This study shows the ability of ventral mesencephalic

tissue to ameliorate some of the lesion-induced deficits, selleck chemical and the power of operant testing in detecting small but significant improvements. The behavioural tests presented are useful drug-free approaches for evaluating cell-based therapies. “
“Repeated administration of psychostimulant drugs or stress can elicit a sensitized response to the stimulating and reinforcing properties of the drug. Here we explore the mechanisms in the nucleus accumbens (NAc) whereby an acute restraint stress augments the acute locomotor response to cocaine. This was accomplished by a combination of behavioral pharmacology, microdialysis measures of extracellular dopamine and glutamate, and Western blotting for GluR1 subunit of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor (AMPAR). A single exposure to restraint stress 3 weeks before testing revealed that enduring locomotor sensitization to cocaine was paralleled by an increase in extracellular dopamine in the core, but not the shell subcompartment, of the NAc. Wistar rats pre-exposed to Buparlisib cell line acute stress showed increased basal levels of glutamate

in the core, but the increase in glutamate by acute cocaine was blunted. The alterations in extracellular glutamate seem to be relevant, as blocking AMPAR by 6-cyano-7-nitroquinoxaline-2,3-dione microinjection into the core prevented both the behavioral cross-sensitization and the augmented increase in cocaine-induced extracellular dopamine. Further implicating glutamate, the locomotor response to AMPAR stimulation in the core was potentiated, but not in the shell of pre-stressed animals, and this was accompanied by an increase in NAc GluR1 surface expression. This study provides evidence that the long-term expression of restraint stress-induced behavioral cross-sensitization to cocaine recapitulates some mechanisms

thought to underpin the sensitization induced by daily cocaine administration, and shows that long-term neurobiological changes induced mafosfamide in the NAc by acute stress are consequential in the expression of cross-sensitization to cocaine. “
“The visual field is retinotopically represented in early visual areas. It has been suggested that when adult primary visual cortex (V1) is deprived of normal retinal input it is capable of large-scale reorganisation, with neurons inside the lesion projection zone (LPZ) being visually driven by inputs from intact retinal regions. Early functional magnetic resonance imaging (fMRI) studies in humans with macular degeneration (MD) report > 1 cm spread of activity inside the LPZ border, whereas recent results report no shift of the LPZ border. Here, we used fMRI population receptive field measurements to study, for the first time, the visual cortex organisation of one macaque monkey with MD and to compare it with normal controls.

With improved turnaround times for VL testing, a woman presenting check details beyond 28 weeks may still be managed with a view to a possible vaginal delivery if she commences HAART and achieves a VL <50

HIV RNA copies/mL by 36 weeks. Where women present between 24 and 28 weeks, the advantages of more detailed assessment and tailoring of the regimen should be weighed against the advantages of initiating HAART immediately. The turnaround time for CD4 cell counts, VL and viral resistance tests will impact on this choice. 5.4.2 If the VL is unknown or >100 000 copies/mL a three- or four-drug regimen that includes raltegravir is suggested. Grading: 2D Where the VL is unknown or >100 000 HIV RNA copies/mL, a fourth drug, raltegravir, may be added to this regimen. Raltegravir has significantly higher first- and second-phase viral decay rates when used as monotherapy (vs. efavirenz) or in combination with other ARVs [134],[135]. It is important

to note that no adequate or well-controlled studies of raltegravir have been conducted in pregnant women. Pharmacokinetic data presented in Recommendation 5.2.4 indicate that no dose change is required in the third trimester. 5.4.3 An untreated woman presenting in labour at term should be given a stat dose of nevirapine 200 mg (Grading: 1B) and commence fixed-dose zidovudine with lamivudine (Grading: 1B) and raltegravir. Grading: 2D 5.4.4 It is suggested that intravenous zidovudine be infused for the duration of labour and delivery. Grading: 2C A single dose of nevirapine, regardless of CD4 cell count (even if available), should be given immediately as this rapidly crosses the placenta and within 2 h achieves, www.selleckchem.com/products/AZD0530.html and then maintains, effective concentrations in the neonate for up to 10 days [73],[136]. HAART should be commenced immediately with fixed-dose zidovudine and lamivudine and with raltegravir as the preferred additional agent because it also rapidly crosses the placenta [137]. Intravenous zidovudine can be administered

