This is a retrospective chart review with convenience sampling of

This is a retrospective chart review with convenience sampling of patients on NSAIDs (at least five tablets a

week, for at least 3 months prior to the study), attending the Rheumatology clinic of a tertiary care institution in south India between June 2004 and November 2004. Those with pre-existing heart disease, hypertension, thrombo-embolic disease, peptic Ipatasertib ulcer and patients on corticosteroids were excluded. All the recorded adverse events were noted and compared between the Celecoxib and non-selective NSAID users. Univariate analysis using Chi-square test was performed. Of the 1387 patients included, 915 were on Celecoxib. In the NSAID group, 204 had used multiple NSAIDs in sequence. Of the Celecoxib users, 164 had switched over to an NSAID during the study period. New onset of hypertension was significantly higher in the Celecoxib users as compared to non-selective NSAID users (3.06% vs. 1.27%, P = 0.04). However, those who had switched over to NSAIDs

did not show this trend. NSAID users, on the other hand, had significant gastrointestinal (GI) toxicity (2.54% vs. 0.327%, P = 0.001). A significant number of Celecoxib users who switched over to NSAIDs also developed GI toxicity (6.1% vs. 1.21%, P = 0.018) over a shorter time span, as compared to the continuous NSAID users. Multiple NSAID users had higher adverse events (6.37% vs. 2.23%, P = 0.023) as compared to single NSAID users. Celecoxib significantly increased the incidence of new onset hypertension in this cohort of Indian patients with rheumatic diseases. No thromboembolic events were documented. Non-steroidal anti-inflammatory drugs MK-8669 price (NSAIDs) are widely acclaimed for their anti-inflammatory, analgesic and antipyretic properties. The non-selective NSAIDs act by inhibiting both isoforms of the enzyme cyclo-oxygenase (COX-1 and COX-2).

COX-2 inhibition is mainly responsible for anti-inflammatory actions and COX-1 inhibition leads to NSAID-induced gastrointestinal damage.[1] Ribose-5-phosphate isomerase The hypothesis that selective inhibition of COX-2 isoform may help in reducing pain and inflammation without compromising the gastric mucosa led to discovery of the selective COX-2 inhibitors. Celecoxib was developed first in this group and was found to possess analgesic and anti-inflammatory efficacy comparable to the non-selective NSAIDs in treatment of inflammatory arthritic conditions.[2] In view of their gastrointestinal safety profile, within a short span of time COX-2 inhibitors gained popularity over non-selective NSAIDs.[3] However, COX-2 inhibition reduces vascular prostacyclin (PGI2) production, thus affecting the balance between prothrombotic and anti-thrombotic eicosanoids.[4] This property can tip the balance in favor of prothrombotic eicosanoids, which can lead to increased cardiovascular thrombotic events.[5] Serious concerns regarding the cardiovascular safety of Rofecoxib were expressed following the Vioxx Gastrointestinal Outcomes Research (VIGOR) study.

WT colonies were visible on agar after 2 days Colonies of 10 mut

WT colonies were visible on agar after 2 days. Colonies of 10 mutants were visible only after 18 days and 13 clones did not form colonies after 21 days. These 23 cold-sensitive mutants were further tested for growth in LB medium with shaking at 30 and 10 °C. After three independent cultures, four clones were reproducibly impaired for growth at 10 °C, 8C12, 11D1, 9H2 and 34G8 mutants (Fig. 1a). These four strains belong to the group of mutants that did not form any colony after 21 days of incubation at p38 MAPK inhibitor a low temperature. All grew as the WT strain at 30 °C (Fig. 1b). Southern hybridizations confirmed that all mutants carried

a single copy of the transposon (data not shown). For the 34G8 and 8C12 mutants, sequencing of the DNA flanking the transposon insertion site revealed that mini-Tn10 was inserted into the same chromosomal region, respectively, in the BC3773 and BC3774 ORFs, coding for the α and β subunits of the pyruvate ferredoxin

