[19] Therefore, information on stool consistency alone was also calculated (a higher number indicated a looser stool). (3) Upper respiratory symptoms: recorded using a modified Jackson system, which detailed the severity of seven items (malaise, chilliness, sneezing, sore throat, runny nose, blocked nose, and cough) each on a 0 to 3 Likert scale (the headache score was removed).[20] As there are no sufficiently

sensitive and specific clinical definitions of presence or absence of upper respiratory infections,[20, 21] the Niemen method of defining presence of upper respiratory symptoms as any score Obeticholic Acid above 1 was used.[22] (4) Anxiety: recorded using the short form state-trait anxiety scale, which recorded the severity of six items on a 0 to 3 Likert scale (adapted from the usual 1–4 scale to ensure consistency with the other self-report measures).[23] Alpha coefficients for the anxiety scale in the present study ranged from 0.83 to 0.92 (above the recommended value for psychological measures of 0.70). (5) Fluid intake: determined daily by using drink bottles of known volume and bead counters to record refills. Total fluid intake was also determined from 24-hour food and fluid

diaries on day 3 (1,100 m) and day 13 (4,700 m), with food and fluid composition determined by computer software (Dietmaster; INCB024360 manufacturer Lifestyles Technologies Inc, Phoenix, AZ, USA). Arterial oxygen saturation and resting heart rate: by finger tip pulse oximeter (9500, Onyx; Nonin, Plymouth, MN, USA), recorded when participants were sheltered from the wind, after wearing gloves and blinded to their results. The lowest and highest values observed over a 1-minute period were recorded and the mean calculated. To achieve the study’s first aim, for each illness, the individual symptom score and the total symptom score were calculated to provide daily expedition mean scores. Statistical Staurosporine mouse differences between days were determined by repeated measures analysis of variance. Significant differences

were followed up by Holm–Bonferroni procedures[24] using 1,435 m as the baseline for comparison (the last day of the baseline period that exhibited normal arterial oxygen saturations). Also, for each illness, the expedition’s daily sum of symptom scores (a marker of expedition symptom burden), daily and total expedition incidence (the number of individuals achieving criteria, when available, for clinical diagnosis), and event rates (expressed per 100 person days) were calculated. Participants with missing data were removed from these analyses. To achieve the study’s second aim, longitudinal linear regression analyses were performed using generalized estimation equations.[25] The predictor variables were day of expedition, height gain, upper respiratory symptoms, stool consistency, anxiety symptoms, arterial oxygen saturation, heart rate, and fluid intake.

Measurements of promoter activity with lacZ transcriptional fusions were performed as described previously (Miller, 1972). The complete coding region of C. crescentus katG was amplified by PCR from genomic DNA of strain NA1000 using primers KatG6 (5′-ATGAAGCTTCAAAATGAGTGGATTC-3′) and KatG10 (5′-TCGAATTCATGGAAACACCTGCGCGGAG-3′), and the 2.33-kb EcoRI/HindIII fragment was cloned into vector pProEX HT (Gibco BRL). The recombinant His-KatG protein was purified from E. coli DH5α by chromatography on a nickel column (Qiagen), according

to the manufacturer’s instructions. The immune serum was obtained in New Zealand rabbits after two subcutaneous injections of 0.7 mg of purified protein in Freund’s adjuvant. Sera were collected from the ear vein using Telazol as an anesthetic according to the Biomedical Sciences Androgen Receptor Antagonist Institute Ethics Committee procedures. Immunoblots were performed essentially as described (Towbin et al., 1979), using a 1 : 1000 dilution of the antiserum and a secondary anti-rabbit-alkaline phosphatase conjugate

(1 : 30 000 dilution). An anti-Fur polyclonal antiserum (da Silva Neto et al., 2009) was used as a control of the amount of protein loaded. The isolation of a partially functional truncated mutant of Rho in a Tn5 mutagenesis screen of C. crescentus represents a new opportunity for studying the physiological functions http://www.selleckchem.com/products/Neratinib(HKI-272).html of Rho. The mutant strain SP3710 does not show pleiotropic deficiencies as do some other rho mutants (Das et al., 1976), in that it exhibits wild-type motility and cell cycling with a doubling time in a rich medium of 200 min compared with 140 min for the wild type. Moreover, the total mRNA half-life in strain SP3710 is similar to the wild type (V.C.S. Italiani & M.V. Marques, unpublished data). Although it is wild type in its sensitivity to other stresses, strain SP3710 is extremely sensitive to Fluorouracil ic50 H2O2 (Italiani et al., 2002), and in this work, we investigate the

