Relationship of heat shock protein and heat stress in broilers.

Due to advances in breeding and nutrition, modern broiler chicken reaches a satisfactory growth performance in a short time because fast growing breeders are showing a more rapidly metabolism, however, the ability to regulate body temperature still remain inefficient under high environment temperatures (above 35°C) and humidity. In this case, cells promote a stress response that allows the expression of heat shock proteins (HSPs) witches has the prime molecular function as chaperones, protecting cells against the damages caused by free radicals produced during stress situations. When animals are exposed to stress in early life (pre-embryogenesis) the HSP70 gene is activated and the protein is expressed and synthesized more quickly when the chicken are exposed later in life to high environment temperature, became thermo resistance. Besides the environment (temperature and humidity) other factors such as genetics, nutrition and health, also predispose stress in chickens during production period. However, if all conditions of welfare were respected, the probability of a stress exposure is reduced in lower level. As final physiologic consequence of heat stress exposure, it can be observed a glycogen muscle depletion during slaughtering, affecting post mortem reactions that contributes to meat quality. This condition has been related to a lower pH, with a reduction in capacity of water retention, and a decrease in meat tenderness, favoring the formation of meat type PSE (pale, soft and exudative), which is not pleasing to the consumer. So, animals with heat tolerance are more resistant to high environment temperatures, reducing mortality of a considering part of the lot. According to described above, this review article will related some issues related to termic stress response of broilers emphasized HSPs contribution for a better meat quality as final product to attend costumer and market demands.Devido aos avanços em melhoramento genético e nutrição, o frango de corte atual atinge elevados índices de desempenho produtivo em um curto período de produção, resultado de um aumento nas taxas metabólicas das linhagens de crescimento rápido. Entretanto, sua capacidade termorreguladora permanece ineficiente, principalmente sob condições de altas temperaturas (acima de 35°C) e umidade. Por conseqüência, as células respondem ao estresse pela expressão das proteínas de choque térmico ou heat shock proteins (HSPs), as quais funcionam como chaperonas moleculares, protegendo as membranas contra os radicais livres formados em situações de estresse. A exposição dos animais ao estresse no início da vida (pré-embriogenese) permitiria que o gene que regula a síntese de HSP70 seja sensibilizado favorecendo uma rápida expressão e síntese desta proteína em situações de estresse térmico, tornando o animal ter-morresistente a temperaturas elevadas. Além do ambiente (temperatura e umidade) outros fatores como, genética, nutrição e sanidade, também predispõem ao estresse do frango durante sua produção. Porém, se respeitadas as condições ambientais exigidas por estes animais, a exposição ao estresse será reduzida. Como conseqüência final da resposta fisiológica a um estresse térmico, observa-se a depleção das reservas de glicogênio muscular no momento do abate, prejudicando as reações post mortem que con-tribuem para a qualidade de carne. Esta condição tem sido relacionada principalmente a um pH ácido, com redução da capacidade de retenção de água e diminuição da maciez da carne, favorecendo a formação da carne tipo PSE (pálida, mole e exsudativa), recusada pelo consumidor. Por isso os animais termotolerantes são mais resistentes, o que reduz o índice de mortalidade do lote. Desta forma, o presente artigo de revisão propõe-se esclarecer aspectos relacionados aos mecanismos envolvidos na resposta ao estresse térmico por calor em frangos de corte, enfatizando a contribuição das HSPs em tal situação contribuindo para a produção de uma carne de melhor qualidade e adequada aos padrões exigidos pelo mercado consumidor

Absence of Morphotropic Phase Boundary Effects in BiFeO3-PbTiO3 Thin Films Grown via a Chemical Multilayer Deposition Method

Here, we report the unusual behaviour shown by the (BiFeO3)1-x-(PbTiO3)x (BF-xPT) films prepared using a multilayer deposition approach by chemical solution deposition method. Thin film samples of various compositions were prepared by depositing several bilayers of BF and PT precursors by varying the BF or PT layer thicknesses. X-ray diffraction showed that final samples of all compositions show mixing of the two compounds resulting in a single phase mixture, also confirmed by transmission electron microscopy. In contrast to bulk equilibrium compositions, our samples show a monoclinic (MA type) structure suggesting disappearance of morphotropic phase boundary (MPB) about x = 0.30 as observed in the bulk. This is accompanied by the lack of any enhancement of remnant polarization at MPB as shown by the ferroelectric measurements. Magnetic measurements show that the magnetization of the samples increases with increasing BF content. Significant magnetization of the samples indicates melting of spin spirals in the BF-xPT arising from random distribution of iron atoms across the film. Absence of Fe2+ ions in the films was corroborated by X-ray photoelectron spectroscopy measurements. The results illustrate that used thin film processing methodology significantly changes the structural evolution in contrast to predictions from the equilibrium phase diagram as well as modify the functional characteristics of BP-xPT system dramatically.Comment: 15 pages, 6 figure