Selleck BI 2536 oxidoreductase (PFOR) involved in the reductive monocarboxylic acid cycle. In the 11D1 mutant, transposon was inserted into the promoter region of the BC3118 gene, encoding a small cytochrome P450-like enzyme with an unknown function. In the mutant 9H2, transposon was inserted into the 5′ untranslated region (UTR) of the BC0259 gene coding for a putative RNA helicase. These mutants were then tested under various stress conditions. Only the mutant 9H2 behaved as the WT over the range of pH (Fig. 2a) and NaCl (Fig. 2b) concentrations tested, suggesting that the

mutation altered a gene important for cold adaptation and not for adaptation to other stresses: this mutant was therefore selected for further characterization. Growth of the mutant 9H2 at 10 °C was delayed by approximately 100 h compared with WT, whereas at Mirabegron 30 °C, growth of both strains was identical (Fig. 1). Stable cell counts during an extended lag at 10 °C suggest cell adaptation rather than death (not shown). The morphology of 9H2 cells at 30 °C was similar to that of WT cells (data not shown). At 10 °C, WT and 9H2 cells were longer than at 30 °C and 9H2 formed large aggregates (single cells were rarely observed). During incubation at 4 °C, viable counts decreased regularly over time, and after 35 days, a viability loss of 5 log CFU was observed for WT cells vs. 4 log CFU for 9H2 cells (Fig. 3). In the presence of chloramphenicol, an inhibitor of protein translation, a viability loss of only 2 log CFU was observed for WT and 9H2 cells. In the 9H2 mutant, transposon was inserted 61 bp upstream of the start codon of the BC0259 gene encoding an RNA helicase (Fig. 4a). We confirmed by sequence analysis that the promoter located in the transposon was oriented opposite to that of BC0259 transcription, which is consequently only driven by its own promoter.

[11, 12] The Chinese study in this issue by Rong MU et al has re

[11, 12] The Chinese study in this issue by Rong MU et al. has revealed poor awareness and deficiency in diagnostic skills amongst doctors including rheumatologists and is a must- read article for all. Some of the points discussed in the preceding paragraphs are realised in this paper. Many rheumatologists who considered themselves non-believers of this vague entity in the recent past, have now turned into believers in view of LDK378 nmr emerging evidences cited above. No rheumatologist can afford to make a mistake today in diagnosing or excluding these modern day illnesses. “
“A 72-year-old woman with slight pulmonary interstitial reticular

markings was initially diagnosed with microscopic polyangiitis (MPA). Two years Kinase Inhibitor Library clinical trial later, cavitated pulmonary masses appeared, and a biopsy specimen revealed granulomas. Granulomatosis with polyangiitis (GPA) was diagnosed. The masses resolved with treatment. Ten years later, the usual interstitial pneumonia (UIP) pattern appeared on chest computed

tomography (CT). The diagnosis of lung toxicity from methotrexate (MTX) or cyclophosphamide (CYC) was precluded by the clinical course. Despite treatment with prednisolone (PSL), the UIP progressed. The change of pulmonary pathology from masses to UIP is rare in patients with GPA. “
“Polyarteritis nodosa in children is a rare necrotizing vasculitis affecting mainly small and medium-size arteries. To describe the different clinical patterns and laboratory profiles of polyarteritis nodosa patients Florfenicol in a tertiary care hospital. This was a retrospective cohort study carried out in the Department of Paediatrics, Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh during the period January 2007 to December 2012. A total of 13 patients fulfilling the European League Against Rheumatism/Paediatric Rheumatology International Trial Organization/Paediatric Rheumatology European Society (EULAR/PRINTO/PRES) classification criteria were enrolled in this study. Data was collected

via a predesigned questionnaire. Age range was 3–12 years, male : female ratio was 9 : 4. The duration of symptoms was 2–16 weeks. All the children had fever, anorexia and generalized weakness. Subcutaneous nodules were present in 77% of cases followed by arthritis and rash (69%), muscle pain (54%) and abdominal pain (38%). Impaired peripheral pulses were present in 54%, ulceration and gangrene was present in 31% and auto-amputation was present in 15% of cases. All the patients had high erythrocyte sedimentation rates followed by neutrophilic leukocytosis and thrombocytosis (85% and 62%). Skin biopsy was positive in 77% of cases and angiographic abnormalities were present in 23% of cases.