for the duration of labour and delivery [138]. If delivery is not imminent, CS should be considered. If delivery occurs <2 h post-maternal nevirapine, the DAPT mouse neonate should also be dosed with nevirapine immediately. 5.4.5 In preterm labour, if the infant is unlikely to be able to absorb oral medications consider the addition of double-dose tenofovir (to the treatment described in Recommendation 5.4.2) to further load the baby. Grading: 2C If the mother is drug naïve, take baseline bloods for CD4 cell count and VL if not known, and commence HAART as per Recommendation 5.4.2. Nevirapine and raltegravir should be included in the regimen as they cross the placenta rapidly (see above). In addition, double-dose tenofovir has been shown to cross the placenta rapidly to preload the infant and should be considered where the prematurity is such that the infant is likely to have difficulty taking PEP in the first few days of life [139]. 5.4.

[4] Immigration could contribute to change the epidemiological pattern of circulating meningococci and sporadic serogroups could become more frequent in Italy, where migration is developing into a structural phenomenon. The aim of this study is to evaluate the prevalence of carriers of N. meningitidis and the pattern of circulating serogroups in a sample of residents in the Asylum Seeker Center of Bari Palese, Italy. The protocol of the study has been approved by the Regional Government Authority and permission was granted to use the results of the tests anonymously for scientific aims. The research

was carried out in compliance with the Helsinki Declaration. Adhesion was completely voluntary and signed informed consent, which was written in the immigrants’ mother tongue, has been requested and obtained.

Study population was invited to undergo the test through mother tongue announcements which were passed on by word of mouth. Nasopharyngeal PLX-4720 supplier samples were obtained using cotton swabs, which were either plated on site or placed in transport medium in the laboratory within 1 hour. Culture for the detection of N. meningitidis and to ascertain the serogroup has been carried out as described elsewhere.[5] Two-hundred and fifty-three refugees (25.1% of the 1007 residents in the Asylum Center during 2008), of which 224 were male www.selleckchem.com/products/abt-199.html (88.5%) and 29 female (11.5%), aged between 2 and 41 years (average = 19.8; SD = Dichloromethane dehalogenase 6.0 years), were enrolled. Twelve and six percent (n = 32) of the study population were less than 5 years old. All migrants came from Africa and 201 (79.4%) originated from countries within the meningitis belt. Thirteen subjects (5.1%) were identified as healthy carriers of N. meningitidis, of which 5.4% (12/221) were aged >14 years and 3.1% (1/32) aged 2 to 14 years. Prevalence of carriage was 4.9% (10/201) among migrants from meningitis belt countries and 5.7% (3/52) in those from other nations. Six

(46.1%) of the isolates were autoagglutinable, four (30.8%) strains belonged to serogroup W135, and three (23.1%) to serogroup Y. The prevalence of carriage of meningococci in our study was higher than that of other investigations carried out among Italian teenagers during the last 40 years.[5] In contrast, studies recently performed in meningitis belt countries showed a similar prevalence of carriers.[6, 7] Moreover, to our knowledge, data on the carriage of meningococci among migrants are not available in Italy. Crowding and close contact in Asylum Seekers Centers could increase the risk of N. meningitidis transmission among migrants and, as in other closed or semi-closed settings, such as military recruit camps, carriage prevalence may be higher.[8] Unlike older surveys carried out in Puglia,[5] our study did not detect meningococci from serogroups B and C. Serogroups Y and W135, that we discovered, are rare in Europe but almost common in countries of origin of migrants.

In Denmark, we recently reported an increasing incidence of, but decreasing in-hospital mortality associated with, adult SAB in the general population [16]. A single study has reported the incidence, clinical characteristics and outcomes of HIV-associated SAB in the early-HAART period [4]. The present study used data from the

ongoing nationwide registration of all Danish cases of SAB, as well as HIV-infected individuals to explore trends and factors associated with the risk of SAB. Denmark, with a population of 5.4 million [17], has an estimated HIV prevalence of 0.07% among adults in the general population [18]. The Danish health care system provides free medical care and treatment for those with HIV infection. The study was carried out by linking three nationwide databases: the Danish Civil Registration click here System (CRS), the Danish Staphylococcal Database and the Danish HIV Cohort Study (DHCS). A unique 10-digit civil registration number is assigned to all residents

