21 In a separate study, rifaximin 600 mg/d effectively prevented experimental shigellosis in a challenge model conducted in healthy volunteers.22

These findings suggest that rifaximin 600 mg/d may be effective in preventing enteric infection caused by diarrheagenic strains of E coli as well as invasive bacterial pathogens. The present phase 3 clinical study assessed Target Selective Inhibitor Library ic50 the safety and efficacy of rifaximin 600 mg/d for 14 days in the prevention of TD in healthy US adults traveling to Mexico. This phase 3, double-blind, randomized, multicenter, 3-week study investigated the efficacy of rifaximin in preventing TD in adults traveling to Mexico. Eligible participants were healthy find more US students aged ≥18 years attending school

in Guadalajara, Mexico, who ingested the study drug within 72 hours of arrival in Mexico. Participants had not experienced diarrhea or received treatment with fluoroquinolones, macrolides, azalides, or trimethoprim-sulfamethoxazole 7 days before taking the study drug or antidiarrheal medications (eg, loperamide, bismuth subsalicylate) 24 hours before taking the study drug. Concomitant medications other than those listed above were permitted. Before the study began, individuals attended an orientation that included instructions on how to avoid diarrhea. Study participants received three tablets of rifaximin 200 mg once daily (ie, 600 mg/d) or a matching placebo for 14 days with a 7-day post-treatment follow-up. Clinical evaluations were conducted at screening (ie, baseline), during treatment (day 8), and at the end of the study (day 15, 16, or 17). Participants recorded the number of formed and unformed stools passed and enteric symptoms experienced on daily diary cards for the duration of the study. Individuals who withdrew from the study prematurely because of diarrhea or requested rescue medication were considered cases of TD. All participants supplied a stool sample at the end of the study regardless of TD acquisition. Individuals who

developed TD during the treatment period discontinued the study medication Immune system and received rescue antibiotic therapy with levofloxacin, ciprofloxacin, or azithromycin. All individuals provided written informed consent. The study was conducted in accordance with ethical standards of the responsible committee on human experimentation and with the Helsinki Declaration of 1975. This trial is registered with the National Library of Medicine (www.clinicaltrials.gov/) under NCT00742469. The primary efficacy end point was the relative risk of developing TD (three or more unformed stools within a 24-h period plus one or more symptom of enteric infection) based on the time to first unformed stool beginning the illness during 14 days of treatment with rifaximin or placebo.

None of the controls were subsequently identified to be HIV positive after inclusion in the study. Throughout this period, there have been no variations in the type of surgery implemented for the treatment of this condition. All preoperative, perioperative and postoperative data were obtained by reviewing standardized clinical dates. For HIV-positive patients, we collected

the following information: date of diagnosis of HIV infection, total duration and types of antiretroviral treatment received, HIV stage [Centers for Disease Control and Prevention (CDC) classification] [24] and most recent CD4 T-lymphocyte count and viral load at the time of THA. The mean time from the onset of INFH symptoms to INFH diagnosis was calculated. The diagnosis Ipilimumab ic50 of INFH was established by conventional radiology (anteroposterior and axial) and, in specific cases, further confirmed by magnetic resonance imaging (MRI) or Technetium-99m (99mTC) gammagraphy. The severity of the lesions was classified according to the Ficat and Arlet radiological classification system [25]. All patients underwent preanaesthetic assessment according

to American Society of Anesthesiologists (ASA) guidelines [26] Data on duration of hospitalization, time spent in surgery, postoperative drop in haemoglobin level and need for transfusion were collected. Preoperative and postoperative function was calculated Copanlisib chemical structure according to the Merlé d’Aubigné and Postel scale [27] For the purposes of the study, we assessed the following postoperative N-acetylglucosamine-1-phosphate transferase complications: infection (pulmonary, urinary, surgical wound, joint, bone, septicaemia or fever of unknown origin), haemorrhage, surgical wound

dehiscence, thromboembolic complications, cardiac complications (myocardial infarction, arrhythmia or heart failure), respiratory complications (atelectasia or pneumonia), renal complications and luxation or displacement of the implant. Short-term (first year) and long-term (subsequent years) follow-up data obtained during regular visit check-ups (first visit 1 month after surgery, second visit 3 months after surgery, third visit 6 months after surgery, and then yearly) were reviewed for the purposes of the study, and clinically meaningful data were recorded for analysis. Quantitative variables were described by the mean and standard deviation (SD) and the median and interquartile range (25th; 75th percentiles). Qualitative variables were described by absolute frequencies and percentages. The Mann–Whitney U-test and Fisher’s exact test were used for statistical analyses in order to compare baseline homogeneity between groups. In order to evaluate the time to diagnosis, surgical duration, duration of hospitalization, evolution of haemoglobin and Merlé d’Aubigné functional scale, means and their 95% confidence intervals (CIs) were used. Odds ratios (ORs) and their 95% CIs were used to estimate risk for the Ficat and Arlet radiological classification system and the need for blood transfusion.