, 2002) Although the cell wall binding domain might be essential

, 2002). Although the cell wall binding domain might be essential for the enzyme’s lytic activity, some endolysins were reported to exhibit higher antibacterial activity after removal of their C-terminal domains (Borysowski Selleckchem PI3K Inhibitor Library et al., 2006). The mechanism of cell wall substrate recognition and the specificity and binding ability of the endolysins have been studied. Significant progress has been made using endolysins linked with green fluorescent protein (GFP). The specific

binding of endolysins to the cell wall substrate has been visualized by fluorescence microscopy (Loessner et al., 2002; Low et al., 2005; Korndoerfer et al., 2006; Briers et al., 2007). Corynephage BFK20, a lytic phage of the industrial producer

Brevibacterium flavum CCM 251, is the first corynephage whose genome was completely sequenced and analyzed (EMBL accession no. AJ278322) (Bukovska et al., 2006). Using a bioinformatics approach, three potential lytic genes in one cluster were identified on the BFK20 genome. In this study, we characterized BFK20 endolysin (gp24′) in detail. We have confirmed the two-domain structure PLX3397 cell line of this endolysin. The catalytic and cell wall binding domains were separately cloned, isolated and characterized. The biological activities of BFK20 endolysin and its catalytic domain were demonstrated. The C-terminal cell wall binding domain appears to be unrelated to any of the previously known cell wall binding domains. Amino acid sequences of endolysins were searched using blastp (Altschul et al., 1997) on the nonredundant database using the sequence of gp24′ as the query. We selected those sequences with E-values over 9e−07 and one sequence from Corynebacterium diphtheriae NCTC 13129 with an E-value 3e−04. These sequences were aligned using clustalw2 (Thompson et al., 1994) and manually adjusted. A domain search was performed against the Pfam databases (Bateman et al., 2004). The bacterial strains used in this study were B. flavum CCM 251 (an l-lysine production strain), B. flavum strains ATCC

21127, 21128, 21129 and 21474, Brevibacterium Orotic acid lactofermentum BLOB (a mutant derived from B. lactofermentum ATCC 21798) (Santamaria et al., 1984), Corynebacterium glutamicum RM3 (Schäfer et al., 1990) and Bacillus subtilis wt PY79 (Youngman et al., 1984). Escherichia coli XL1 Blue (Stratagene) was used for cloning experiments and E. coli BL21(DE3) (Novagen) was used as a host for the expression of recombinant proteins. Escherichia coli strains were grown at 37 °C, and corynebacteria and bacilli were grown at 30 °C in Luria–Bertani medium (Sambrook & Russel, 2001). Corynephage BFK20 was propagated on B. flavum CCM 251 according to Bukovska et al. (2006). BFK20 phage particle isolation and phage DNA purification were performed according to Sambrook & Russell (2001).

Those requiring 3–6 monthly anti-HCV testing are MSM with normal

Those requiring 3–6 monthly anti-HCV testing are MSM with normal transaminases but with regular high risk exposure (e.g., unprotected sex between men [especially in the context of concurrent STI, high risk sexual practices, and recreational drug use]), and those

regularly sharing drug equipment or snorting cocaine but with normal transaminases. However, despite the known link between cocaine snorting and acute HCV, the best screening strategy for patients remains unclear. We recommend commencing ART when the CD4 count is less than 500 cells/μL in all patients who are not to commence anti-HCV treatment immediately (1B). We suggest commencing ART when the CD4 count is greater than 500 cells/μL in all patients who are not to

