22q11 deletion syndrome (22q11DS) is one of the most common multiple anomaly syndromes, and many dentists are likely to meet patients with the syndrome. Odontological research has focused on describing and analysing conditions/concepts

based on the current state of knowledge within the dental profession. Yet, these research topics are not necessarily the most important issues for the patients. Aims.  To explore and describe, by use of Grounded theory, parents’ experiences of oral health issues and needs for dental care in their children with 22q11DS. Design.  Twelve parents from different regions in Sweden were interviewed. Analyses were carried out according to Grounded theory. Results.  Parents recognised good oral NVP-LDE225 in vivo health as important for the wellbeing of their children. Oral health was a concern and the parents described the fight for this as struggling in vain for good oral health in their child. Conclusions.  Parents not only described their children’s oral health as important but also hard to gain. Thus, it is important that all patients with disabilities, regardless of whether there is a defined medical diagnosis or not, are identified and see more well taken care of in the dental care system.

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“International Journal of Paediatric Dentistry 2010; 20: 102–111 Purpose.  The purpose was to describe pathologic paediatric conditions associated with airway compromise adversely affecting dental treatment with sedation and general anaesthesia. Methods.  A review of available literature was completed, identifying pathologic paediatric conditions predisposing to airway compromise. Results.  Airway-related deaths are uncommon, but respiratory complication represents the greatest cause of morbidity and mortality during the administration of general anaesthesia. Differences in anatomy and physiology of the paediatric and adult airway

contribute to the child’s predisposition to rapid development of airway compromise and respiratory failure; juvenile rheumatoid arthritis, cervical spine injury, morbid obesity, and prematurity represent only a few conditions contributing to potential airway compromise of which the paediatric clinician needs to be aware. In all cases, thorough physical examination prior to treatment is mandated VDA chemical to affect a positive treatment outcome. Conclusions.  Successful management of children and adolescents with a compromised airway begins with identification of the problem through a detailed medical history and physical examination. Due to the likely fragile nature of many of these patients, and possibility of concomitant medical conditions affecting airway management, dental treatment needs necessitating pharmacological management are best treated in a controlled setting such as the operating room, where a patent airway can be maintained. “
“International Journal of Paediatric Dentistry 2010; 20: 366–373 Background.

caseolyticus and 99±1% (97.3±1.5% at 24 h) – untreated cells. Thus, there are no apparent or systematic differences in macrophage viability during the initial 6-h incubation period of the experiment, corresponding to the period of cytokine peak. In light

PF-02341066 chemical structure of the in vitro proinflammatory cytokine induction of S. iniae EPS, we were next interested in determining whether similar events also occur in vivo, and in revealing the clinical outcomes following EPS inoculation. To accomplish this we first constructed a dose-effect (lethal) model. Mortality rates were affected by both time and group (EPS/LPS dosages). As shown in Fig. 3, EPS induced death of fish in a dose-dependent fashion: low doses (0.55 mg per fish) resulted in 10% mortality, while higher doses resulted in increased

mortality rates (P<0.001). Administration of 2.2 mg of EPS per fish resulted in 60% mortality within the first 24 h, while 1.1 mg of EPS per fish yielded 40% mortality during the same period (P<0.01 between these doses). Mortality in fish injected with the higher doses continued for several more days, cumulating in 90% at 144-h postinoculation, resembling that of the LPS-induced septic shock in a mouse model (An et al., 2008) and the (24-h delayed) LPS-induced mortality (80%) of trout observed in the present work (Fig. 3). None of the PBS-injected fish succumbed. 3-deazaneplanocin A manufacturer Gross pathological findings in dead and moribund fish consisted in discoloration of skin (mainly around the tail), presence of ascitic fluids in the celomic cavity and inflammation with ecchymotic hemorrhages in the gut and peritoneum. Thus, 1.1 mg of EPS per fish was used as the effective dosage in subsequent experiments where cytokine-specific mRNA transcripts levels were assessed. Relative cytokine mRNA levels analysis revealed that augmentation of specific transcripts was significantly superior to that of the in vitro system. Following inoculation