F-MRI in the evaluation of motor activation in patients with multiple sclerosis and fatigue

22nd European Congress of Radiology - Vienna 4-8 marzo 201

Modernity and the cities of the Jews

Collection of articles devoted to Modernity and Jewish diaspora. Urban history and Jew

Effect of guanylin peptides on pancreas steatosis and function in experimental diet-induced obesity and after bariatric surgery

Introduction: Obesity contributes to ectopic fat deposition in non-adipose organs, including the pancreas. Pancreas steatosis associates with inflammation and beta-cell dysfunction, contributing to the onset of insulin resistance and type 2 diabetes. An improvement of pancreatic steatosis and indices of insulin resistance is observed following bariatric surgery, but the underlying mechanisms remain unknown. We sought to analyze whether guanylin (GUCA2A) and uroguanylin (GUCA2B), two gut hormones involved in the regulation of satiety, food preference and adiposity, are involved in the amelioration of pancreas fat accumulation after bariatric surgery. Methods: Pancreas steatosis, inflammation, islet number and area were measured in male Wistar rats with diet-induced obesity (n=125) subjected to surgical (sham operation and sleeve gastrectomy) or dietary (pair-fed to the amount of food eaten by gastrectomized animals) interventions. The tissue distribution of guanylate cyclase C (GUCY2C) and the expression of the guanylin system were evaluated in rat pancreata by real-time PCR, Western-blot and immunohistochemistry. The effect of guanylin and uroguanylin on factors involved in insulin secretion and lipogenesis was determined in vitro in RIN-m5F beta-cells exposed to lipotoxic conditions. Results: Sleeve gastrectomy reduced pancreas steatosis and inflammation and improved insulin sensitivity and synthesis. An upregulation of GUCA2A and GUCY2C, but not GUCA2B, was observed in pancreata from rats with dietinduced obesity one month after sleeve gastrectomy. Interestingly, both guanylin and uroguanylin diminished the lipotoxicity in palmitate-treated RIN-m5F beta-cells, evidenced by lower steatosis and downregulated lipogenic factors Srebf1, Mogat2 and Dgat1. Both guanylin peptides reduced insulin synthesis (Ins1 and Ins2) and release from RIN-m5F beta-cells, but only guanylin upregulated Wnt4, a factor that controls beta-cell proliferation and function. Discussion: Together, sleeve gastrectomy reduced pancreatic steatosis and improved beta-cell function. Several mechanisms, including the modulation of inflammation and lipogenesis as well as the upregulation of GUCA2A in the pancreas, might explain this beneficial effect of bariatric surgery

Increased expression levels of netrin-1 in visceral adipose tissue during obesity favour colon cancer cell migration

Simple Summary Netrin-1 (NTN-1) regulates obesity-associated low-grade inflammation, being also involved in the control of cell migration and proliferation. We aim to study whether excess visceral adipose tissue in patients with obesity and colon cancer is associated with increased NTN1 and the expression levels of its main receptors, promoting an inflammatory microenvironment that favours colon cancer development. Increased expression levels of NTN1 and its receptor NEO1 in the visceral adipose tissue from patients with obesity and colon cancer together with elevated DCC and UNC5B mRNA levels in patients with colon cancer were found. Moreover, the treatment of colorectal cancer cells with NTN-1 and with the adipocyte-derived secretome obtained from patients with obesity increased the migration of colorectal cancer cells. These results suggest that NTN-1 plays an important role in obesity-associated colon cancer development. Netrin (NTN)-1, an extracellular matrix protein with a crucial role in inflammation, is dysregulated during obesity (OB) and influences colon cancer (CC) progression. To decipher the mechanisms underlying CC development during obesity, we examined the expression of NTN1 and its receptors in the visceral adipose tissue (VAT) of 74 (25 normal weight (NW)) (16 with CC) and 49 patients with OB (12 with CC). We also evaluated the effect of caloric restriction (CR) on the gene expression levels of Ntn1 and its receptors in the colon from a rat model fed a normal diet. The impact of adipocyte-conditioned media (ACM) from patients with OB and NTN-1 was assessed on the expression levels of neogenin 1(NEO1), deleted in colorectal carcinomas (DCC) and uncoordinated-5 homolog B (UNC5B) in Caco-2 and HT-29 human colorectal cell lines, as well as on Caco-2 cell migration. Increased NTN1 and NEO1 mRNA levels in VAT were due to OB (p < 0.05) and CC (p < 0.001). In addition, an upregulation in the expression levels of DCC and UNC5B in patients with CC (p < 0.01 and p < 0.05, respectively) was observed. Decreased (p < 0.01) Ntn1 levels in the colon from rats submitted to CR were found. In vitro experiments showed that ACM increased DCC (p < 0.05) and NEO1 (p < 0.01) mRNA levels in HT-29 and Caco-2 cell lines, respectively, while UNC5B decreased (p < 0.01) in HT-29. The treatment with NTN-1 increased (p < 0.05) NEO1 mRNA levels in HT-29 cells and DCC (p < 0.05) in both cell lines. Finally, we revealed a potent migratory effect of ACM and NTN-1 on Caco-2 cells. Collectively, these findings point to increased NTN-1 during OB and CC fuelling cancer progression and exerting a strong migratory effect on colon cancer cells