commence anti-HCV treatment immediately (2D). We recommend commencing ART to allow ALK inhibitor drugs immune recovery before anti-HCV therapy is initiated when the CD4 count is less than 350 cells/μL. We recommend commencing ART to optimise immune status before anti-HCV therapy is initiated when the CD4 count is 350–500 cells/μL unless there is an urgent indication for anti-HCV treatment when ART should be commenced as soon as the patient has been stabilised on HCV therapy. Proportion of patients with a CD4 count < 500 cells/μL commencing ART CAL-101 cost The assessment and recommendations on when to initiate ART in patients with HCV/HIV infection are based on theoretical considerations and indirect data as no RCT evidence exists. Observational data demonstrate that individuals with HCV coinfection have faster rates of fibrosis progression and an increased risk of cirrhosis, ESLD, HCC and liver-related death than those with HCV monoinfection, and the risk of liver-related mortality and HCC increases as the CD4 cell count declines [43]. Successful treatment outcome with pegylated interferon (PEG-IFN) and ribavirin (RBV) therapy for Nabilone hepatitis C in the context of HCV/HIV infection lessens as the CD4 cell count declines [44–48]. ART slows the progression of liver disease by improving immune function and reducing HIV-immune

activation [49–51], although patients with coinfection are more likely to experience drug-induced liver injury (DILI), especially in the context of advanced liver disease. ART-mediated benefits to the prognosis of hepatitis C outweigh the risks of DILI, even in the setting of cirrhosis, but the importance of correct ART choice in HCV coinfection should be emphasised [52–53]. The advent of direct acting antivirals (DAAs) for HCV has increased the need of awareness of drug–drug interactions (DDI) in planning treatment strategies. There are no direct data to support early initiation of ART in individuals with HCV/HIV infection. It is important to time the start of ARVs to fit with whether or not HCV therapy is required imminently.

Palumbo and J Martinis for their help in the experiments We tha

Palumbo and J. Martinis for their help in the experiments. We thank I. Gianicolo, A. Zambonelli, M. Iotti, A. Mello, B. Finot and A. de Miguel for providing fruiting bodies of Tuber species, and E. Martino for providing O. maius isolates. M.V. and C.M. acknowledge financial support by the University of Turin. E.Z. PhD fellowship was funded by the University of Turin. This research was funded by the University I-BET-762 concentration of Turin, by Fondazione Sanpaolo and by Regione Piemonte. C.M. and E.Z. contributed equally to this work. “
“Although the biosynthesis of oxalic acid is known to occur in a number of bacteria, the mechanism(s) regulating its production remains largely unknown. To date, there is no report on

the identification of an oxalic acid ZD1839 molecular weight biosynthetic pathway gene from bacteria. In an attempt to identify such a gene(s), a mutant screen was conducted using the simple oxalic acid-producing phytopathogenic bacterium, Burkholderia glumae. Four mutants that failed to produce oxalic acid were isolated from

a transposon-mutagenized B. glumae library and named Burkholderia oxalate defective (Bod)1. DNA sequence analysis revealed that each mutant contained an insertion event at different sites in the same ORF, which we referred to as the oxalate biosynthetic component (obc)A locus. Complementation of the Bod1 mutant with the obcA gene, however, resulted only in a partial restoration of the oxalic acid-producing phenotype. Further complementation studies utilizing a larger DNA fragment encompassing the obcA locus coupled with deletion mutagenesis led to the identification of another ORF that we named the obcB locus,