of EPS, TNF-α2 Amobarbital transcription levels peaked at 12-h postinjection (1320-fold increase) and remained elevated for a considerable time (71-fold increase at 24 h), whereas TNF-α1 transcription levels, peaking at 12-h postinjection, were relatively lower (18.1-fold increase) and decreased to a 2.8-fold increase at 24 h (P<0.01 for the difference between the two cytokines) (Fig. 4). LPS injection (Fig. 5) resulted in 115.4-fold increase of TNF-α2 transcripts (remaining elevated throughout the experiment) and 25.9-fold increase of TNF-α1 transcripts (at 9 h). Differences between the two cytokines were nonsignificant. Injection of PBS (negative control) did not affect cytokine transcription levels. IL-1 transcript level among the EPS-injected fish was increased by 209-fold; IL-6 transcript level of the same fish was increased 560.9-fold. LPS-injected fish showed a 252.1-fold increase of IL-1 transcripts and a 536.7-fold increase of IL-6 transcripts (P<0.001). All of the IL transcripts peaked at 6–9-h postinjection.

One limitation of our study may be that the population of cases was highly heterogeneous, particularly

in terms of history of antiretroviral therapy. The cases were diagnosed between 1988 and 2007, i.e. before and during the cART era. We tried to minimize this effect by matching cases and controls for CH5424802 time period as well as for CD4 cell counts, in order that cases and controls should be similar in terms of antiretroviral regimens received. Another limitation of this study is that results of EBER staining were not available and therefore some lymphoma cases may have been EBER negative and not EBV-driven NHL. This may have minimized the predictive value of high EBV loads in PBMCs for progression to systemic lymphoma in our study. However, this potential

bias does not invalidate our finding that a high EBV load in PBMCs was associated with an increased risk of developing systemic B lymphoma. Finally, one could argue that EBV load may only be a surrogate marker for immunosuppression rather than an independent marker for the risk of occurrence of B systemic lymphoma. However, a high level of EBV DNA in PBMCs remained significantly associated with a higher risk of subsequent progression to systemic B lymphoma, after adjustment for CD4 cell count at sample date or for CD4 cell count nadir. Immune reconstitution is probably the main explanation for the lower MYO10 incidence of ARL following the widespread use Olaparib mw of cART. Nevertheless, some treated patients with satisfactory immune recovery (CD4 cell count > 350 cells/μL) still develop systemic B lymphoma [7, 27]. This underlines the need to identify additional risk factors for lymphoma in HIV-infected patients. Gasser et al. demonstrated that a lack of EBV-specific CD4 T-cell immunity was associated with

the occurrence of PBL irrespective of CD4 cell count [28]. Different groups reported that uncontrolled HIV replication during cART, assessed by HIV cumulative viraemia, was predictive of the development of AIDs-related lymphoma independently of the CD4 cell count, but the underlying mechanisms of this association remain unclear [6, 27, 29]. Recently, Bohlius et al. reported that, among patients under cART, those who had experienced decreasing CD4 cell counts despite suppression of HIV-1 replication were at a higher risk of developing Hodgkin lymphoma [30]. Jaffe et al. reported that, in untreated patients, initially low and further decreasing CD4 cell counts within 12 months before the diagnosis were predictive of both NHL and Kaposi sarcoma [31]. High EBV DNA blood loads have been reported in up to 20% of asymptomatic HIV carriers and high viral loads persisted over time in more than 80% of this subset of patients [32].

g., Flood et al., 1987; Turner & Deupree, 1991; Flood, 1993), and alterations in dendritic spines are region-specific, and will be discussed in terms of synapse number below. In rodents, there is loss of axospinous synapses from the layer 2 medial entorhinal cortex projection to granule cells (Geinisman http://www.selleckchem.com/products/gsk1120212-jtp-74057.html et al., 1992) and reduced synaptophysin staining in the dendritic region of CA3 pyramidal cells (Smith et al., 2000) during aging. The synaptic input to CA1 pyramidal cells from CA3, however,

does not show synapse reduction (Geinisman et al., 2004). However, a subset of the synaptic contacts in this region exhibit reduced postsynaptic density size (Nicholson et al., 2004), and electrophysiological evidence suggests that this group of synapses may reflect nonfunctional ‘silent’ synapses (Barnes et al., 1997; Burke & Barnes, 2010). Clearly, anatomical changes do occur within the hippocampus in normal aging, although they are rather subtle compared with those known to occur in pathological conditions that arise during aging, such as AD (e.g., Ballard et al., 2011). The impact

that these neurological changes have on plasticity and circuit function is discussed below. Hippocampal cell function in aging animals is strikingly well preserved. In rats it is possible to study the detailed biophysics of individual hippocampal principal cells using in vitro recording methods. Most biophysical properties in these aging cells do not change Epacadostat in vivo (for reviews, Burke & Barnes, 2006; Hoang et al., 2012), with a small number of exceptions including a larger after-hyperpolarizing potential in CA1 pyramidal cells of old rats (e.g., Landfield & Pitler, 1984). This change may be due to an increased number of L-type calcium channels in old CA1 cells (e.g., Thibault & Landfield, 1996). This increase in channel Selleck Verteporfin numbers is hypothesized to lead to age-related disruption of neuronal calcium homeostasis, suggesting an interesting potential therapeutic target