biochemical reasons for this defect in SP3710 oxidative stress response. Because of the severe sensitivity of rho mutant strain SP3710 to exogenously added H2O2 (Italiani et al., 2002), the response of SP3710 to other reactive oxygen species (ROS) was also tested. Increased sensitivity of SP3710 to tert-butyl hydroperoxide was demonstrated by larger zones of inhibition compared with strain NA1000 in a plate assay (Table 1). This difference was evident for both exponential- and stationary-phase cells, and was not observed for the katG mutant strain SGC111. The response to superoxide was analyzed by determining cell viability in the presence of paraquat, which generates superoxide intracellularly.

Prior to appetitive training (Pavlovian, instrumental and transfer sessions), rats were food restricted to 85% of their ad-libitum weight and maintained this weight. During the 14 days of cocaine self-administration training,

rats were allowed ad-libitum access to food but were allowed 30 min access to water following each session. For the reacquisition transfer sessions, rats were returned to the food-restricted diet (85%ad libitum) with free access to water. After Pavlovian and instrumental training, but prior to cocaine self-administration, rats were prepared for surgery as in Experiment 1. All rats were implanted with a custom-made chronic indwelling catheter into their right jugular vein under aseptic conditions. Catheter construction and surgical implantation have been described previously (Carelli & Deadwyler, 1994). During the same surgery, a subset of rats (n = 9) high throughput screening were then chronically implanted with bilateral electrophysiological arrays aimed at the NAc core in one hemisphere and the NAc shell in the contralateral hemisphere, Linsitinib price as described in Experiment 1. Two rats were prepared for self-administration but

did not receive arrays. All rats were allowed at least 7 days to recover before self-administration training. Rats were run in two different contexts. For appetitive training (Pavlovian, instrumental and transfer sessions), rats were run in the same behavioral test chambers as described in Experiment 1, except that an infrared beam (MED Associates) was positioned on either side of the foodcup to allow precise detection of the timing of foodcup entries

and exits. For cocaine self-administration, rats were trained in a separate context in another room in the laboratory. These smaller test chambers (25 × 25 × 30 cm; MED Associates) were comprised of two clear Plexiglas walls in the front and rear, and two stainless-steel walls on the left and right side of the chamber. Each behavioral chamber was housed in a larger sound-attenuating cabinet equipped with CYTH4 a fan to mask noise. Unlike the solid plastic floor in the appetitive test chambers, the floorgrid in these contexts was comprised of evenly-spaced stainless-steel bars (0.5 cm diameter, 1.5 cm apart). On the left wall a centrally-located houselight was positioned 1 cm below the Plexiglas ceiling. On the right wall, 5 cm below the ceiling, two jewel lights were spaced 14 cm apart. An illuminated nosepoke hole (2.5 cm diameter) was located 1 cm above the floorgrid in the middle of the left wall, and a recessed foodcup was located on the opposite wall. Cocaine was administered via an intrajugular catheter attached to a syringe. Cocaine infusion was controlled via a motor-driven syringe pump (MED Associates), and tubing was tethered using a counterweighted arm to provide for animal mobility. Pavlovian training.

After the preparatory period, we measured the monkeys’ ability to recognize the objects across changes in viewing angle, by introducing the object set to the Object task. Results indicated significant view-invariant recognition after the second but not first preparatory task. These results suggest

that discrimination of objects from distractors at each of several viewing angles is required http://www.selleckchem.com/products/Trichostatin-A.html for the development of view-invariant recognition of the objects when the distractors are similar to the objects. “
“Members of the miR-183 family are unique in that they are highly abundant in sensory organs. In a recent study, significant downregulation was observed for miR-96 and miR-183 in the L5 dorsal root ganglion (DRG) 2 weeks after spinal nerve ligation (SNL). In this study, we focused on miR-183, which is the most regulated member of the miR-183 family, to look at the specific role on neuropathic pain. Persistent mechanical allodynia was induced with the L5 SNL model in 8-week-old male SCH727965 solubility dmso Sprague-Dawley rats. Paw withdrawal thresholds in response to mechanical stimuli were assessed with Von Frey filaments. Expression of miR-183 in the L5 DRG was assessed with quantitative real-time polymerase chain reaction (qPCR)

