A STUDY TO EVALUATE THE EFFECT OF ADDING CLONIDINE TO ROPIVACAINE FOR AXILLARY PLEXUS BLOCKADE

Aims and objectives- The present study was undertaken to evaluate the effect of adding Clonidine to Ropivacaine for axillary plexus blockade. Material and methods- A total of 60 adult patients having physical status grade I or II according to American Society of Anaesthesiologists ( ASA ) undergoing hand or forearm surgery under axillary plexus blockade using nerve stimulator were included in the study. Patients were randomly allocated to one of the two groups. Each group consisted of 30 patients. Group 1 patients received 35 ml of Ropivacaine 0.5 % + 1 ml of normal saline.Group 2 patients received 35 ml of Ropivacaine + 1 ml of clonidine ( 150 µg). Sensory block, motor block and sedation were assessed every 5 minutes for 30 minutes. Postoperatively assessment was done every 15 minutes till complete regression of sensory and motor block. Results- Mean sensory onset time in patients of group 1 was 26.48 ± 7.88 min and in patients of group 2 was 26.55 ± 8.06 min, which was insignificant statistically. Patients of group 1 had a mean motor onset time 35.51 ± 10.4 min and patients of group 2 had a mean motor onset time 37.06 ± 14.19min, the difference being statistically comparable. Mean duration of sensory block in patients of group 1 was 422 ± 163.10 min and in patients of group 2 was 438 ± 133.93 min, which was statistically comparable. Patients belonging to group 1 had a mean duration of motor block 404 ± 160.60 min and patients belonging to group 2 had a mean duration of motor block 388 ± 151.63 min, which was statistically comparable. Conclusion- Addition of Clonidine ( 150 µg) is of no benefit in the onset and duration of axillary plexus block

Susceptibility of Multi-Drug-Resistant Organisms (MDROs), Isolated from Cases of Urinary Tract Infection to Fosfomycin (The New Antibiotic) vis-a-vis Other Antimicrobial Agents

Introduction: Urinary tract infection (UTI) is one of the commonest infections encountered in the hospital. Most of the hospital UTIs are caused by MDROs. There is scarcity of available drugs to treat MDR infections. In this scenario, reevaluation of the old antimicrobial agents is being done. Fosfomycin is one such old molecule. The studies suggest that Fosfomycin may provide a useful option for the treatment of patients with the MDR/XDR difficult-to-treat infections.Materials and Methods: Urine samples (including catheter samples) were collected in sterile containers; cultured on CHROME agar, using calibrated loop; colony count was done in positive cultures; identification and antimicrobial susceptibility of the organism was done by VITEK2 compact system. Susceptibility pattern of antimicrobial agents used for treatment of UTI including Fosfomycin was analyzed.Results: Of the 502 urinary MDRO isolates, 74.9% were ESBLs and 29.49% were CROs. MDRO susceptibility was 88% to Fosfomycin, 70.52% to Ertapenem, 53.98% to Nitrofurantoin, 37.05% to Trimethoprim-Sulfamethoxazole, 22.31% to Norfloxacin, 20.91% to Ciprofloxacin, and 10.96% to Ampicillin respectively.Discussion: Gupta et al.10 reported 52.6% E. coli urinary isolates to be ESBLs and all were susceptible to Fosfomycin. In the present study, 76.8% Escherichia coli isolates were ESBLs and 98.5% only were susceptible to Fosfomycin

A framework for human microbiome research

A variety of microbial communities and their genes (the microbiome) exist throughout the human body, with fundamental roles in human health and disease. The National Institutes of Health (NIH)-funded Human Microbiome Project Consortium has established a population-scale framework to develop metagenomic protocols, resulting in a broad range of quality-controlled resources and data including standardized methods for creating, processing and interpreting distinct types of high-throughput metagenomic data available to the scientific community. Here we present resources from a population of 242 healthy adults sampled at 15 or 18 body sites up to three times, which have generated 5,177 microbial taxonomic profiles from 16S ribosomal RNA genes and over 3.5 terabases of metagenomic sequence so far. In parallel, approximately 800 reference strains isolated from the human body have been sequenced. Collectively, these data represent the largest resource describing the abundance and variety of the human microbiome, while providing a framework for current and future studies