(for review, Kumar et al., 2009). There are two additional electrophysiological changes that are observed in all three subregions of the hippocampus. These include reduced amplitude of the stimulation-induced cholinergic slow excitatory postsynaptic potential (Shen & Barnes, 1996), and an increase in gap junction-mediated electrotonic coupling between aged CA1 and CA3 pyramidal cells, as well as granule cells (Barnes et al., 1987). The former age-related change suggests reduced effectiveness of a modulatory input, and the latter increased electrical communication between cells. The alterations described above are consistent with both increased excitability (increased calcium conductance, increased electrotonic coupling) and decreased excitability (reduced cholinergic modulation) of old cells. Taken together the data suggest a complex set of mechanisms at play that may tend to keep overall cell function stable in the aged brain.

In this issue of the Journal of Travel Medicine, Rossi and Genton have contributed to our limited understanding of the pre-travel encounter by assessing the effect of actual versus intended travel plans on pre-travel health recommendations.[8] One could interpret their findings in a number of ways, including the following: the pre-travel risk assessment cannot predict actual travel exposures, and thus may not help to manage travel-related

risk, the assessment is sensitive and robust enough to deal with travel-related risk, even if travelers substantially change their itinerary, or the assessment itself may have been part of the intervention, and can lead to alterations in a traveler’s original plans. It is hard to know the correct Tamoxifen research buy interpretation, but this research is a good first step. However, there remains much to study to fully understand the complexity of the pre-travel visit. If the encounter is seen more as a conversation, then one

can appreciate the back and forth discussion of uncertainties needed to characterize travel-related risks of a given traveler. These identified risks may be further categorized into three or four groups, as follows: Preventable risks: those risks identified pre-travel that can be completely or nearly eliminated through an intervention, such as immunization or chemoprophylaxis Avoidable risks: those risks identified pre-travel that can be avoided by the traveler through counseling leading to awareness and/or behavior changes, such as safe sex practices or preparedness for Scuba diving Manageable risks: those risks identified pre-travel selleck that can be self-managed through standby treatment

for such conditions as traveler’s diarrhea or human immunodeficiency virus (HIV) exposure Unexpected risks: those risks Leukotriene-A4 hydrolase that may not be anticipated pre-travel but can be addressed through appropriate contingency planning, such as carrying adequate travel medical insurance and/or medical evacuation insurance. Assessing the need for specific interventions should also not be solely based on a traveler’s current plans, but also on future traveling intentions. Exposures to travel-related hazards may occur in different time patterns resulting in very different types of risks, such as: One-time or singular events [eg, first-time yellow fever (YF) immunization and the risk of YEL-AVD; an involuntary blood exposure and the risk of HIV-1 infection; flight from sea level to altitude >3,000 m and the risk of acute mountain sickness]. Intermittent (eg, malaria risk in rotational business travel with a return to the home country after each tour; island hopping using ferries and risk of drowning; deep vein thrombosis risk during a series of long-haul air flights). Continuous or ongoing (eg, malaria risk in expatriates living in endemic regions; YF infection risk in YF endemic area among unimmunized travelers).