analysis. Lentivirions expressing miR-183 were injected intrathecally into SNL rats. Changes in mechanical allodynia were assessed with Von Frey filaments. In addition, changes in the predicted target genes of miR-183 were assessed with qPCR. L5 SNL produced marked mechanical allodynia in the ipsilateral hindpaws of adult rats, beginning at postoperative day 1 and continuing to day 14. L5 SNL caused significant downregulation of miR-183 in adult DRG cells. Intrathecal administration of lentivirions expressing miR-183 downregulated Methamphetamine SNL-induced increases

in the expression of Nav1.3 and brain-derived neurotrophic factor (BDNF), which correlated with the significant attenuation of SNL-induced mechanical allodynia. Our results show that SNL-induced mechanical allodynia is significantly correlated with the decreased expression of miR-183 in DRG cells. Replacement of miR-183 downregulates SNL-induced increases in Nav1.3 and BDNF expression, and attenuates SNL-induced mechanical allodynia. “
“The microtubule-associated protein Tau is responsible for a large group of neurodegenerative disorders, known as tauopathies, including Alzheimer’s disease. Tauopathy result from augmented and/or aberrant phosphorylation of Tau. Besides aging and various genetic and epigenetic defects that remain largely unknown, an important non-genetic agent that contributes is hypothermia, eventually caused by anesthesia. Remarkably, tauopathy in brains of hibernating mammals is not pathogenic, and, because it is fully reversible, is even considered to be neuroprotective. Here, we assessed the terminal phase of Tau.

, 2000). The translation products of MAT1-1-1 and MAT1-2-1, the major motors of sexual communication (Turgeon, 1998), are regulatory proteins that contain DNA-binding motifs with conserved regions of the α-box domain and the HMG-box (high mobility group) domain, respectively. These proteins act as transcriptional factors and regulate pheromone precursor and pheromone selleck kinase inhibitor receptor genes in heterothallic ascomycetes (Debuchy, 1999; Pöggeler & Kück, 2001; Kim & Borkovich, 2004). Pheromone communication is required between mating partners (Bistis, 1983) in

heterothallic species. On the contrary, in homothallic species, such as Fusarium graminearum, the expression of the pheromone precursor and pheromone receptor genes is nonessential in sexual development, although these genes are controlled by the MAT locus (Kim et al., 2008; Lee et al., 2008). Fusarium species are well known because of the richness of their secondary metabolism including the production of a range of pigments. Relevant examples are the carotenoids, fat-soluble terpenoid pigments produced by photosynthetic organisms and a variety of heterotrophic bacteria and fungi (Britton et al., 1998). In response to light,

different Fusarium species produce the carboxylic apocarotenoid neurosporaxanthin (Avalos & Estrada, 2010; Jin et al., 2010). The genes and enzymes needed for the synthesis of this xanthophyll have been investigated in detail in Fusarium fujikuroi (Linnemannstöns et al., 2002; Prado-Cabrero et al., 2007a). The enzymatic steps from the diterpenoid precursor geranylgeranyl pyrophosphate, i.e., a condensation, five desaturations, a cyclization and an oxidative Hydroxychloroquine manufacturer cleavage reaction, are depicted in Fig. 1. The pathway includes a side Demeclocycline branch through a second cyclization reaction to produce β-carotene,

the substrate of the retinal-forming enzyme CarX (Prado-Cabrero et al., 2007b). Retinal is the light-absorbing prosthetic group of opsins (Spudich, 2006). Cultures of Fusarium verticillioides (teleomorph: Gibberella moniliformis), a cosmopolitan pathogen of maize that produces fumonisins, exhibit an orange pigmentation when grown in the light, not apparent in dark-grown cultures, suggesting the occurrence of a similar regulation of carotenoid biosynthesis as described in F. fujikuroi. Interestingly, when the wild type and its ΔFvMAT1-2-1 mutants were cultured on synthetic minimal medium, marked morphological differences were observed between the wild type and the mutants: the mutant colonies became pale and they seemingly lost their ability to produce carotenoids. The objective of the present work was to demonstrate that inactivation of the MAT1-2-1 gene causes a drastic reduction of carotenoid production paralleled with a significant decrease in the photo-induced mRNA levels of the carB, carRA, and carT genes encoding key enzymes of the carotenoid biosynthetic pathway.

