RAMAN-SPECTRA OF DOLOMITE [CAMG(CO3)2]

14104676467

Nephroprotective Effect of the Virgin Olive Oil Polyphenol Hydroxytyrosol in Type 1-like Experimental Diabetes Mellitus: Relationships with Its Antioxidant Effect

The aim of this study was to determine whether hydroxytyrosol administration prevented kidney damage in an experimental model of type 1 diabetes mellitus in rats. Hydroxytyrosol was administered to streptozotocin-diabetic rats: 1 and 5 mg/kg/day p.o. for two months. After hydroxytyrosol administration, proteinuria was significantly reduced (67–73%), calculated creatinine clearance was significantly increased (26–38%), and the glomerular volume and glomerulosclerosis index were decreased (20–30%). Hydroxytyrosol reduced oxidative and nitrosative stress variables and thromboxane metabolite production. Statistical correlations were found between biochemical and kidney function variables. Oral administration of 1 and 5 mg/kg/day of hydroxytyrosol produced an antioxidant and nephroprotective effect in an experimental model of type 1-like diabetes mellitus. The nephroprotective effect was significantly associated with the systemic and renal antioxidant action of hydroxytyrosol, which also influenced eicosanoid production

Interleukin-1 polymorphisms associated with increased risk of gastric cancer

Helicobacter pylori infection is associated with a variety of clinical outcomes including gastric cancer and duodenal ulcer disease. The reasons for this variation are not clear, but the gastric physiological response is influenced by the severity and anatomical distribution of gastritis induced by H. pylori. Thus, individuals with gastritis predominantly localized to the antrum retain normal (or even high) acid secretion, whereas individuals with extensive corpus gastritis develop hypochlorhydria and gastric atrophy, which are presumptive precursors of gastric cancer. Here we report that interleukin-1 gene cluster polymorphisms suspected of enhancing production of interleukin-1-beta are associated with an increased risk of both hypochlorhydria induced by H. pylori and gastric cancer. Two of these polymorphism are in near-complete linkage disequilibrium and one is a TATA-box polymorphism that markedly affects DNA-protein interactions in vitro. The association with disease may be explained by the biological properties of interleukin-1-beta, which is an important pro-inflammatory cytokine and a powerful inhibitor of gastric acid secretion. Host genetic factors that affect interleukin-1-beta may determine why some individuals infected with H. pylori develop gastric cancer while others do no

Cognitive Performance and Heart Rate Variability: The Influence of Fitness Level

In the present study, we investigated the relation between cognitive performance and heart rate variability as a function of fitness level. We measured the effect of three cognitive tasks (the psychomotor vigilance task, a temporal orienting task, and a duration discrimination task) on the heart rate variability of two groups of participants: a high-fit group and a low-fit group. Two major novel findings emerged from this study. First, the lowest values of heart rate variability were found during performance of the duration discrimination task, compared to the other two tasks. Second, the results showed a decrement in heart rate variability as a function of the time on task, although only in the low-fit group. Moreover, the high-fit group showed overall faster reaction times than the low-fit group in the psychomotor vigilance task, while there were not significant differences in performance between the two groups of participants in the other two cognitive tasks. In sum, our results highlighted the influence of cognitive processing on heart rate variability. Importantly, both behavioral and physiological results suggested that the main benefit obtained as a result of fitness level appeared to be associated with processes involving sustained attention.This research was supported by the Spanish Ministerio de Educación y Cultura with a predoctoral grant (FPU-AP2010-3630) to the first author, Spanish grants SEJ2007-63645 from the Junta de Andalucía to Daniel Sanabria, Mikel Zabala and Esther Morales, and the CSD2008-00048 CONSOLIDER INGENIO (Dirección General de Investigación) to Daniel Sanabria

Sensitivity is not an intrinsic property of a diagnostic test: empirical evidence from histological diagnosis of Helicobacter pylori infection