which was essential for higher levels of oxalic acid production. Transcript analysis indicated that both obcA and obcB are coexpressed and encoded on a single polycistron message. Oxalic acid is the simplest of the organic dicarboxylic acids. It is considered a relatively strong acid with good reductive power, making it prevalent in a variety of industrial applications (Strasser et al., 1994; Rymowicz & Lenart, 2003; Meyer-Pinson et al., 2004). Currently, the bulk of the acid is produced chemically, but there has been some interest in the development of fermentative processes utilizing oxalic acid-producing microorganisms (Strasser et al., 1994; Rymowicz & Lenart, 2003; Meyer-Pinson et al., 2004). As in the SPTLC1 chemical industry, oxalic acid is also common in nature; its biosynthesis has long been known to occur in a variety of organisms such as bacteria, fungi, plants, and animals (Hodgkinson, 1977; Franceschi & Nakata, 2005). The functional role of oxalate in each organism can differ along with its chemical form and distribution (Hodgkinson, 1977; Dutton & Evans, 1996; Franceschi & Nakata, 2005). In microorganisms, oxalic acid has been shown to serve a number of important functions, which include roles in metal tolerance (Dutton & Evans, 1996; Sayer & Gadd, 1997; Appanna & Hamel, 1999; Green & Clausen, 2003), nutrient acquisition (Shimada et al.

Palumbo and J Martinis for their help in the experiments We tha

Palumbo and J. Martinis for their help in the experiments. We thank I. Gianicolo, A. Zambonelli, M. Iotti, A. Mello, B. Finot and A. de Miguel for providing fruiting bodies of Tuber species, and E. Martino for providing O. maius isolates. M.V. and C.M. acknowledge financial support by the University of Turin. E.Z. PhD fellowship was funded by the University of Turin. This research was funded by the University Dabrafenib concentration of Turin, by Fondazione Sanpaolo and by Regione Piemonte. C.M. and E.Z. contributed equally to this work. “
“Although the biosynthesis of oxalic acid is known to occur in a number of bacteria, the mechanism(s) regulating its production remains largely unknown. To date, there is no report on

the identification of an oxalic acid R428 purchase biosynthetic pathway gene from bacteria. In an attempt to identify such a gene(s), a mutant screen was conducted using the simple oxalic acid-producing phytopathogenic bacterium, Burkholderia glumae. Four mutants that failed to produce oxalic acid were isolated from

a transposon-mutagenized B. glumae library and named Burkholderia oxalate defective (Bod)1. DNA sequence analysis revealed that each mutant contained an insertion event at different sites in the same ORF, which we referred to as the oxalate biosynthetic component (obc)A locus. Complementation of the Bod1 mutant with the obcA gene, however, resulted only in a partial restoration of the oxalic acid-producing phenotype. Further complementation studies utilizing a larger DNA fragment encompassing the obcA locus coupled with deletion mutagenesis led to the identification of another ORF that we named the obcB locus,

which was essential for higher levels of oxalic acid production. Transcript analysis indicated that both obcA and obcB are coexpressed and encoded on a single polycistron message. Oxalic acid is the simplest of the organic dicarboxylic acids. It is considered a relatively strong acid with good reductive power, making it prevalent in a variety of industrial applications (Strasser et al., 1994; Rymowicz & Lenart, 2003; Meyer-Pinson et al., 2004). Currently, the bulk of the acid is produced chemically, but there has been some interest in the development of fermentative processes utilizing oxalic acid-producing microorganisms (Strasser et al., 1994; Rymowicz & Lenart, 2003; Meyer-Pinson et al., 2004). As in the Idoxuridine chemical industry, oxalic acid is also common in nature; its biosynthesis has long been known to occur in a variety of organisms such as bacteria, fungi, plants, and animals (Hodgkinson, 1977; Franceschi & Nakata, 2005). The functional role of oxalate in each organism can differ along with its chemical form and distribution (Hodgkinson, 1977; Dutton & Evans, 1996; Franceschi & Nakata, 2005). In microorganisms, oxalic acid has been shown to serve a number of important functions, which include roles in metal tolerance (Dutton & Evans, 1996; Sayer & Gadd, 1997; Appanna & Hamel, 1999; Green & Clausen, 2003), nutrient acquisition (Shimada et al.