Tanespimycin mouse in Denmark, and this prevents multiple registrations and allows easy tracking of individuals across various databases and registers. The CRS contains information on birth, immigration, emigration and death [19]. Continuous, nationwide registration of patients with SAB in Denmark has been carried out at the Staphylococcal Laboratory at the Statens Serum Institut (SSI), Copenhagen, since 1956 and the database has been described in detail elsewhere [16,20,21]. In brief, the Staphylococcal Laboratory receives positive blood culture isolates from all cases of SAB from 14 of 15 departments of clinical microbiology in Denmark for typing and national surveillance. Clinical data are extracted annually from discharge records. Data used in this study included:

date of SAB during the study period, age, gender, origin of bacteraemia (HA or CA) and antibiotic susceptibility testing. HA SAB is defined as SAB diagnosed more than 48 h after admission, catheter-related infections or otherwise health care-associated infections. CA SAB is defined as SAB diagnosed <48 h after hospital admission and none of the above. Cases diagnosed more than 12 weeks DNA ligase apart were considered repetitive SABs, whereas cases diagnosed within 12 weeks were considered relapses. If an individual had repetitive SABs in the study period, only the first episode was used to explore risk factors associated with SAB, whereas all cases of SAB were used to calculate incidence rates (IRs). The DHCS is a prospective, observational, nationwide, multicentre, population-based cohort study of all HIV-infected individuals seen in Danish HIV clinics since 1 January 1995. The cohort has been described in detail elsewhere [18,22].

This may be an important consideration in the design of new drug therapy regimens that aim to minimize the detrimental effects of long-term HAART in HIV-1-infected patients. The authors would like to express their gratitude to all of the patients who participated in the TORO 1 and TORO 2 studies, as well as to the numerous Roche and Trimeris study personnel who have worked

on these trials. We would also like to acknowledge the other members of the TORO 1 and TORO 2 study teams: Belinda Atkins, Silvia find more Bader-Weder, MD, Laurence Bourdeau, PhD, Neil E. Buss, PhD, Bonaventura Clotet, MD, PhD, Calvin Cohen, MD, MSc, Jean-François Delfraissy, MD, Ralph DeMasi, PhD, Lucille Donatacci, MS, Claude Drobnes, MD, Joseph J. Eron, Jr, MD, Fiona Hughes, BSc, Christine Katlama, MD, Tosca Kinchelow, MD, Daniel Kuritzkes, MD, Emily Labriola-Tomkins, BA, Jacob Lalezari, MD, Joep Lange, MD, PhD, Adriano Lazzarin, MD, Julio Montaner, MD, Christopher Natale, MSc, Peter Piliero, MD, Miklos P. Salgo, MD, PhD, Anna Shikhman, BSN, MBA, Lynn Smiley, MD, Hans-Jürgen Stellbrink, MD, Benoit Trottier, MD, Adeline Valentine, MSc, Sharon Walmsley, MD, Cynthia Wat, MBBS and Martin Wilkinson, MSC. These studies were supported by F. Hoffmann-La Roche Ltd, Basel, Switzerland and Trimeris,

Inc., Morrisville, Epigenetics inhibitor NC, USA. Under the guidance of the lead author,

Caudex Medical created the initial draft of this manuscript. “
“Background. This study assesses, for the first time, the incidence, etiology, and determinants associated with traveler’s diarrhea (TD) among French forces deployed to N’Djamena, Chad. Methods. A prospective study was conducted based on physician consultation for diarrhea during a 5-month French forces mandate. Diarrhea was defined as ≥3 loose stools in a 24-hour period or ≥2 loose stools within the last 8 hours. For each diarrheic episode, an anonymous from physician-administered questionnaire was completed and a stool sample collected. Samples were tested for parasites, bacteria, and enteric viruses. Global incidence rate was calculated using the mean number of soldiers based in N’Djamena (n = 1,024) over the 5-month period, as denominator. Incidence rates were also estimated for each of the eleven 2-week periods of stay. A case-crossover analysis estimated determinants associated with diarrhea. Results. A total of 240 cases of diarrhea were notified by military physicians, resulting in a global incidence rate of 49 cases per 1,000 person-months (PM). The cumulative individual risk of developing diarrhea during the study period was 0.23. The incidence per 2-week stay began at 8.8/1,000 PM, rose to 54.4/1,000 PM after 1 month, and decreased after 2 months.