diphtheriae KCTC3075 has been characterized (Kim et al., 2010), which is the orthologue of DIP0543 C. diphtheriae NCTC check details 13129 (Fig. 4), confirming that this organism has both normal sialidase but also a reported trans-sialidase activity (Mattos-Guaraldi et al., 1998). Other data suggested that C. diphtheriae harbours sialic acid on its cell envelope (Mattos-Guaraldi

et al., 1999). This could originate from the trans-sialidase activity moving sialic acid directly from host sialoglycans onto the bacterium’s surface. Both the lack of association of the sialidase with production of the diphtheria toxin (Warren & Spearing, 1963; Moriyama & Barksdale, 1967) and the lack of a need for uptake for cell surface modification were perhaps the reason why no study has ever examined the capability of C. diphtheriae to use sialic acid as a nutrient in vivo, which this study would suggest it is capable of. While the identity of a sialidase click here in C. diphtheriae has been known for

nearly 50 years, the presence of a sialidase in C. glutamicum has not been suspected. This enzyme is not orthologous to the sialidases seen in C. diphtheriae, C. ulcerans and C. pseudotuberculosis, but rather is most similar to Arthrobacter sp. The essential nature of the ABC transporter in the same gene cluster as the sialidase (cg2935) suggests that Cg2935 is a sialidase; however, this will need experimental confirmation. This study presents the first evidence for an active transporter for Neu5Ac in an actinobacterium and increases the range of bacteria that appear to use an ABC transporter for this purpose. Other bacteria where sialic acid transporters have been characterized use tripartite ATP-independent periplasmic (TRAP) transporters (Severi et al.,

2005; Mulligan et al., 2009, 2012; Chowdhury et al., 2012), classical secondary transporters of the Morin Hydrate major facilitator superfamily (Martinez et al., 1995; Mulligan et al., 2012) or sodium solute symporter family (SSS) transporters (Severi et al., 2010), although perhaps significantly all these are Gram-negative bacteria. The only clear work on sialic acid transport in Gram-positives are from Streptococcus pneumoniae, which also uses an ABC transporter (Marion et al., 2011a, b). The reduced growth lag when cells are precultured in the presence of sialic acid suggests either the presence of a sialic acid-specific activator or the inactivation of a repressor. Given the presence of a GntR-family transcription factor in the cluster (cg2936), it is probable that the presence of Neu5Ac or one of its catabolic product acts as the ligand to cause depression of the cluster. The additional observation is that derepression by Neu5Ac is not seen in the presence of glucose, suggesting a catabolic repression-type mechanism is in operation. The mechanisms of catabolite repression are not well studied in C. glutamicum, and in many cases, different carbon sources are co-metabolized.

The potential drug–drug interactions that may occur in HIV-infected individuals with comorbidities such as diabetes, hypertension, dyslipidaemia and hyperuricaemia are a subject of much debate. There is clearly a risk of impaired drug tolerance and efficacy. PIs TSA HDAC solubility dmso and nonnucleoside reverse transcriptase inhibitors (NNRTIs) are all metabolised in the liver by the cytochrome (CYP) 450 system, a common metabolic pathway for many other drugs, including statins. Some PIs and NNRTIs inhibit statin excretion and therefore a lower starting dose is required. Conversely, others

reduce the efficacy of the statin, meaning that a higher dose may be needed [5]. Regular monitoring and dose titration are therefore essential in patients taking ART and statin therapy. Fibrates are not considered to potentially interact with ritonavir, or PIs in general [40]. The challenge of treating diabetes and dyslipidaemias in HIV-infected patients receiving ART, including PIs, and especially ritonavir, has been reviewed by Fantoni [41]. Drug–drug interactions may occur between ritonavir and rosiglitazone in the management of diabetes, leading to a reduced metabolism and potential overdosage of the anti-diabetic drug. Knowledge of when to refer to other specialist colleagues has become very important; similarly, proactive communication of the need for lifestyle changes related

to diet, smoking, alcohol use and physical activity is paramount. Clinicians www.selleckchem.com/epigenetic-reader-domain.html should be given the opportunities to educate each other, within their own hospitals, and HIV physicians should be discouraged from working in isolation. Programmes such as the ongoing HIV and the Body initiative (http://www.hivandthebody.com) can help address some of these issues. As well as a programme of international and national medical education meetings, expert-led treatment and management algorithms are available for physicians