Structure, function and diversity of the healthy human microbiome

Author Posting. © The Authors, 2012. This article is posted here by permission of Nature Publishing Group. The definitive version was published in Nature 486 (2012): 207-214, doi:10.1038/nature11234.Studies of the human microbiome have revealed that even healthy individuals differ remarkably in the microbes that occupy habitats such as the gut, skin and vagina. Much of this diversity remains unexplained, although diet, environment, host genetics and early microbial exposure have all been implicated. Accordingly, to characterize the ecology of human-associated microbial communities, the Human Microbiome Project has analysed the largest cohort and set of distinct, clinically relevant body habitats so far. We found the diversity and abundance of each habitat’s signature microbes to vary widely even among healthy subjects, with strong niche specialization both within and among individuals. The project encountered an estimated 81–99% of the genera, enzyme families and community configurations occupied by the healthy Western microbiome. Metagenomic carriage of metabolic pathways was stable among individuals despite variation in community structure, and ethnic/racial background proved to be one of the strongest associations of both pathways and microbes with clinical metadata. These results thus delineate the range of structural and functional configurations normal in the microbial communities of a healthy population, enabling future characterization of the epidemiology, ecology and translational applications of the human microbiome.This research was supported in part by National Institutes of Health grants U54HG004969 to B.W.B.; U54HG003273 to R.A.G.; U54HG004973 to R.A.G., S.K.H. and J.F.P.; U54HG003067 to E.S.Lander; U54AI084844 to K.E.N.; N01AI30071 to R.L.Strausberg; U54HG004968 to G.M.W.; U01HG004866 to O.R.W.; U54HG003079 to R.K.W.; R01HG005969 to C.H.; R01HG004872 to R.K.; R01HG004885 to M.P.; R01HG005975 to P.D.S.; R01HG004908 to Y.Y.; R01HG004900 to M.K.Cho and P. Sankar; R01HG005171 to D.E.H.; R01HG004853 to A.L.M.; R01HG004856 to R.R.; R01HG004877 to R.R.S. and R.F.; R01HG005172 to P. Spicer.; R01HG004857 to M.P.; R01HG004906 to T.M.S.; R21HG005811 to E.A.V.; M.J.B. was supported by UH2AR057506; G.A.B. was supported by UH2AI083263 and UH3AI083263 (G.A.B., C. N. Cornelissen, L. K. Eaves and J. F. Strauss); S.M.H. was supported by UH3DK083993 (V. B. Young, E. B. Chang, F. Meyer, T. M. S., M. L. Sogin, J. M. Tiedje); K.P.R. was supported by UH2DK083990 (J. V.); J.A.S. and H.H.K. were supported by UH2AR057504 and UH3AR057504 (J.A.S.); DP2OD001500 to K.M.A.; N01HG62088 to the Coriell Institute for Medical Research; U01DE016937 to F.E.D.; S.K.H. was supported by RC1DE0202098 and R01DE021574 (S.K.H. and H. Li); J.I. was supported by R21CA139193 (J.I. and D. S. Michaud); K.P.L. was supported by P30DE020751 (D. J. Smith); Army Research Office grant W911NF-11-1-0473 to C.H.; National Science Foundation grants NSF DBI-1053486 to C.H. and NSF IIS-0812111 to M.P.; The Office of Science of the US Department of Energy under Contract No. DE-AC02-05CH11231 for P.S. C.; LANL Laboratory-Directed Research and Development grant 20100034DR and the US Defense Threat Reduction Agency grants B104153I and B084531I to P.S.C.; Research Foundation - Flanders (FWO) grant to K.F. and J.Raes; R.K. is an HHMI Early Career Scientist; Gordon&BettyMoore Foundation funding and institutional funding fromthe J. David Gladstone Institutes to K.S.P.; A.M.S. was supported by fellowships provided by the Rackham Graduate School and the NIH Molecular Mechanisms in Microbial Pathogenesis Training Grant T32AI007528; a Crohn’s and Colitis Foundation of Canada Grant in Aid of Research to E.A.V.; 2010 IBM Faculty Award to K.C.W.; analysis of the HMPdata was performed using National Energy Research Scientific Computing resources, the BluBioU Computational Resource at Rice University

Evaluation of outer-surface proteins in the reduction of iron(III) oxide in Geobacter sulfurreducens