Alternative approaches or strategies may be reasonable depending

on the individual patient’s circumstances, preferences and values. A weak or conditional recommendation usually starts with the standard wording ‘We suggest’. The strength of a recommendation is determined not only by the quality of evidence for defined outcomes but also the balance between desirable and undesirable effects of a treatment or intervention, differences in values and preferences, and where appropriate resource use. Each recommendation concerns a defined target population and is actionable. The quality of evidence is graded from A to D and for the purpose of these guidelines is defined as follows: Grade A evidence means high-quality evidence that comes from consistent AZD9291 mouse results from well- performed randomised controlled trials (RCTs), or overwhelming evidence from another source (such as well-executed observational

studies with consistent strong effects and exclusion of all potential sources of bias). Grade A implies confidence that the true effect lies close to the estimate of the effect. Grade B evidence means moderate-quality evidence from randomised trials that suffers from serious flaws in conduct, inconsistency, indirectness, Everolimus imprecise estimates, reporting bias, or some combination of these limitations, or from other study designs with specific strengths such as observational studies with consistent effects and exclusion of the majority of the potential sources of bias. Grade C evidence is low-quality evidence from controlled trials with several serious limitations, or observational studies with limited evidence on effects and exclusion of most potential sources of bias. Grade D evidence is based only on case studies, expert judgement or observational studies with inconsistent effects and a potential for substantial bias, such that there can be little confidence

in the effect estimate. In addition to graded recommendations, the BHIVA Writing Group has also included good practice points Tyrosine-protein kinase BLK (GPP), which are recommendations based on the clinical judgement and experience of the working group. GPPs emphasise an area of important clinical practice for which there is not, nor is there likely to be, any significant research evidence. They address an aspect of treatment and care that is regarded as such sound clinical practice that health care professionals are unlikely to question it and where the alternative recommendation is deemed unacceptable. It must be emphasised that GPPs are not an alternative to evidence-based recommendations.

The work reported here from our own laboratories was funded by the Medical Research Council, the Biotechnology and Biological Sciences Research Council, the Wellcome Trust, the Engineering and Physical Sciences Research Council (COLAMN), EU Framework 6 (FACETS), Novartis Pharma Basel and Glaxo Smith Kline. Abbreviations

BZ1, BZ2 and BZ3 benzodiazepine (binding site) type 1, 2 and 3 CASK Calcium/calmodulin-dependent serine protein kinase CCK cholecystokinin ER endoplasmic reticulum GABAAR GABAA receptor IAα5 α5-subunit-selective partial inverse agonist IPSC inhibitory postsynaptic current IPSP inhibitory postsynaptic potential LNS laminin neurexin sex hormone binding protein mGluR metabotropic glutamate receptor type NCAM neural cell adhesion molecules NL2 neuroligin 2 selleck kinase inhibitor NMDA N-methyl-D-aspartate OLM Oriens lacunosum moleculare PSD postsynaptic density PV parvalbumin RIM1α Regulating synaptic membrane exocytosis protein 1α “
“A successful Staphylococcus aureus vaccine should elicit a long-term antibody response that prevents establishment of the infection. The aim of the present study was to evaluate the functional role of antibodies raised against different S. aureus CP5 vaccines in invasion to bovine mammary epithelial

cells (MAC-T) and phagocytosis by bovine milk macrophages in vitro. Sera and whey from cows immunized with a whole-cell S. aureus CP5 vaccine adjuvanted with Al(OH)3 or with ISCOM Matrix, significantly reduced internalization of S. aureus in MAC-T cells without significant selleck chemical differences between both groups. The effect of antibodies generated by a S. aureus whole-cell and a lysate vaccine formulated with ISCOM Matrix was also evaluated. Sera and whey from both immunized groups significantly reduced S. aureus internalization in MAC-T cells without significant differences between both groups. Whey antibodies against whole-cell why and

lysate vaccines were also able to inhibit internalization in MAC-T cells of a heterologous S. aureus strain. In addition, sera from animals vaccinated with S. aureus lysate or bacterin promoted milk macrophage phagocytosis. These results provide an insight into the potential mechanisms by which these vaccines can afford protection to the mammary gland against S. aureus intramammary infection. “
“Fluorescent amplified fragment length polymorphism (FAFLP) analysis was applied to genetically fingerprint ‘working culture control strains’ used by accredited food microbiology laboratories. A working culture control strain is defined as a subculture from a strain initially obtained from an authenticated source [such as the National Collection of Type Cultures (NCTC)] that is maintained for use with routine testing within the laboratory.