, 2011) In humans, the default mode network not only

, 2011). In humans, the default mode network not only PD0325901 datasheet consists

of mPFC areas but also medial parietal areas (including midline anterior and posterior cingulate cortices; Raichle et al., 2001). Recent investigations in macaques have identified electrophysiological correlates of default mode processing in both mPFC and posterior cingulate cortices (Hayden et al., 2009; Kojima et al., 2009). The positron emission tomography imaging study of Kojima et al. (2009) in awake unanaesthetized monkeys clearly demonstrated a default mode of cortical activity with higher rest-related activity in mPFC areas compared with working memory tasks. The activity in macaque mPFC reported here before and during eye-closure may therefore represent in part alterations in the activity of mPFC areas associated with the default mode network in monkeys. It is of interest that Rudolph et al. (2007)

reported that a significant proportion (~45%) of presumed pyramidal (broad spike/regularly spiking) neurons in parietal association cortex also discharged during SWS and were silent during waking. In relation to these default mode network studies, the value of the present investigation is that it shows electrophysiologically that the firing rates of a significant NVP-BKM120 mouse number of mPFC neurons (those of cell Type 1 representing about 28% of sampled neurons) in the monkey were low in the awake state (mean 3.1 spikes/s) and increased significantly during sleep (mean 10.2 spikes/s). The firing rates of the neurons involved in default mode network activities, and exactly how they may change, is not directly measured in human neuroimaging studies. Given the increase in the human BOLD (blood oxygen level-dependent) response during operation of the default mode network, it is tempting to speculate that some of the neurons whose firing rates increased during periods of ‘eye-closure’ may have intracortical axonal arbors instrinsic to the mPFC that innervated nitric oxide (NO)-producing cells (Gabbott and Bacon, 1996). The activity of such cells would lead to local vasodilatation

(through NO-mediated mechanisms) and thus increased blood flow in specific mPFC regions with raised metabolic demands during periods of augmented information processing Methane monooxygenase (Duchemin et al., 2012). The data from the present study have implications for the generation of sleep activity in humans, both in health and in disease. Many neuropsychiatric and neurodevelopmental disorders, for example depression, schizophrenia and autism, which include functional modifications of the default mode network, have symptoms that include poor sleep architecture (Drevets et al., 1997; Wichniak et al., 2000; Vogt, 2009; Gregory et al., 2011; Vukadinovic, 2011; Price & Drevets, 2012). Patterns of abnormal sleep structure (narcolepsy, sleep inertia, parasomnias, non-REM and REM sleep behaviour disorders, etc.

All of these were abundantly produced by S mycoparasitica on F

All of these were abundantly produced by S. mycoparasitica on F. graminearum Selleckchem ABT199 hyphae. Formation of these structures as well as haustorial penetration appeared 2 days later in F. graminearum than in F. avenaceum and F. oxysporum (Goh & Vujanovic, 2010). Soon after, S. mycoparasitica sporulated on F. avenaceum and F. oxysporum (Goh & Vujanovic, 2010), as well as on both F. graminearum chemotypes as presented in this study. Sporulation is an additional criterion for determining mycoparasite host ranges because melanosporaceous biotrophic mycoparasites were observed to undergo sporulation on specific Fusarium isolates only (Harveson & Kimbrough, 2001a, b). The germination test of S. mycoparasitica

ascospores in Fusarium filtrates showed that F. graminearum is one of the principal hosts of the mycoparasite, together with F. avenaceum and F. oxysporum. In contrast, F. proliferatum and F. sporotrichioides do not appear to be hosts. A few biotrophic,

mycoparasitic fungi (Gonatobotrys, Dicyma, Stephanoma, Melanospora and Piptocephalis) acquire certain nutrients (mycotrophein, biotin or aneurin) from their hosts for growth and generation of sexual reproductive organs (Hawker, 1938; Jeffries & Young, 1994; Rakvidhyasastra & Butler, 1973; Whaley & Barnett, 1963). During interactions with F. graminearum 3-ADON (but not with 15-ADON) and by an as yet unknown mechanism, S. mycoparasitica removed the pathogen red-colored compounds, possibly aurofusarin (Kim et al., CP-868596 ic50 2005), and subsequently released crystal-like red-colored substances (Fig. 3). We hypothesize that S. mycoparasitica absorbs aurofusarin from attacked Fusarium cells through lysis of the pathogen membrane components, such as chitin by production of chitinase and chitosanases (Goh & Vujanovic, 2010; Manocha, 1987). This property of S. mycoparasitica could imply detoxification or neutralization of aurofusarin, a notable F. graminearum mycotoxin new (Dvorska et al., 2001; Dvorska & Surai, 2004). Moreover, trichothecene mycotoxins