Reduction of Fe(III) in the subsurface environment is of immense environmental significance due to its impact on remediation of toxic metals and organic pollutants. Iron is mostly present in these environments as insoluble Fe(III) oxide. Geobacter are the largest known group of Fe(III) reducing microorganisms in the subsurface environment. Previous studies to understand the mechanism of Fe(III) oxide reduction have demonstrated the need for direct contact. Current study was aimed at identifying the outer surface proteins that are involved in establishing contact, electron transfer and subsequent reduction of Fe(III) oxides. Work presented here demonstrates novel function of type IV pili in Geobacter sulfurreducens in the reduction of insoluble Fe(III) oxides. It has been established by subsequent studies in the laboratory that G. sulfurreducens uses type IV pili for direct electron transfer to insoluble Fe(III). A homologue of pilA, the type IV pilin, gspG was identified as part of a type II secretion system involved specifically in the reduction of insoluble Fe(III), a unique mechanism for dissimilatory Fe(III) reduction. Cytochromes, OmcE and OmcS were identified in an attempt to identify outer surface proteins involved in Fe(III) reduciton. OmcS and its paralogue, OmcT are the first pair of c-type cytochromes identified that are expressed specifically for the reduction of Fe(III) oxides and are crucial for their reduction. OmcE was also demonstrated to be involved in the reduction of insoluble Fe(III). The studies also emphasize the importance of evaluating mechanisms for Fe(III) reduction with environmentally relevant Fe(III) oxide, rather than the more commonly utilized Fe(III) citrate, because additional electron transfer components are required for Fe(III) oxide reduction that are not required for Fe(III) citrate reduction

Anti-Myeloma Effect of Imidazole and Methyl Derivatives of a Synthetic Oleanane Triterpenoid 2-Cyano-3,12-Dioxooleana-1,9-Dien-28-Oic Acid (CDDO)

INTRODUCTION: Multiple myeloma (MM) is a plasma cell cancer characterized by accumulation of malignant cells preferentially in the bone marrow. The synthetic oleanane triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) and its imidazole derivative CDDO-Im and methyl derivative CDDO-Me have been reported with therapeutic potential in treating various cancers, including hematological cancers. The objective of this study is to determine if CDDO-Im and CDDO-Me inhibit growth and induce apoptosis of multiple myeloma cells. METHODS: Cultured MM cell lines RPMI 8226, U266 and NCI-H929 were exposed to CDDO-Im and CDDO-Me (0 ~ 0.5 μM) for 24, 48, or 72 hours, respectively. Cell viability was measured using Presto Blue assay. Apoptosis of RPMI 8226 cells after 24 hour incubation with CDDO-Im or CDDO-Me (0 ~ 0.5 μM) were determined through flow cytometric analysis and western blot analysis. RESULTS: Both CDDO-Im and CDDO-Me prevented proliferation of all MM cells examined in a dose and time dependent fashion. Increase of percentage of apoptotic cells was observed with increase of concentrations of both CDDO derivatives. Expression of caspase-3, a pro-apoptotic factor, was significantly altered in a pattern suggesting the occurrence of apoptosis. CONCLUSIONS: Both CDDO-Im and CDDO-Me inhibit growth of multiple myeloma cells in a dose and time-dependent manner possibly through induction of apoptosis. Further study is needed to elucidate the mechanism of anti-myeloma action of CDDO-Im and CDDO-Me

Extracellular Electron Transfer Via Microbial Nanowires

Microbes that can transfer electrons to extracellular electron acceptors, such as Fe(iii) oxides, are important in organic matter degradation and nutrient cycling in soils and sediments1, 2. Previous investigations on electron transfer to Fe(iii) have focused on the role of outer-membrane c-type cytochromes. However, some Fe(iii) reducers lack c-cytochromes. Geobacter species, which are the predominant Fe(iii) reducers in many environments, must directly contact Fe(iii) oxides to reduce them, and produce monolateral pili that were proposed on the basis of the role of pili in other organisms to aid in establishing contact with the Fe(iii) oxides. Here we report that a pilus-deficient mutant of Geobacter sulfurreducens could not reduce Fe(iii) oxides but could attach to them. Conducting-probe atomic force microscopy revealed that the pili were highly conductive. These results indicate that the pili of G. sulfurreducens might serve as biological nanowires, transferring electrons from the cell surface to the surface of Fe(iii) oxides. Electron transfer through pili indicates possibilities for other unique cell-surface and cell–cell interactions, and for bioengineering of novel conductive materials