The median (range) gestation at delivery was 40 (27–42) weeks and the median (range) birthweight was 3.1 (1.2–4.5) kg. There were no HIV-positive infants. Antepartum and postpartum LPV and RTV pharmacokinetic data from 46 patients are summarized in Table 2. Geometric mean (95% CI) total LPV concentrations were comparable during the first, second [3525 (2823–4227) ng/mL] and third trimesters [3346 (2813–3880) ng/mL; P=0.910], but were ∼35% lower relative to LPV

concentrations Selleck Roxadustat observed during the postpartum period [5136 (3693–6579) ng/mL; P=0.006; all comparisons]. Equally, RTV Ctrough values were significantly reduced antepartum vs. postpartum (P=0.017; all comparisons). Inter-subject variation in LPV Ctrough was moderately high both antepartum (24–45%) and postpartum (44%). The time of post-dose sampling was consistent across the trimesters of pregnancy and postpartum, at approximately 13 h (P=0.924). Overall, six of 46 patients (13%)

had LPV concentrations below the proposed MEC (<1000 ng/mL) in pregnancy; one patient (8%) in the second trimester and five patients (12%) in the third trimester (LPV=<73–831 ng/mL; 14.5–26 h post-dose); all were receiving standard dosing of the LPV/r tablet at baseline. All 12 patients at postpartum had plasma concentrations in excess of the LPV MEC. A single patient below target in the second trimester (LPV Ctrough=790ng/mL; 29 weeks; 15 h post-dose) was dose-adjusted to three tablets (600/150 mg) twice daily at 32 weeks which achieved above-target Selleckchem Etoposide concentrations (LPV=4575 ng/mL; 34 weeks; 12.7 h). She was later reduced back to two tablets twice daily post-delivery and remained therapeutic at 6 weeks postpartum. Of the five patients below target in the third trimester, one patient had an LPV Ctrough of 831 ng/mL (32 weeks; 17 h post-dose); no changes were made to the LPV/r dose, and she underwent no further TDM sampling having

check delivered elsewhere. Another had an LPV Ctrough of 647 ng/mL (26 weeks; 15.7 h post-dose). No dose adjustments were made and an additional TDM was performed at 32 weeks, in which she remained below target (641 ng/mL). Both patients discontinued ART post-delivery. The remaining three patients had LPV concentrations below our predefined cut-off for adherence (<384 ng/mL) and were therefore excluded from subsequent statistical analyses. These subjects were suspected by the study personnel as being nonadherent to treatment with one patient admitting to having missed doses one day. In two instances the time of pharmacokinetic sampling was greater than 20 h and this may also have contributed to the low LPV concentrations observed. Of the six patients who were below the MEC during pregnancy, five had undetectable pVL (<50 copies/mL) at the time of TDM sampling. The remaining subject had a pVL of 209 copies/ml in the third trimester. LPV unbound trough concentrations (Table 2) were lower in the first, second and third trimesters relative to postpartum (P=0.

No φC31 plaques were selleck kinase inhibitor observed on the Δpmt mutant carrying the cloned Rv1002c gene for PmtMtu [IB25(pBL9)], whereas they could be observed when the

Δpmt mutant carried an equivalent construct with the S. coelicolor pmt gene also under the control of PtipA [IB25(pBL12); Fig. 4a, plates 3 and 4; Table S2]. To explain this observation, we hypothesized that perhaps PmtMtu was functional, but failed to recognize the φC31 receptor. Therefore, plasmids pBL9 and pBL12 carrying the cloned genes for PmtMtu and PmtSco were also introduced into the S. coelicolor Δpmt mutant IB25 expressing the apa gene (from pBL1), and Apa produced by these strains was analyzed; only pBL12 carrying the gene for PmtSco complemented the ability to glycosylate the Apa protein (Fig. 4b and c, lane 3),

whereas pBL9 did not (Fig. 4b and c, lane 4). Again a few degradation products were observed, and these were more apparent when Apa was not glycosylated, which is consistent with the notion that protection from degradation might be one of the functions for protein glycosylation. These results mean that the PmtMtu enzyme learn more is unable to complement Pmt activity in the S. coelicolor mutant, even when the glycosylation target is Apa, a protein that, unlike the φC31 receptor, is normally recognized by PmtMtu. One possibility to explain these results is that PmtMtu is not being correctly localized to the S. coelicolor membrane, unlike PmtSco. To test this, both PmtSco and PmtMtu were tagged at the C-terminus with a hemagglutinin