to download from http://www.hivandthebody.com and use in everyday practice. There is an increasing click here need for ongoing monitoring of interventions that aim to reduce the risk of development and progression of comorbidities in individuals infected with HIV. Awareness of the findings of clinical endpoint studies, such as fracture prevalence studies, and the use of surrogate markers in CVD are important in achieving a clear picture of the impact of the intervention. Risk stratification tools are not sufficient to demonstrate the effectiveness of an intervention. Patient-related outcomes and the evaluation of quality of life are also important, particularly in the assessment of interventions to address comorbidities that affect body image, such as lipodystrophy [9]. An ageing HIV-infected population demands a new approach to the management of HIV infection.

, 2008). Two additional genes, contained CYC202 ic50 in an

operon with amtB, have also been proposed to be under GlnR control: glnK (msmeg_2426; PII-type protein) and glnD (msmeg_2427; an adenylyl-transferase enzyme) (Amon et al., 2008). Therefore, glnA1, amtB and amt1 were selected for analysis in this study. Four other genes were also chosen for investigation owing to their proposed role in nitrogen metabolism in Mycobacteria (Amon et al., 2009). These were amtA (msmeg_4635), an ammonium transporter; nirB (msmeg_0427), a nitrite reductase enzyme; gltD (msmeg_3226), a glutamate synthase enzyme involved in glutamate synthesis during nitrogen limitation; and glnE (msmeg_4293), a bifunctional adenylyl-transferase thought to modulate GS enzymatic activity. Expression of glnR (msmeg_5784) itself was also included. Wild-type and mutant strains were grown in nitrogen-limiting or nitrogen-excess conditions for 13 h. Expression values for each gene analysed were compared with the housekeeping gene sigA (msmeg_2758) whose expression did not alter in the conditions tested (data not shown). Genes previously shown to be under GlnR control, glnA1, amtB and amt1, were all highly up-regulated in the wild type during nitrogen limitation when compared with their expression in nitrogen-excess conditions (Fig. 2). glnA1 expression was induced approximately 13-fold, amtB 153-fold and amt1 219-fold (Table 3). However, there was no induction of these genes in either GlnR mutant

grown under nitrogen limitation (-)-p-Bromotetramisole Oxalate (Fig. 2 and Table 3). To account for the fact that the GlnR mutants deplete the external ammonium at a slower rate than the wild type (Fig. 1) and Angiogenesis inhibitor may not be stressed at 13 h, we repeated the qRT-PCR using samples taken at 19 h, when external nitrogen was no longer detectable. However, there was also no induction of gene expression in either mutant at this later time point (data not shown). Transcriptional control of other genes proposed to be involved in mycobacterial nitrogen metabolism, not shown previously to be under GlnR control, was subsequently investigated. Figure 3 shows that amtA, gltD and nirB were up-regulated in the wild-type strain in response

to nitrogen limitation at 13 h, compared with nitrogen excess, while glnE expression was down-regulated. During nitrogen limitation, amtA was induced approximately 337-fold, nirB 103-fold and gltD 8-fold; glnE was down-regulated 3-fold. Again, no significant change in the expression levels of these genes was observed in the GlnR mutants at either 13 h (Fig. 3 and Table 3) or 19 h (data not shown). To exclude the possibility that the GlnR_D48A mutation inhibited glnR expression, leading to the observed null phenotype of this strain, transcriptomic analysis of glnR was performed. No significant change in glnR expression was observed under nitrogen-limiting conditions for either the wild type or GlnR_D48A mutant (Table 3 and Fig. 2), confirming previous observations that M.

