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Search Results: 1 - 10 of 219344 matches for " C. Sivagnanam "
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 C. Sivagnanam International Journal of Digital Information and Wireless Communications , 2012, Abstract: In a graph G, a vertex dominates itself and its neighbours. A subset S of V is called a dominating set in G if every vertex in V is dominated by at least one vertex in S. The domination number is the minimum cardinality of a dominating set. A set is called a double dominating set of a graph G if every vertex in V is dominated by at least two vertices in S. The minimum cardinality of a double dominating set is called double domination number of G and is denoted by dd(G). The connectivity of a connected graph G is the minimum number of vertices whose removal results in a disconnected or trivial graph. In this paper we find an upper bound for the sum of the double domination number and connectivity of a graph and characterize the corresponding extremal graphs.
 Opuscula Mathematica , 2011, Abstract: Let G = (V;E) be a graph without isolated vertices. A dominating set S of G is called a neighbourhood total dominating set (ntd-set) if the induced subgraph has no isolated vertices. The minimum cardinality of a ntd-set of G is called the neighbourhood total domination number of G and is denoted by \$gamma _{nt}(G)\$. The maximum order of a partition of V into ntd-sets is called the neighbourhood total domatic number of G and is denoted by \$d_{nt}(G)\$. In this paper we initiate a study of these parameters.
 Tamkang Journal of Mathematics , 2012, DOI: 10.5556/j.tkjm.43.2012.69-80 Abstract: Let G = (V,E) be a connected graph. An edge dominating set X of G is called a neighborhood connected edge dominating set (nced-set) if the edge induced subgraph < N(X) > is connected. The minimum cardinality of a nced-set of G is called the neighborhood connected edge domination number of G and is denoted by. In this paper we initiate a study of this parameter.
 Tamkang Journal of Mathematics , 2012, DOI: 10.5556/j.tkjm.43.2012.557-562 Abstract: Let \$G = (V, E)\$ be a connected graph. A set \$S\$ of vertices in \$G\$ is a perfect dominating set if every vertex \$v\$ in \$V-S\$ is adjacent to exactly one vertex in \$S\$. A perfect dominating set \$S\$ is said to be a neighborhood connected perfect dominating set (ncpd-set) if the induced subgraph \$\$ is connected. The minimum cardinality of a ncpd-set of \$G\$ is called the neighborhood connected perfect domination number of \$G\$ and is denoted by \$gamma_{ncp}(G)\$. In this paper we initiate a study of this parameter.
 Physics , 2002, DOI: 10.1051/0004-6361:20021227 Abstract: We have undertaken a comprehensive search for 5-cm excited OH maser emission from evolved stars representative of various stages of late stellar evolution. Observed sources were selected from known 18-cm OH sources. This survey was conducted with the 100-m Effelsberg telescope to achieve high signal to noise ratio observations and a sensitivity limit of about 0.05 to 0.1 Jy. A total of 64 stellar sources were searched for both main line and satellite line emission. We confirm the previous detection of 5 cm OH in Vy 2-2, do not confirm emission from NML-Cyg and do not report any other new detection within the above sensitivity limit. Implications of these results on the pumping mechanism of the OH radical in circumstellar envelopes are briefly discussed.