UDTR employs different rules that converge on specific levels of accuracy. We used a three-up, one-down rule, meaning that for three consecutive hits we adjusted the stimulus one step harder and for any miss we adjusted the stimulus one step easier. This rule necessarily selleck kinase inhibitor converges on an accuracy level of 79.4%. During the experimental session, participants were instructed to respond as quickly and accurately

as possible to the detection of targets within the cued modality and to withhold responses otherwise. Participants were further instructed to refrain from eyeblinks during each trial as much as possible. Each participant completed one visual and one auditory pure-task block of 100 trials, followed by ~20 mixed-task blocks of 30 trials AZD6738 each, resulting in the collection of ~300 trials per cue condition. Continuous EEG was recorded, with a bandpass of DC to 134 Hz, from 168 scalp electrodes (Biosemi ActiveTwo System, Amsterdam, Netherlands) at an analog-to-digital sampling rate of 512 Hz. Biosemi replaces the ground electrodes that are used in conventional systems with two separate electrodes: a Common Mode Sense and a Driven Right Leg passive electrode. These two electrodes

create a feedback loop, thus rendering them references. With the Biosemi system, every electrode or combination of electrodes can be assigned as a reference, which is done purely in software after acquisition. EEG data were processed using

the FieldTrip toolbox Vitamin B12 (Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen, The Netherlands). This MATLAB (The MathWorks Inc., Natick, MA, USA) toolbox and supporting materials can be accessed at http://www.ru.nl/neuroimaging/fieldtrip. The continuous EEG data were stored and then re-referenced to the average reference and low-pass filtered with a cutoff frequency of 40 Hz. Trials with blinks and excessive eye movements were rejected based on the horizontal and vertical electro-occulogram. Over all other electrodes, a trial rejection threshold of ±100 μV was used. Trials were then epoched from −200 to +1805 ms around the onset of the S1 cue-stimulus. The period of −100 to 0 ms was defined as baseline. To obtain so-called global switching costs, we quantified the difference in reaction times (RTs) and response accuracy (d-prime; see below) between mixed and pure task blocks. To obtain local switching costs, we analysed differences in RT and d-prime between switch and repeat trials within the mixed blocks. The RT was measured from all correct ‘go’ trials (i.e. trials with a target in the cued modality). Responses were only considered valid if they occurred in the window 200–1500 ms following the onset of the gabor in attend-visual conditions and the second tone stimulus in the attend-auditory conditions.

CMC is widely used as an index of functional connectivity between the primary motor cortex and limb muscles, and Granger causality is used across many fields of science to detect the direction of coherence. To calculate CMC and Granger causality, we used electroencephalography

(EEG) to measure activity over the cortical region that governs leg muscles, and surface electromyography (EMG) over the right and left tibialis anterior muscles, Natural Product Library in 15 healthy term and preterm neonates, during spontaneous movements without any external stimulation. We found that 17 leg muscles (10 right, seven left) in 12 neonates showed significant CMC, whose magnitude significantly correlated with postnatal age only in the beta frequency band. Further analysis revealed Granger causal drive from EEG to EMG in 14 leg muscles. Our findings suggest that the primary motor cortex drives muscle activity when neonates move their limbs. Moreover, the positive correlation between CMC magnitude and postnatal age suggests that corticomuscular communication begins to develop during the neonatal selleck chemicals llc stage. This process may facilitate

sensory-motor integration and activity-dependent development. “
“Muscle β-catenin has been shown to play a role in the formation of the neuromuscular junction (NMJ). Our previous studies showed that muscle-specific conditional knockout of β-catenin (HSA-β-cat−/−) results in early postnatal death in mice. To understand the underlying mechanisms, we investigated the electrophysiological

properties of muscle cells from HSA-β-cat−/− and control mice, and found Protirelin that, in the absence of muscle β-catenin, the resting membrane potential (RMP) depolarised in muscle cells from the diaphragm, gastrocnemius and extensor digitorum longus muscles. Furthermore, in a primary line of mouse myoblasts (C2C12 cells) transfected with small-interfering RNAs targeting β-catenin, the RMP was depolarised as well. Finally, the expression levels of the α2 subunit of sodium/potassium adenosine triphosphatase were reduced by β-catenin knockdown in vitro or deletion in vivo. These results suggest a possible mechanism underlying the depolarised RMP in the absence of muscle β-catenin, and provide additional evidence supporting a role for β-catenin in the development of NMJs. “
“CCAAT enhancer-binding protein β is a transcription factor that is involved in many brain processes, although its role in neuronal survival/death remains unclear. By using primary cultures of rat cerebellar granule neurons, we have shown here that CCAAT enhancer-binding protein β is present as all of its isoforms: the transcriptional activators liver activator proteins 1 and 2, and the transcriptional inhibitor liver inhibitory protein. We have also shown that liver activator protein 1 undergoes post-translational modifications, such as phosphorylation and sumoylation.