, 2009). IIANtr is a component of the Ntr-phosphotransferase system that is conserved in many proteobacteria (Deutscher et al., 2006). In this system, EINtr (encoded by ptsP) transfers phosphoryl groups to NPr, which subsequently phosphorylates protein IIANtr (Rabus et al., 1999; Zimmer et al., 2008). The Ntr-PTS works in parallel to the phosphoenolpyruvate : carbohydrate phosphotransferase system (transport-PTS) in E. coli. Because no obvious phosphoryl group acceptor was identified for phospho-IIANtr, it was

speculated that this system has regulatory rather than transport function. Earlier it was shown that dephosphorylated IIANtr binds and inhibits the low-affinity K+ transporter TrkA, suggesting that the Ntr-PTS somehow regulates K+ homeostasis (Lee et al., 2007). Thereupon, it was demonstrated that kdp promoter activity is stimulated

find more by the dephosphorylated form of IIANtr (Fig. 2c). The connection between the Ntr-PTS and the Kdp system was found in a search for a potential phospho-acceptor for IIANtr. Overproduction of IIANtr resulted in the accumulation of a phosphorylated protein that was identified as phospho-KdpB (Lüttmann et al., 2009). In parallel, a transposon clone library was screened for enhanced expression of kdpFABC in the presence of 5 mM K+, a concentration that normally represses the expression of the target operon. Two independent transposon mutants were isolated out of 9000 tested, in which kdpFABC expression was significantly elevated. Both insertions

mapped in gene ptsP that encodes EINtr, providing independent evidence for the inter-relation between Kdp and Ntr-PTS (Lüttmann et al., 2009). Two-hybrid data and biochemical NVP-BKM120 supplier analysis revealed Carnitine palmitoyltransferase II that the nonphosphorylated IIANtr interacts with KdpD and stimulates its autokinase activity. Subsequently, the level of phospho-KdpE is increased and kdpFABC is induced. It was also found that the supplied carbon source influenced kdpFABC expression, which might be related to a ‘cross-talk’ between the Ntr-PTS and the transport-PTS. When cells utilized preferred carbohydrates such as glucose, which results in dephosphorylation of the transport-PTS and also of IIANtr, kdpFABC expression was enhanced. In summary, the Ntr-PTS links carbohydrate metabolism and K+ homeostasis via the KdpD/KdpE system. Based on the results described above, the following model for activation, internal signaling, and signal integration of the KdpD/KdpE system is proposed (Fig. 2). The histidine kinase KdpD perceives different chemical stimuli from the cytoplasm (K+ concentration, ionic strength, and ATP content) that modulate the ratio between kinase and phosphatase activity. Upon activation, KdpD is transferred into the ‘ON’ state that is characterized by a high kinase to phosphatase ratio. The transition between ‘OFF’ and the ‘ON’ involves alterations of electrostatic interactions within KdpD. KdpD is a dimer, and autophosphorylation occurs in trans.

, 1987), which was different from what was observed in C. albicans with fluconazole (Andes et al., 2006). A possible explanation for the difference in the best dosing strategy in the different systems was proposed by Andes et al. (2006) to be the differences in modes of action on the target organisms. Aminoglycoside antimicrobials have cidal activities

against the bacteria tested while fluconazole is a fungistatic agent for C. albicans. The cidal activity of CP-690550 concentration the aminoglycoside antimicrobials can effectively reduce the population size of the pathogens and thus reduce the supply of beneficial mutations. Under this type of selection, genetic drift may play a more important role because of the smaller population sizes, leading to the higher frequency of loss of rare beneficial mutations; thus exposure to a cidal agent may result in a more click here homogeneous population structure containing few drug-resistant mutants. However, a fungistatic agent may not effectively reduce the size of the population significantly to prevent the emergence of rare beneficial mutations, possibly leading to a more heterogeneous population containing multiple beneficial mutants. Thus, depending on the mode of action of the antimicrobial agent, different population dynamics may emerge. Additional studies with C. albicans using

fungicidal agents will help to shed additional insight on the effects of the mode of action of the drug on the population dynamics during drug exposure.

The fitness effect associated with a resistance mutation plays a key role in determining whether the resistant genotype can survive drift and whether it will become dominant in the population (Andersson, 2003; Andersson & Hughes, 2010). It is expected that if drug-resistant mutations carry a fitness cost in the absence of drug, the proportions of the drug-resistant phenotypes will decrease and may even be eliminated from the population when the drug is removed and further compensatory evolution is absent. This type of trade-off in the relative fitness between different environments is commonly Progesterone observed (Johanson et al., 1996; Schrag & Perrot, 1996; Schrag et al., 1997; Bjorkman et al., 1998, 1999; Sandegren et al., 2008). Several scenarios have been used to describe such differences in fitness effects in different environmental conditions (Elena & Lenski, 2003). The first scenario is antagonistic pleiotropy (AP), which describes mutations that are beneficial in one condition but are deleterious in another environment. The second is mutation accumulation (MA), in which neutral mutations that accumulated in one environment are deleterious in another condition. The third scenario is independent adaptation (IA), which describes mutations with beneficial effects in one environment but neutral in another.