<p>Abstract</p> <p>Background</p> <p>We aimed to provide empirical evidence of how spectrum effects can affect the sensitivity of histological assessment of <it>Helicobacter pylori </it>infection, which may contribute to explain the heterogeneity in prevalence estimates across populations with expectedly similar prevalence.</p> <p>Methods</p> <p>Cross-sectional evaluation of dyspeptic subjects undergoing upper digestive endoscopy, including collection of biopsy specimens from the greater curvature of the antrum for assessment of <it>H. pylori </it>infection by histopathological study and polymerase chain reaction (PCR), from Portugal (n = 106) and Mozambique (n = 102) following the same standardized protocol.</p> <p>Results</p> <p>In the Portuguese sample the prevalence of infection was 95.3% by histological assessment and 98.1% by PCR. In the Mozambican sample the prevalence was 63.7% and 93.1%, respectively. Among those classified as infected by PCR, the sensitivity of histological assessment was 96.2% among the Portuguese and 66.3% among the Mozambican. Among those testing positive by both methods, 5.0% of the Portuguese and 20.6% of the Mozambican had mild density of colonization.</p> <p>Conclusions</p> <p>This study shows a lower sensitivity of histological assessment of <it>H. pylori </it>infection in Mozambican dyspeptic patients compared to the Portuguese, which may be explained by differences in the density of colonization, and may contribute to explain the heterogeneity in prevalence estimates across African settings.</p

IL-17 Produced during Trypanosoma cruzi Infection Plays a Central Role in Regulating Parasite-Induced Myocarditis

Chagas disease is caused by the intracellular parasite Trypanosoma cruzi. This infection has been considered one of the most neglected diseases and affects several million people in the Central and South America. Around 30% of the infected patients develop digestive and cardiac forms of the disease. Most patients are diagnosed during the chronic phase, when the treatment is not effective. Here, we showed by the first time that IL-17 is produced during experimental T. cruzi infection and that it plays a significant role in host defense, modulating parasite-induced myocarditis. Applying this analysis to humans could be of great value in unraveling the elements involved in the pathogenesis of chagasic cardiopathy and could be used in the development of alternative therapies to reduce morbidity during the chronic phase of the disease, as well as clinical markers of disease progression. The understanding of these aspects of disease may be helpful in reducing the disability-adjusted life years (DALYs) and costs to the public health service in developing countries

<em>Enterococcus faecalis</em> Infection Causes Inflammation, Intracellular Oxphos-Independent ROS Production, and DNA Damage in Human Gastric Cancer Cells

Background: Achlorhydria caused by e.g. atrophic gastritis allows for bacterial overgrowth, which induces chronic inflammation and damage to the mucosal cells of infected individuals driving gastric malignancies and cancer. Enterococcus faecalis (E. faecalis) can colonize achlohydric stomachs and we therefore wanted to study the impact of E. faecalis infection on inflammatory response, reactive oxygen species (ROS) formation, mitochondrial respiration, and mitochondrial genetic stability in gastric mucosal cells. Methods: To separate the changes induced by bacteria from those of the inflammatory cells we established an in vitro E. faecalis infection model system using the gastric carcinoma cell line MKN74. Total ROS and superoxide was measured by fluorescence microscopy. Cellular oxygen consumption was characterized non-invasively using XF24 microplate based respirometry. Gene expression was examined by microarray, and response pathways were identified by Gene Set Analysis (GSA). Selected gene transcripts were verified by quantitative real-time polymerase chain reaction (qRT-PCR). Mitochondrial mutations were determined by sequencing. Results: Infection of MKN74 cells with E. faecalis induced intracellular ROS production through a pathway independent of oxidative phosphorylation (oxphos). Furthermore, E. faecalis infection induced mitochondrial DNA instability. Following infection, genes coding for inflammatory response proteins were transcriptionally up-regulated while DNA damage repair and cell cycle control genes were down-regulated. Cell growth slowed down when infected with viable E. faecalis and responded in a dose dependent manner to E. faecalis lysate. Conclusions: Infection by E. faecalis induced an oxphos-independent intracellular ROS response and damaged the mitochondrial genome in gastric cell culture. Finally the bacteria induced an NF-kappa B inflammatory response as well as impaired DNA damage response and cell cycle control gene expression