may play an important role in the aggressiveness of F. graminearum towards plant hosts (Doohan et al., 1999). In this study, S. mycoparasitica demonstrated a capacity to markedly reduce the amount of Tri5 gene fragments in both 3-ADON and 15-ADON strains (P=0.05). Mycoparasitic biodegradation of mycotoxins is often related to production of lactonase enzymes involved in mycotoxin hydrolysis. Gliocladium roseum, a mycoparasite, showed detoxification of zearalenone mycotoxin through hydrolysis of fungitoxic zearalenone by these catalysts, followed by a spontaneous decarboxylation (Utermark & Karlovsky, 2007). A previous study highlighted degeneration of the cytoplasm of F. avenaceum and F. oxysporum hyphal cells challenged with S. mycoparasitica (Goh & Vujanovic, 2010). In this study, linear growth of both F. graminearum chemotypes was significantly decreased in the presence of S. mycoparasitica (Fig. 4), with similar cytoplasmic breakdown.


“The evolution of microbial genomes is greatly influenced


“The evolution of microbial genomes is greatly influenced by horizontal gene transfer (HGT), where large blocks of horizontally acquired foreign sequences, often encoding virulence determinants, occur in chromosomes of pathogenic bacteria. A program design-island developed in our laboratory was used on three completely sequenced Vibrio cholerae genomes,

V. cholerae Classical O395, El Tor N16961 and MJ1236, in order to identify the putative horizontally acquired regions. The putative genomic islands this website (GIs) were graphically represented and analyzed. The study identified distinct regions in the GIs of V. cholerae MJ1236 which were shared either with the Classical or the El Tor strain of Natural Product Library V. cholerae. A cluster comprising of 38 ORFs was common to V. cholerae strains of MJ1236 and Classical O395 but absent in El Tor N16961. About 5% of the predicted GIs of V. cholerae MJ1236 were unique to itself. Among these unique ORFs, a region of mostly hypothetical genes was identified, where the ORFs were present in a large cluster. The results show that the HGT had played a significant role in the evolution and the differentiation of V. cholerae MJ1236. Vibrio cholerae, a Gram-negative bacterium, is the etiological agent of epidemic cholera,

that causes a severe and sometimes lethal diarrheal disease. Vibrio cholerae is classified into two serogroups: O1 and non-O1. So far, the toxigenic strains of serogroups O1

and O139 have been found to cause cholera epidemics. There are two biotypes of V. cholerae O1, Classical and El Tor. There have been seven major pandemics since 1817. Isolates of the sixth pandemic were of O1 classical biotype, whereas the seventh pandemic, which Fludarabine started in 1961, is associated with El Tor biotype (Chaudhuri & Chatterjee, 2009). This indicated that a transition might have occurred, which largely replaced the V. cholerae Classical by V. cholerae El Tor as the causative organism for pandemicity between 1905 and 1961. In 1994, the new Matlab variants of V. cholerae El Tor replaced the seventh pandemic O1 El Tor strains in Asia and Africa as the predominant isolate from clinical cases of cholera (Safa et al., 2008). In V. cholerae, the two major virulence factors, cholera toxin (CT) and toxin coregulated pili (TCP), have been reported to be encoded on mobile genetic elements. The ctxAB genes, coding for A and B subunits of CT, are encoded on a filamentous bacteriophage CTXϕ. TCP, an essential colonization factor, was originally designated as part of a pathogenicity island named Vibrio pathogenicity island (VPI), but this island has more recently been proposed to be the genome of a filamentous phage, VPIϕ (Karaolis et al., 1999).