF-κB pathway

Posted by Ly Chen, Yj Chen, H Yun, et al. on 2019-05-26 20:13:00

ABSTRACT
Acute pancreatitis (AP) is a digestive disease characterized by pancreatic inflammation. Tetramethylpyrazine (TMP) has been effectively used to ameliorate the damage on intestinal mucosa injury in rats with acute necrotizing pancreatitis (ANP). We aim to study the protective effect of TMP on caerulein-induced AP and to explore the possible mechanism. The mice randomized into control and different experimental groups. AP was induced in mice by 6-hourly intraperitoneal (i.p) injections of caerulein (50?μg/kg at 1?h interval). TMP (i.p, 10?mg/kg, 1?h interval) was administered 3 h before caerulein injection. Administration of TMP attenuated the severity of AP as shown by the histopathology, reduced serum amylase activity and pro-inflammatory cytokines TNF-α and IL-6. Further, TMP enhances the beneficial effect by reducing caerulein-induced NF-κB activation and inducing cell apoptosis in pancreas. Therefore, inhibition of nuclear factor-kappa B(NF-κB) signals by TMP represents a potential therapeutic strategy for the treatment of acute pancreatitis.

interleukin-31 promotes helper t cell type-2 inflmmation in children with allergic rhinitis

Posted by Wenlong L, Renzhong L, Yanqiu C, et al. on 2015-01-13 17:05:00

Background:

Interleukin-31 (IL-31) is a recently described cytokine that is involved in helper T cell type-2 (Th2)-mediated diseases. However, its regulatory effect in the pathogenesis of children allergic rhinitis (AR) needs to be further characterized. This study sought to evaluate the expression and role of IL-31 in children with AR.

Methods:

Sixty children with AR and 20 normal controls were included. IL-31 and Th2 cytokines production in tissue, serum, and nasal lavage was examined by immunohistochemistry, quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay, respectively. Peripheral blood mononuclear cells (PBMCs) were purified for in vitro regulation experiment of IL-31. Nasal epithelial cells (NECs) were cultured and stimulated by recombinant IL-31.

Results:

The IL-31 mRNA and protein levels in both serum and nasal lavage were significantly enhanced in AR compared with normal controls, especially in children with asthma. The nasal IL-31 was associated with enhanced local Th2 cytokines and mucin 5AC (MUC5AC) expression. In vitro study showed that IL-31 promotes Th2 cytokines expression and MUC5AC upregulation and thus amplified Th2 inflammation.

Conclusion:

Our results demonstrate that IL-31 expression in AR aggravated and amplified Th2 inflammation as well as mucin production, and provide a possible explanation for IL-31’s regulatory role in the pathogenesis of AR.


Abstract

 

Intermittent hypoxic training (IHT) is a discrete cost-effective method for improving athletic performance and high altitude acclimatization. Unfortunately, IHT protocols widely vary in terms of hypoxia severity, duration, and number of cycles affecting physiological outcomes. In the present study, we evaluated the efficacy of a moderate normobaric IHT protocol (12% FiO2 for 4 h, 4 days) on acclimatization to high altitude (3250 m). Global plasma proteomics studies revealed that IHT elicited acute-phase response proteins like C-reactive protein (CRP), serum amyloid A-1 protein (SAA), and alpha-1-acid glycoprotein 2 (AGP 2) as well as altered levels of several apolipoproteins. On subsequent exposure to high altitude, the IH trained volunteers exhibited significant higher arterial oxygen saturation with concomitant lower incidences of acute mountain sickness (AMS) as compared to controls. Interestingly, IH trained subjects exhibited lower levels of positive acute-phase proteins like C-reactive protein (CRP), serum amyloid A-1 protein (SAA), and fibrinogen (FGA, FGB, and FGG) both after days 4 and 7 of high altitude ascent. High altitude exposure also decreased the levels of HDL, LDL, and associated proteins as well as key enzymes for assembly and maturation of lipoprotein particles like lecithin-cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP), and phospholipid transfer protein (PLTP). In contrast, IHT curtailed hypoxia-induced alterations of HDL, LDL, Apo-AI, Apo-B, LCAT, CETP, and PLTP. Further validation of results also corroborated attenuation of hypoxia-induced inflammation and dyslipidemia by IHT. These results provide molecular evidences supporting the use of moderate IHT as a potential non-pharmacological strategy for high altitude acclimatization.

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