136 research outputs found

    Assessing Heart Rate Variability Using A 12 lead ECG In Patients With Alcohol Dependence Syndrome

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    Heavy or hazardous drinking is associated with an increased risk of cardiac morbidity and mortality and this has been attributed to abnormalities in cardiac autonomic regulation. Current study aimed to assess the role of simple indices derived from 12 lead ECG in subjects with chronic alcohol dependence. Data suggested that alcohol group had significantly lower 12 lead ECG derived RR variability compared to age and gender matched controls. Study further supports the implication of 12 lead derived RR variability indices in various clinical settings

    Extensive Analysis on Generation and Consensus Mechanisms of Clustering Ensemble: A Survey

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    Data analysis plays a prominent role in interpreting various phenomena. Data mining is the process to hypothesize useful knowledge from the extensive data. Based upon the classical statistical prototypes the data can be exploited beyond the storage and management of the data. Cluster analysis a primary investigation with little or no prior knowledge, consists of research and development across a wide variety of communities. Cluster ensembles are melange of individual solutions obtained from different clusterings to produce final quality clustering which is required in wider applications. The method arises in the perspective of increasing robustness, scalability and accuracy. This paper gives a brief overview of the generation methods and consensus functions included in cluster ensemble. The survey is to analyze the various techniques and cluster ensemble methods

    Spatial analysis of malaria incidence at the village level in areas with unstable transmission in Ethiopia

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    <p>Abstract</p> <p>Background</p> <p>Malaria is the leading cause of morbidity and mortality in Ethiopia, accounting for over five million cases and thousands of deaths annually. The risks of morbidity and mortality associated with malaria are characterized by spatial and temporal variation across the country. This study examines the spatial and temporal patterns of malaria transmission at the local level and implements a risk mapping tool to aid in monitoring and disease control activities.</p> <p>Methods</p> <p>In this study, we examine the global and local patterns of malaria distribution in 543 villages in East Shoa, central Ethiopia using individual-level morbidity data collected from six laboratory and treatment centers between September 2002 and August 2006.</p> <p>Results</p> <p>Statistical analysis of malaria incidence by sex, age, and village through time reveal the presence of significant spatio-temporal variations. Poisson regression analysis shows a decrease in malaria incidence with increasing age. A significant difference in the malaria incidence density ratio (IDRs) is detected in males but not in females. A significant decrease in the malaria IDRs with increasing age is captured by a quadratic model. Local spatial statistics reveals clustering or hot spots within a 5 and 10 km distance of most villages in the study area. In addition, there are temporal variations in malaria incidence.</p> <p>Conclusion</p> <p>Malaria incidence varies according to gender and age, with males age 5 and above showing a statistically higher incidence. Significant local clustering of malaria incidence occurs between pairs of villages within 1–10 km distance lags. Malaria incidence was higher in 2002–2003 than in other periods of observation. Malaria hot spots are displayed as risk maps that are useful for monitoring and spatial targeting of prevention and control measures against the disease.</p

    Vibrio fluvialis in Patients with Diarrhea, Kolkata, India

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    We identified 131 strains of Vibrio fluvialis among 400 nonagglutinating Vibrio spp. isolated from patients with diarrhea in Kolkata, India. For 43 patients, V. fluvialis was the sole pathogen identified. Most strains harbored genes encoding hemolysin and metalloprotease; this finding may contribute to understanding of the pathogenicity of V. fluvialis

    Trends in the prevalence of diarrheagenic Escherichia coli among hospitalized diarrheal patients in Kolkata, India

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    BACKGROUND:γ€€ To analyse the trends in the prevalence of different pathogroups of diarrheagenic Escherichia coli (DEC) among hospitalized acute diarrheal patients.γ€€ METHODOLOGY/PRINCIPAL FINDINGS:γ€€ From the active surveillance of diarrheal disease at the Infectious Diseases Hospital, Kolkata, 3826 stool specimens collected during 2008-2011 were screened for DEC and other enteric pathogens. PCR was used in the detection of enterotoxigenic, enteropathogenic and enteroaggregative E. coli and 10 major colonization factor antigens (CFs) of enterotoxigenic E. coli. The relationship between DEC infected patient's age group and clinical symptoms were also investigated. Multiplex PCR assay showed that the prevalence of EAEC was most common (5.7%) followed by ETEC (4.2%) and EPEC (1.8%). In diarrheal children >2 year of age, EAEC and EPEC were detected significantly (pβ€Š=β€Š0.000 and 0.007, respectively). In children >2 to 5 and >5 to 14 years, ETEC was significantly associated with diarrhea (pβ€Š=β€Š0.000 each). EAEC was significantly associated with diarrheal patients with age groups >14 to 30 and >30 to 50 years (pβ€Š=β€Š0.001, and pβ€Š=β€Š0.009, respectively). Clinical symptoms such as vomiting, abdominal pain, watery diarrhea, were recorded in patients infected with ETEC. Dehydration status was severe among patients infected by ST-ETEC (19%) and EPEC (15%). CS6 was frequently detected (37%) among ETEC.γ€€ CONCLUSIONS/SIGNIFICANCE:γ€€ Hospital based surveillance reviled that specific pathogroups of DEC are important to certain age groups and among ETEC, CS6 was predominant