 Soupramanien Sivagnanam Critical Care , 2002, DOI: 10.1186/cc1500 Abstract: Insect damage costs the world loses approximately 6 billion pounds sterling every year. Use of pesticides has increased food production in parallel with population growth in many parts of the world. Many insect-borne diseases have been eliminated or controlled by the use of insecticides. Organophosphorus compounds are widely used as insecticides and as agents of chemical warfare. According to the World Health Organization [2], 1 million serious accidental and 2 million suicidal poisonings with insecticides occur worldwide every year, and of these approximately 200,000 die, mostly in developing countries.Atropine and oximes are traditionally used in the management of such poisonings but they have failed to reduce the attendant mortality and morbidity. Some agents have been found to reduce the toxicity of organophosphorus compounds in animal experiments, and they have potential as therapeutic agents in the management of organophosphorus poisoning. These agents are magnesium, clonidine and fluoride.Kiss and Fazekas [3] reported control of premature ventricular contractions with intravenous magnesium. Magnesium was considered to counteract the direct toxic inhibitory action of organophosphorus compounds on sodium—potassium ATPase. It also inhibits acetylcholine release [4]. Singh and coworkers [5] found that intravenous magnesium reversed the neuro-electrophysiological effect of organophosphorus poisoning.Pretreatment of mice with clonidine (0.1—1 mg/kg) resulted in protection against toxic manifestations of soman — an organophosphorus compound [6]. Increased survival rates, reduction in centrally mediated symptoms such as tremor and straub tail, and reduction in excessive salivation were noted. The protective effects of clonidine are probably due to blockade of acetylcholine release and postmuscarinic receptors, together with transient inhibition of acetylcholinesterase. Thus, clonidine may prove useful in the management of organophosphorus poisoning.Pretreatment of mi
 Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-4 Abstract: KCNN3 mRNA (real-time RT-PCR) and SK3 immunoreactivity were examined in rat microglia. Lipopolysaccharide was then used to activate microglia (monitored by iNOS, nitric oxide, activation of NF-κB and p38 MAPK) and transform them to a neurotoxic state. Microglia-mediated neuron damage (TUNEL, activated caspase 3) and nitrotyrosine levels were quantified using a two-chamber system that allowed microglia to be treated with channel blockers, washed and then added to neuron/astrocyte cultures. Contributions of SK3 to these processes were discriminated using a subtractive pharmacological approach with apamin and tamapin. ANOVA and post-hoc tests were used to assess the statistical significance of differences between treatment groups. SK3 immunoreactivity was then compared in the normal and damaged adult rat striatum, by injecting collagenase (a hemorrhagic stroke) or endothelin-1 (a transient ischemic stroke).KCNN3 mRNA was prevalent in cultured microglia and increased after lipopolysaccharide-induced activation; SK3 channel blockade inhibited microglial activation and reduced their ability to kill neurons. SK3 immunoreactivity was prevalent in cultured microglia and throughout the adult rat striatum (except white matter tracts). After strokes, SK3 was highly expressed in activated microglia/macrophages within the lesions, but reduced in other cells.SK3 is expressed in microglia in both the healthy and damaged adult striatum, and mechanistic in vitro studies show it contributes to transformation of microglia to an activated neurotoxic phenotype. Thus, SK3 might be a therapeutic target for reducing inflammation-mediated acute CNS damage. Moreover, its roles in microglia must be considered when targeting this channel for CNS diseases, disorders and reducing neuron hyper-excitability.After acute CNS injuries such as stroke or trauma, there is a prolonged inflammatory response involving microglial activation and infiltration of macrophages and neutrophils, which has the poten