The relative risk for hepatitis A in travelers to high-risk destinations was probably mitigated by less intended risk-seeking behavior and by higher protection rates against hepatitis A as compared with travelers to low-to-intermediate-risk destinations. Logistic regression analyses showed that an age >60 years was the only significant determinant for improvement of their knowledge. Trend analyses showed a significant change over time in attitude toward more risk-avoiding behavior and toward higher protection

Ibrutinib rates against hepatitis A in travelers to high-risk destinations. The KAP profile of the risk groups travelers VFR (irrespective of hepatitis A risk of their destination) and solo as well as last-minute travelers to high-risk destinations substantially increased their relative risk for hepatitis A. Conclusions. The results of this longitudinal survey in Dutch travelers suggest an annual 5% increase in protection rates against hepatitis A coinciding with an annual 1% decrease in intended risk-seeking behavior. This improvement may reflect the continuous efforts of travel health advice providers to create awareness and to propagate safe and healthy travel. The KAP profile of travelers visiting friends and relatives (VFR) and solo as well as last-minute travelers

to high-risk destinations substantially increased their relative risk for hepatitis A. These risk groups should be candidates for targeted interventions. Hepatitis A is considered as one of the most common vaccine-preventable travel-related diseases globally.1 Osimertinib Despite access to efficient and safe vaccines, ADAM7 the immunization level in travelers to endemic areas is shown to be low in most countries1 and hepatitis A is still a frequently reported disease among international travelers.2–4 In addition, travel may also play an important role

in unexpected outbreaks of hepatitis A in non-endemic countries like the Netherlands.5 In fact, it has been shown that due to import of hepatitis A by immigrant children returning from family visits in Morocco and Turkey and secondary cases in the Netherlands among siblings and schoolmates caused a time-related increase in notifications of adults who became infected in the Netherlands.6 In the years 2002 to 2003, the European Travel Health Advisory Board conducted a cross-sectional pilot survey in several European airports including the Dutch Schiphol Airport to evaluate current travel health knowledge, attitudes, and practices (KAP) and to determine where travelers going to developing countries obtain travel health information, what information they receive, and what preventive travel health measures they adopt.7,8 The results of that particular study demonstrated an important educational need among those traveling to risk destinations.

, 1996). Subsequent studies revealed that the O1 serogroup, which replaced the O139, was a new clone of the O1 El Tor biotype (Faruque et al., 1997; Sharma et al., 1997; Yamasaki et al., 1997). Due to the quiescent period in the incidence of V. cholerae O139, it was thought that the appearance of O139 was a one-time event. But a resurgence of O139 was recorded in August 1996 in Kolkata (Mitra et al., 1996) and this serogroup remained dominant until 1997 (Fig. 1). Between December 1999 and December 2000, escalating association of V. cholerae

O139 with outbreaks of cholera were recorded in many parts of India, including Kolkata Selleckchem ICG-001 (Sinha et al., 2002). After this period, V. cholerae O1 continued to be a dominant serogroup in Kolkata, and the incidence of O139 gradually decreased over the years (Raychoudhuri

et al., 2007) (Fig. 1). Cholera toxin (CT) is the principal toxin of epidemic-causing V. cholerae serogroup O1 and O139 and is encoded by ctxA and ctxB, the major enzymatic subunit and the binding subunit, respectively. Generally, ctxB is polymorphic in nature and exists APO866 solubility dmso in three major genotypes, namely genotype 1, found among strains of the classical biotype worldwide and the US Gulf Coast, genotype 2, found among El Tor biotype strains from Australia and genotype 3, found in El Tor biotype strains from the seventh pandemic and the Latin American epidemic (Olsvik et al., 1993). Previous studies have shown that the V. cholerae serogroup O139 originated from the seventh pandemic El Tor biotype by horizontal transfer of novel O antigen genes (Bik et al., 1995; Comstock et al., 1996).

Cytidine deaminase A recent study revealed that the prototype seventh pandemic El Tor biotype of V. cholerae O1 was completely replaced in 1995 by El Tor strains that had classical type ctxB in Kolkata (Raychoudhuri et al., 2009). This shift of CT from genotype 3 to genotype 1 in V. cholerae O1 strains of Kolkata and detection of diversity in the CTX phage repressor, rstR (Kimsey et al., 1998; Davis et al., 1999; Nusrin et al., 2004), has formed the impetus for a retrospective analysis of CT genotypes along with rstR of CTX prophages in O139 strains isolated from Kolkata over a period of 13 years. A total of 125 O139 strains were selected for this study from the strain repository of the National Institute of Cholera and Enteric Diseases, Kolkata, and were isolated in different time frames between 1993 and 2005. All the strains were grown in Luria–Bertani (LB) broth (Difco) for 18 h and then streaked on Luria agar plates. These strains were confirmed serologically by slide agglutination with O139-specific antiserum. A 1-mL aliquot of overnight LB broth culture was taken into a sterile 1.