epitope, to allow their identification using commercial anti-hemagglutinin antibodies, and cloned under the control of the PtipA promoter (pB14 and pB15, respectively; Table 1). Both plasmids were introduced into the Δpmt mutant IB25, and after induction of the cultures with thiostrepton, mycelium was harvested and subject many to fractionation, and the cytoplasmic and membrane fractions were analyzed by Western blot using anti-hemagglutinin antibodies. Hemagglutinin-tagged PmtSco could only be found in the membrane fraction (Fig. 5, lane 1) and not in the cytoplasmic fraction (Fig. 5, lane 2), meaning that the hemagglutinin tag did not affect its correct localization. In addition, the hemagglutinin-tagged PmtSco was shown to complement the Δpmt mutant IB25 for the ability to form plaques when infected with φC31 (data not shown). These results show that the hemagglutinin tag did not affect either the correct localization or the functionality of PmtSco. Hemagglutinin-tagged PmtMtu was also found only in the membrane fraction (Fig. 5, lane 3) and not in the cytoplasmic fraction (Fig.

It appears that the most conserved function of the CtrA and CckA proteins in disparate species is related to motility (Quon et al., 1996; Lang & Beatty, 2002; Miller & Belas, 2006; Brilli et al., 2010; Mercer et al., 2010; Bird & MacKrell, 2011). Unlike C. crescentus, the CckA and CtrA proteins are not essential in regulation of the R. capsulatus cell cycle, but CtrA is required for the proper expression of more than 225 genes (Mercer et al., 2010).

However, it is not known whether phosphorylated or unphosphorylated CtrA is the active form of the protein in this species. Recently, Brilli et al. (2010) analyzed 37 α-proteobacterial genomes and identified orthologs of the 14 genes involved in CtrA-dependent cell cycle regulation in C. crescentus. Their bioinformatic analyses of possible CtrA networks further strengthened some GSK458 research buy of the previous work indicating that

CtrA regulation buy Epacadostat and function has a patchwork of conservation in different α-proteobacteria, and they identified a possible chpT ortholog in Rhodobacter. To further understand the CtrA network in R. capsulatus, we have analyzed the motility and RcGTA production phenotypes of strains lacking the putative CtrA regulators sciP and chpT in comparison with ctrA and cckA mutants. We also investigated the effects of CtrA phosphorylation state using a phosphomimetic protein, CtrAD51E, and a version of the protein that is unable to be phosphorylated, CtrAD51A. These CtrA mutants have been used in C. crescentus and Rhodospirillum centenum to study CtrA activities (Domian et al., 1999; Jacobs et al., 1999; Ryan et al., 2002; Siam & Marczynski, 2003; Bird & MacKrell, 2011). The CtrAD51E protein mimics CtrA~P in vivo (Domian et al., 1997; Siam & Marczynski, 2003), and

the CtrAD51A mutant serves as a constitutively Protein kinase N1 unphosphorylated form (Ryan et al., 2002). The experimental strains, plasmids, and PCR primers used for this study are listed in Table 1. Rhodobacter capsulatus was grown at 35 °C in anaerobic photoheterotrophic conditions in complex YPS medium (Wall et al., 1975) or aerobically in RCV medium (Beatty & Gest, 1981) supplemented with appropriate antibiotics when necessary: kanamycin (10 μg mL−1) and tetracycline (0.5 μg mL−1). Escherichia coli was grown in LB medium at 37 °C and supplemented with the appropriate antibiotics when necessary: ampicillin (100 μg mL−1), kanamycin (25 μg mL−1), and tetracycline (10 μg mL−1). The ORFs encoding the predicted ChpT (rcc03000) and SciP (rcc01662) homologs were amplified by PCR from genome of R. capsulatus strain SB1003 using the primers chpT-F and chpT-R, and sciP-F and sciP-R, respectively (Table 1). The amplified products were cloned into pGEM-T-Easy. The genes were disrupted by insertion of a ~1.4-kb SmaI fragment of the kanamycin resistance-encoding KIXX cartridge (Barany, 1985) at specific restriction sites within the ORFs.