Amylase solution (1 mL) was incubated at 70 °C with 0.5% soluble starch in Tris–HCl buffer (pH 10.0) containing 10% NaCl. Aliquots were drawn at different time intervals, and hydrolysis was stopped by boiling at 100 °C. After centrifugation at 12 000 g for 15 min, each sample was Compound C purchase analyzed by HPLC analysis on a micro

Bond pack Amino Carbohydrate column (4.1 × 300 mm). Samples (15 μL) were injected and eluted with acetonitrile/water (70 : 30 ratio) at a flow rate of 1 mL min−1. The hydrolyzed products were detected using a refractive index detector. Glucose, maltose, maltotriose, and maltopentaose (Sigma) were used as standards. Based on morphological, physiological, and biochemical characteristics, the isolate LY20 is a Gram-positive, motile, rod-shaped and aerobic bacterium.

Colonies are PLX4032 solubility dmso light yellow, uniformly round, circular, and convex on CM agar plate. It was able to grow in medium containing 0.5–25% (w/v) NaCl and grew optimally at 10% (w/v) NaCl. No growth was observed in the absence of NaCl. Thus, this bacterium can be considered as a moderately halophilic microorganism (Ventosa et al., 1998). Optimal temperature and pH for bacterial growth were 37 °C and 10.0. H2S production, methyl red, and Tween-80 hydrolysis were negative, while Voges–Proskauer test, nitrate reduction, oxidase, catalase, and gelatin hydrolysis were positive. Acid is produced from maltose, fructose, sucrose, and glucose. OSBPL9 Phylogenetic analysis based on 16S rRNA gene sequence comparisons revealed that the isolate LY20 belonged to Salimicrobium species and was most closely related to Salimicrobium halophilum DSM 4771T (98.9% 16S rRNA gene sequence similarity; Fig. 1). As shown in Fig. 2, both enzymes started

to produce from the early-exponential phase of bacterial growth (4 h for amylase and 10 h for protease) and reached a maximum level during the early-stationary phase (42 h). Both enzymes were purified by ammonium sulfate precipitation, Q-Sepharose ion exchange, and Sephacryl S-200 gel filtration chromatography. The amylase was purified 21.5-fold with recovery of 31.9% and specific activity of 573.5 units mg−1 protein, while protease was purified 27.5-fold with recovery of 32.4% and specific activity of 832.7 units mg−1 protein. Molecular weights of the β-amylase and protease were determined to be 81 and 30 kDa, respectively (Fig. 3, lanes 2 and 3), corresponding with those determined by gel filtration. These results indicated that both enzymes from LY20 were monomeric ones. Also, zymographic activity staining revealed the activity bands for purified samples at corresponding positions on SDS-PAGE (Fig. 3, lanes 4 and 5). The amylase hydrolyzed soluble starch to form maltose as the main product. This product was readily apparent during the early stages of the reaction and increased in concentration along with the time course of the reaction.

The 18 clinical isolates

and the two type strains (B. megaterium ATCC14581T and B. frigoritolerans DSM 8801T) were characterized using a standard set of biochemical tests (Weyant et al., 1996). For the production of B. anthracis-specific, d-PGA capsular antigens, the fresh vegetative growth of each isolate was used to inoculate 450 μL of heart infusion broth (Remel) supplemented with 50% heat-inactivated horse serum and 0.8% sodium bicarbonate, and incubated at 35 °C for 3 h. Detection of the d-PGA by the CAP-DFA assay was performed as described previously (De et al., 2002). SP600125 in vitro Capsule visualization using India ink was performed as described in Luna et al. (2006), with the following exceptions: (1) cells were grown overnight on SBA at 30 °C, under 5% CO2,

and used to inoculate TSA plates containing 0.8% sodium bicarbonate (bicarbonate agar), which were then incubated under the same conditions; (2) two to three drops of India ink were added directly to the bacterial suspension; and (3) 5 μL of selleck chemical the suspension was added to a microscope slide and covered with a coverslip. Cells from both the DFA assay and India ink stain were viewed and photographed under oil immersion at × 1000 (UV and phase contrast, respectively), using a Nikon Eclipse 50i UV microscope and a Nikon Digital Sight DS-1 camera (Melville, NY). To test whether the capsules were covalently attached to the cell surface, the cells were heated at 60 °C for 30 min, and then stained with India ink as just described (Candela & Fouet, 2005). The colony morphology