 Proteome Science , 2011, DOI: 10.1186/1477-5956-9-66 Abstract: We identified 894 different proteins in C. acetobutylicum from ABE fermentation process by two dimensional - liquid chromatography - tandem mass spectrometry (2D-LC-MS/MS) method. This includes 717 proteins from glucose and 826 proteins from the xylose substrate. A total of 649 proteins were found to be common and 22 significantly differentially expressed proteins were identified between glucose and xylose substrates.Our results demonstrate that flagellar proteins are highly up-regulated with glucose compared to xylose substrate during ABE fermentation. Chemotactic activity was also found to be lost with the xylose substrate due to the absence of CheW and CheV proteins. This is the first report on the shotgun proteomic analysis of C. acetobutylicum ATCC 824 in ABE fermentation between glucose and xylose substrate from a single time data point and the number of proteins identified here is more than any other study performed on this organism up to this report.Clostridium acetobutylicum is a gram positive, spore forming, obligate anaerobic bacteria and is one of the few microorganisms capable of converting a wide variety of sugars into three main products acetone, butanol and ethanol (ABE) [1]. ABE fermentation process was the primary source of butanol for over 40 years until the mid-1950s and is one of the oldest large-scale industrial fermentations [2]. ABE fermentation could not compete with the chemical synthesis of ABE solvents from petroleum since the mid-1950s [3]. However, increased concern over depletion of fossil fuels has led to renewed research interest in producing solvents via microbial fermentation processes.Lignocellulosic biomass is an abundant renewable resource that can be used for the production of alternative fuels [4]. It is advantageous to use lignocellulosic biomass such as rice straw, wheat straw, corn stover and agricultural residues for biofuel production as they have limited impact on food supplies [5]. Glucose is the most abundant sugar fou
 Physics , 2010, DOI: 10.1051/0004-6361/200913387 Abstract: The aim of this study is to investigate the physical properties of molecular envelopes of planetary nebulae in their earliest stages of evolution. Using the 100m telescope at Effelsberg, we have undertaken a high sensitivity discrete source survey for the first excited state of OH maser emission (J=5/2, 2PI3/2 at 6GHz) in the direction of planetary and proto-planetary nebulae exhibiting 18cm OH emission (main and/or satellite lines), and we further validate our detections using the Nan\c{c}ay radio telescope at 1.6-1.7GHz and MERLIN interferometer at 1.6-1.7 and 6GHz. Two sources have been detected at 6035MHz (5cm), both of them are young (or very young) planetary nebulae. The first one is a confirmation of the detection of a weak 6035MHz line in Vy 2-2. The second one is a new detection, in K 3-35, which was already known to be an exceptional late type star because it exhibits 1720MHz OH emission. The detection of 6035MHz OH maser emission is confirmed by subsequent observations made with the MERLIN interferometer. These lines are very rarely found in evolved stars. The 1612MHz masers surround but are offset from the 1720 and 6035MHz masers which in turn lie close to a compact 22GHz continuum source embedded in the optical nebula.
 Critical Care , 2002, DOI: 10.1186/cc1871 Abstract: The incidence of nosocomial infections in hospitalized patients varies between 5 and 15% [1]. Nosocomial infection can lead to complications in 25–33% of those patients admitted to intensive care units. Vancomycin is often used in intensive care units. It is the drug of choice for the treatment of infections due to methicillin-resistant staphylococci, Corynebacterium jeikeium, and resistant strains of Streptococcus pneumoniae. Vancomycin is an alternative drug for serious staphylococcal and streptococcal infections, including endocarditis, when allergy precludes the use of penicillins and cephalosporins.Vancomycin can cause two types of hypersensitivity reactions, the red man syndrome and anaphylaxis [2]. Red man syndrome is an infusion-related reaction peculiar to vancomycin [3]. It typically consists of pruritus, an erythematous rash that involves the face, neck, and upper torso. Less frequently, hypotension and angioedema can occur. Patients commonly complain of diffuse burning and itching and of generalized discomfort. They can rapidly become dizzy and agitated, and can develop headache, chills, fever, and paresthesia around the mouth. In severe cases, patients complain of chest pain and dyspnea. In many patients, the syndrome is a mild, evanescent pruritus at the end of the infusion that goes unreported.Signs of red man syndrome would appear about 4–10 min after an infusion started or may begin soon after its completion. It is often associated with rapid (<1 hour) infusion of the first dose of vancomycin. The reaction may not be of the same severity with successive exposures, but it can occur for the first time after several doses or with a slow infusion [4]. Delayed reactions at or near the end of a 90 or 120 min infusion have been seen in patients who had been on vancomycin therapy for longer than 7 days without prior incident [5]. Most of the hospital protocols require vancomycin to be infused over 60 min, as a minimum [5,6]. Sporadic reports of red man synd
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