    KLF2 Is a Novel Transcriptional Regulator of Endothelial Proinflammatory Activation

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    The vascular endothelium is a critical regulator of vascular function. Diverse stimuli such as proinflammatory cytokines and hemodynamic forces modulate endothelial phenotype and thereby impact on the development of vascular disease states. Therefore, identification of the regulatory factors that mediate the effects of these stimuli on endothelial function is of considerable interest. Transcriptional profiling studies identified the Kruppel-like factor (KLF)2 as being inhibited by the inflammatory cytokine interleukin-1Ξ² and induced by laminar shear stress in cultured human umbilical vein endothelial cells. Overexpression of KLF2 in umbilical vein endothelial cells robustly induced endothelial nitric oxide synthase expression and total enzymatic activity. In addition, KLF2 overexpression potently inhibited the induction of vascular cell adhesion molecule-1 and endothelial adhesion molecule E-selectin in response to various proinflammatory cytokines. Consistent with these observations, in vitro flow assays demonstrate that T cell attachment and rolling are markedly attenuated in endothelial monolayers transduced with KLF2. Finally, our studies implicate recruitment by KLF2 of the transcriptional coactivator cyclic AMP response element–binding protein (CBP/p300) as a unifying mechanism for these various effects. These data implicate KLF2 as a novel regulator of endothelial activation in response to proinflammatory stimuli

    Interaction of Virstatin with Human Serum Albumin: Spectroscopic Analysis and Molecular Modeling

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    Virstatin is a small molecule that inhibits Vibrio cholerae virulence regulation, the causative agent for cholera. Here we report the interaction of virstatin with human serum albumin (HSA) using various biophysical methods. The drug binding was monitored using different isomeric forms of HSA (N form ∼pH 7.2, B form ∼pH 9.0 and F form ∼pH 3.5) by absorption and fluorescence spectroscopy. There is a considerable quenching of the intrinsic fluorescence of HSA on binding the drug. The distance (r) between donor (Trp214 in HSA) and acceptor (virstatin), obtained from Forster-type fluorescence resonance energy transfer (FRET), was found to be 3.05 nm. The ITC data revealed that the binding was an enthalpy-driven process and the binding constants Ka for N and B isomers were found to be 6.09Γ—105 Mβˆ’1 and 4.47Γ—105 Mβˆ’1, respectively. The conformational changes of HSA due to the interaction with the drug were investigated from circular dichroism (CD) and Fourier Transform Infrared (FTIR) spectroscopy. For 1∢1 molar ratio of the protein and the drug the far-UV CD spectra showed an increase in Ξ±- helicity for all the conformers of HSA, and the protein is stabilized against urea and thermal unfolding. Molecular docking studies revealed possible residues involved in the protein-drug interaction and indicated that virstatin binds to Site I (subdomain IIA), also known as the warfarin binding site

    M402, a Novel Heparan Sulfate Mimetic, Targets Multiple Pathways Implicated in Tumor Progression and Metastasis

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    Heparan sulfate proteoglycans (HSPGs) play a key role in shaping the tumor microenvironment by presenting growth factors, cytokines, and other soluble factors that are critical for host cell recruitment and activation, as well as promoting tumor progression, metastasis, and survival. M402 is a rationally engineered, non-cytotoxic heparan sulfate (HS) mimetic, designed to inhibit multiple factors implicated in tumor-host cell interactions, including VEGF, FGF2, SDF-1Ξ±, P-selectin, and heparanase. A single s.c. dose of M402 effectively inhibited seeding of B16F10 murine melanoma cells to the lung in an experimental metastasis model. Fluorescent-labeled M402 demonstrated selective accumulation in the primary tumor. Immunohistological analyses of the primary tumor revealed a decrease in microvessel density in M402 treated animals, suggesting anti-angiogenesis to be one of the mechanisms involved in-vivo. M402 treatment also normalized circulating levels of myeloid derived suppressor cells in tumor bearing mice. Chronic administration of M402, alone or in combination with cisplatin or docetaxel, inhibited spontaneous metastasis and prolonged survival in an orthotopic 4T1 murine mammary carcinoma model. These data demonstrate that modulating HSPG biology represents a novel approach to target multiple factors involved in tumor progression and metastasis
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