of the isolates on bicarbonate agar was also noted, as encapsulated cells usually appear as mucoid or shiny colonies. DNA contained in the cell lysates of each isolate was used for all molecular testing (Hoffmaster et al., 2002). 16S rRNA gene sequencing was performed as described previously using the primers 8F and 1492R for amplification (Sacchi et al., 2002). BigDye 3.1 (Applied Biosystems, Foster City, CA) was used for sequencing the reactions and products were run on an ABI 3130xl (Sacchi et al., 2002). Analysis of the 16S rRNA genes was performed using gcg ver 10.3 (Accelrys, San Diego, CA) to assemble, compare, and align sequences. The 16S rRNA gene sequences were used in blast searches to determine the best similarity to sequences in the NCBI database (http://blast.ncbi.nlm.nih.gov/Blast.cgi). Neighbor-joining analysis was performed using Kimura-2 parameter correction and 1000-step bootstrap in mega 4 (Tamura et al., 2007). The 16S rRNA gene sequences obtained were deposited in the GenBank sequence database under accession numbers GU252108–GU252128. PCR amplification to detect the presence of four B. anthracis capsule genes (capA, capB, capC, and capD) was performed using previously published primers (Hoffmaster et al., 2006; Luna et al., 2006) and carried out in separate, 10-μL reaction volumes containing 1.5 mM MgCl2, 1 × buffer, 200 μM dNTPs, 2.5 U Platinum Taq polymerase (Invitrogen, Foster City, CA), 0.

The subsequent sequencing at ctxB loci revealed the presence of genotype 5 of ctxB in CTX prophage with rstRET and genotype 4 of ctxB in CTX prophage with rstRcalc. The prominent

events in the changing profile of CTX prophages with respect to CT genotypes and rstR alleles among O139 strains from January 1993 to December 2005 are shown in Fig. 1 along with the isolation status of V. cholerae O139 strains from patients hospitalized due to acute secretory diarrhoea at the Infectious Diseases Hospital, Kolkata. Nested PCR results depicted the schematic representation (Fig. 2) of variable combinations of CT genotypes, and rstR alleles prevailed among O139 Alectinib ic50 strains in Kolkata. Since its first appearance in 1993, five types of O139 strains have been detected successively with the following important changes: (1) strains with CT genotype 3 only; (2) strains with CT genotype 4 only; (3) strains with CT genotype 5 only; (4) strains with CT genotypes 3 and 4; and (5) strains with CT genotypes 4 and 5. All the O139 strains yielded an amplicon of 766 bp, when a PCR was performed using CIIF and CIIR primers, which indicated lack of the CTX element in the small chromosome. All the O139 strains isolated

from 1993 to 2000 and 40% of O139 strains of 2001 yielded an amplicon of nearly 2.4 kb with ctxB forward (F) and rtxA1 primers. Strain N16961, which possessed RS1 downstream

of CTX prophage, and O395, which lacked selleck products RS1, were used as controls considering the fact that selleck chemical N16961 has CTX prophage only in the large chromosome, whereas the other strain O395 possessed CTX prophage in both the large and the small chromosome. N16961 yielded a product of > 5 kb with ctxB common forward (F) and rtxA1 primers and 766-bp amplicons with CIIF and CIIR primers. O395 yielded a product of 2.4 kb with ctxB forward (F) and rtxA1 primer pairs but no product with CIIF and CIIR primer sets. About 60% of the O139 strains of 2001 and all the tested strains isolated from 2002 to 2005 did not produce any amplicon using ctxB forward (F) and rtxA1 primer pairs. But an amplicon of ∼2.35 kb was obtained from these strains using another primer pair, zotF and rtxA1. Thus, our results depicted that V. cholerae O139 strains isolated over the period of 1993–2005 harboured CTX prophage in the large chromosome having no RS1 downstream of CTX prophage and with an empty site in the small chromosome. Some of the strains of 2001 and most of the strains isolated during 2002–2005 had a truncated CTX prophage adjacent to rtx gene cluster. These strains were further analyzed for the detection of RS1 and TLC (toxin-linked cryptic) element to understand the upstream region of CTX prophage. Detection of RS1 was carried out by PCR assay using the primers rstC1 and rstC2.