The Relationship Between Rating of Perceived Exertion and Muscle Activity During Exhaustive Constant-Load Cycling

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)The aims of this study were to verify the relationship between rating of perceived exertion (RPE) and electromyography (EMG) increases during exhaustive constant-load cycling bouts and, to compare and to correlate the power outputs corresponding to perceived exertion threshold (PET) and neuromuscular fatigue threshold (NFT). 11 men completed 3-4 different exhaustive constant-load cycling bouts on a cycle ergometer, being RPE and EMG measured throughout the bouts. The linear regression of the RPE(slope) and EMG(slope) against the power output identified the PET and NFT intensity, respectively. There was a significant relationship between RPE slope and EMG(slope) (R(2) = 0.69; P < 0.01). However, the linearity of RPE(slope) (R(2) = 0.93 +/- 0.07) was significantly higher (P < 0.001) than EMG(slope) (R(2) = 0.63 +/- 0.25). In addition, the RPE(slope) and EMG(slope) were related to time to exhaustion (r = -0.59 and r = -0.60; P < 0.001). There was no significant difference (P = 0.42) between PET (201.5 +/- 27.9W) and NFT (210.3 +/- 22.6W) and they were significantly correlated (r = 0.78; P = 0.005). Therefore, the RPE and EMG increases during exhaustive constant-load cycling bouts are related and, PET and NFT intensities are similar and closely associated.3110683688Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP [04/12589-0

Ileal Intussusception Caused by Vanek's Tumor: A Case Report

Inflammatory fibroid polyps (Vanek's tumor) are rare benign localized lesions originating in the submucosa of the gastrointestinal tract. Intussusceptions due to inflammatory fibroid polyps are uncommon; moreover, ileo-ileal intussusception with small bowel necrosis and perforation has rarely been reported. We report a 56-year-old woman who was admitted two days after complaints of nausea and vomiting. Abdominal examination revealed distension, signs of gastrointestinal perforation and clanging intestinal sounds. The patient underwent a emergency laparotomy which found a 17-cm invaginated mid-ileal segment with necrosis, perforation and fecal peritonitis. The ileal segment was resected and single-layer end-to-end anastomosis was performed. Histopathological analysis showed an ulcerative lesion with variable cellularity, formed by spindle cells with small number of mitosis and an abundant inflammatory infiltrate comprising mainly eosinophils. Immunohistochemistry confirmed the diagnosis of ileal Vanek's tumor. Although inflammatory fibroid polyps are seen very rarely in adults, they are among the probable diagnoses that should be considered in obstructive tumors of the small bowel causing intussusception with intestinal necrosis and perforation

Dysregulated Recruitment of the Histone Methyltransferase EZH2 to the Class II Transactivator (CIITA) Promoter IV in Breast Cancer Cells

One mechanism frequently utilized by tumor cells to escape immune system recognition and elimination is suppression of cell surface expression of Major Histocompatibility Class II (MHC II) molecules. Expression of MHC II is regulated primarily at the level of transcription by the Class II Transactivator, CIITA, and decreased CIITA expression is observed in multiple tumor types. We investigate here contributions of epigenetic modifications to transcriptional silencing of CIITA in variants of the human breast cancer cell line MDA MB 435. Significant increases in histone H3 lysine 27 trimethylation upon IFN-γ stimulation correlate with reductions in transcription factor recruitment to the interferon-γ inducible CIITA promoter, CIITApIV, and with significantly increased CIITApIV occupancy by the histone methyltransferase enhancer of zeste homolog 2 (EZH2). Most compelling is evidence that decreased expression of EZH2 in MDA MB 435 variants results in significant increases in CIITA and HLA-DRA mRNA expression, even in the absence of interferon-γ stimulation, as well as increased cell surface expression of MHC II. Together, these data add mechanistic insight to prior observations of increased EZH2 expression and decreased CIITA expression in multiple tumor types

Lipopolysaccharides Impair Insulin Gene Expression in Isolated Islets of Langerhans via Toll-Like Receptor-4 and NF-κB Signalling

BACKGROUND:Type 2 diabetes is characterized by pancreatic β-cell dysfunction and is associated with low-grade inflammation. Recent observations suggest that the signalling cascade activated by lipopolysaccharides (LPS) binding to Toll-Like Receptor 4 (TLR4) exerts deleterious effects on pancreatic β-cell function; however, the molecular mechanisms of these effects are incompletely understood. In this study, we tested the hypothesis that LPS alters insulin gene expression via TLR4 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in islets. METHODOLOGY/PRINCIPAL FINDINGS:A 24-h exposure of isolated human, rat and mouse islets of Langerhans to LPS dose-dependently reduced insulin gene expression. This was associated in mouse and rat islets with decreased mRNA expression of pancreas-duodenum homebox-1 (PDX-1) and mammalian homologue of avian MafA/l-Maf (MafA). Accordingly, LPS exposure also decreased glucose-induced insulin secretion. LPS repression of insulin, PDX-1 and MafA expression, as well as its inhibition of insulin secretion, were not observed in islets from TLR4-deficient mice. LPS inhibition of β-cell gene expression in rat islets was prevented by inhibition of the NF-κB pathway, but not the p38 mitogen-activated protein kinase (p38 MAPK) pathway. CONCLUSIONS/SIGNIFICANCE:Our findings demonstrate that LPS inhibit β-cell gene expression in a TLR4-dependent manner and via NF-κB signaling in pancreatic islets, suggesting a novel mechanism by which the gut microbiota might affect pancreatic β-cell function