Uroguanylin prevents hepatic steatosis, mitochondrial dysfunction and fibrosis in obesity-associated NAFLD

Background: The biological mediators supporting the resolution of liver steatosis, inflammation and fibrosis after bariatric surgery in patients with obesity and NAFLD remain unclear. We sought to analyze whether uroguanylin and guanylin, two gut hormones involved in the regulation of satiety, food preference and adiposity, are involved in the amelioration of obesity-associated NAFLD after bariatric surgery. Methods: Proguanylin (GUCA2A) and prouroguanylin (GUCA2B) were measured in 214 participants undergoing bariatric surgery with biopsy-proven NAFLD diagnosis. Pathways involved in lipid metabolism, mitochondrial network and fibrogenesis were evaluated in liver biopsies (n = 137). The effect of guanylin and uroguanylin on these metabolic functions was assessed in HepG2 hepatocytes and LX-2 hepatic stellate cells (HSC) under lipotoxic and profibrogenic conditions. Results: Plasma and hepatic expression of GUCA2B were decreased in obesity-associated NAFLD. Both GUCA2A and GUCA2B levels were increased after sleeve gastrectomy and Roux-en-Y gastric bypass in parallel to the improved liver function. The liver of patients with type 2 diabetes showed impaired mitochondrial β-oxidation, biogenesis, dynamics as well as increased fibrosis. Uroguanylin diminished the lipotoxicity in palmitate-treated HepG2 hepatocytes, evidenced by decresased steatosis and lipogenic factors, as well as increased mitochondrial network expression, AMPK-induced β-oxidation and oxygen consumption rate. Additionally, uroguanylin, but not guanylin, reversed HSC myofibroblast transdifferentiation as well as fibrogenesis after TGF-β1 stimulation. Conclusions: Uroguanylin constitutes a protective factor against lipotoxicity, mitochondrial dysfunction and fibrosis. Increased GUCA2B levels might contribute to improve liver injury in patients with obesity-associated NAFLD after bariatric surgery

Uroguanylin prevents hepatic steatosis, mitochondrial dysfunction and fibrosis in obesity-associated NAFLD

Background: The biological mediators supporting the resolution of liver steatosis, inflammation and fibrosis after bariatric surgery in patients with obesity and NAFLD remain unclear. We sought to analyze whether uroguanylin and guanylin, two gut hormones involved in the regulation of satiety, food preference and adiposity, are involved in the amelioration of obesity-associated NAFLD after bariatric surgery. Methods: Proguanylin (GUCA2A) and prouroguanylin (GUCA2B) were measured in 214 participants undergoing bariatric surgery with biopsy-proven NAFLD diagnosis. Pathways involved in lipid metabolism, mitochondrial network and fibrogenesis were evaluated in liver biopsies (n = 137). The effect of guanylin and uroguanylin on these metabolic functions was assessed in HepG2 hepatocytes and LX-2 hepatic stellate cells (HSC) under lipotoxic and profibrogenic conditions. Results: Plasma and hepatic expression of GUCA2B were decreased in obesity-associated NAFLD. Both GUCA2A and GUCA2B levels were increased after sleeve gastrectomy and Roux-en-Y gastric bypass in parallel to the improved liver function. The liver of patients with type 2 diabetes showed impaired mitochondrial β-oxidation, biogenesis, dynamics as well as increased fibrosis. Uroguanylin diminished the lipotoxicity in palmitate-treated HepG2 hepatocytes, evidenced by decresased steatosis and lipogenic factors, as well as increased mitochondrial network expression, AMPK-induced β-oxidation and oxygen consumption rate. Additionally, uroguanylin, but not guanylin, reversed HSC myofibroblast transdifferentiation as well as fibrogenesis after TGF-β1 stimulation. Conclusions: Uroguanylin constitutes a protective factor against lipotoxicity, mitochondrial dysfunction and fibrosis. Increased GUCA2B levels might contribute to improve liver injury in patients with obesity-associated NAFLD after bariatric surgery