How the information was searched Databases: Medline, Embase, Cochrane Library Conference abstracts:2008–2011 Language: restrict to English only Date parameters: –2011 Published abstracts: 152 Conference abstracts: 25 To date such

an increase has not been http://www.selleckchem.com/products/epacadostat-incb024360.html detected. (Data from the Antiretroviral Pregnancy Registry http://www.apregistry.com, accessed 27 April 2012; data to end July 2011.) Abacavir Atazanavir Efavirenz Emtricitabine Indinavir Lamivudine* Lopinavir Nevirapine Ritonavir* Stavudine Tenofovir Zidovudine* *Sufficient data to detect a 1.5-fold increase in overall birth defects. In reviewing all reported defects from the prospective registry, informed by clinical studies and retrospective reports of antiretroviral exposure, the MK0683 in vitro Registry finds no apparent increases in frequency of specific defects with first trimester exposures and no pattern to suggest a common cause. The Registry notes modest but statistically significant elevations of overall defect rates with didanosine and nelfinavir compared with its population-based comparator, the MACDP. While the Registry population exposed and monitored to date is

2-hydroxyphytanoyl-CoA lyase not sufficient to detect an increase in the risk of relatively rare defects,

these findings should provide some assurance when counselling patients. However, potential limitations of registries such as this should be recognized. The Registry is ongoing. Health care providers are encouraged to report eligible patients to the Registry at http://www.APRegistry.com. “
“The aim of the study was to describe trends in CD4 cell counts in HIV-infected patients after initiation of combination antiretroviral therapy (cART), according to CD4 cell count at initiation (baseline), and to quantify the implications of virological failure for these trends. Eligible participants from the UK Collaborative HIV Cohort (CHIC) were antiretroviral-naïve and started cART after 1997. Random effects were used to model CD4 cell count trends, accounting for multiple measurements within participants. We assessed whether CD4 cell count trends varied according to baseline CD4 cell count and separately in participants with and without post-cART virological failure. Effects of post-cART virological failure (>1000 HIV-1 RNA copies/mL) on subsequent CD4 cell counts were evaluated.

In this analysis of the imp and idpA genes of PoiBI, we confirmed the previously published assertions

that these two genes are not homologous, and that imp is well conserved over a wide range of phytoplasma strains (Kakizawa et al., 2009). Although the Imp of WX has been previously reported to be IdpA (Blomquist et al., 2001), histone deacetylase activity the identity of the Imp of PoiBI was not studied. In the present study, we were able to detect the expression of Imp in PoiBI-infected poinsettia plants using both immunohistochemical and Western blot analyses (Fig. 3a and b Fig. 4). In contrast, although we were able to detect expression of IdpA in PoiBI-infected plants immunohistochemically, we were not able to detect it by Western blotting, probably because immunohistochemical analysis is generally the more sensitive technique (Jiang et al., 1988; Friedlander et al., 1989; Gala et al., 1994). Our findings suggest that Imp is expressed at a higher level than IdpA in PoiBI. In comparing PoiBI strains from 26 different poinsettia cultivars, we found no variation

in their idpA, dnaD, or 16S rRNA genes. On the other hand, imp did exhibit some variation. All of the nucleotide substitutions in PoiBI imp resulted in amino acid changes; that is, no silent mutations were CDK inhibitor observed, suggesting that imp is prone to mutation. Although adaptive evolution of imp was not detected (Table 2), strong positive selection has been reported for the imp genes of AY-group phytoplasmas, indicating that Imp plays an important role in phytoplasma fitness (Kakizawa et al., 2006b, 2009). The imp gene of PoiBI might also play a crucial role correlated to the accumulation of amino acid substitutions. AY-group phytoplasmas express approximately ten times as much Amp as Imp, indicating that the Imp in this group is Amp (Kakizawa et al., 2009). Among phytoplasma

strains, amp gene sequences exhibit this website much more variation than imp gene sequences, and are subject to strong positive selection pressure (Kakizawa et al., 2009). In PoiBI, Imp was expressed at a higher level than IdpA (Fig. 3a and b), suggesting that the major membrane protein of PoiBI is Imp rather than IdpA, even though the Imp in closely related WX is IdpA (Blomquist et al., 2001). Therefore, the genes encoding Imps appear to differ among even closely related phytoplasma strains. Further analyses of imp and idpA sequences and gene expression among many strains of 16SrIII ribosomal group phytoplasmas, which include PoiBI and WX should yield more information about the diversity of Imps. The average nucleotide sequence identity between PoiBI imp genes and WX imp in our study was 97.2%, whereas that between PoiBI and WX idpA was 77.7%. Nonsynonymous substitutions outnumbered synonymous substitutions for both genes from the two strains, and dN/dS was > 1 for both comparisons (Table 2). The high value of dN/dS for idpA resulted solely from the differences between WX and PoiBI idpA, as there was no variation among the 26 PoiBI sequences.

A few years later, an epidemic of neurocysticercosis-related epilepsy was documented in that population.[2] On the other hand, the option that another food, that is, vegetables or fruits, infected with taenia eggs travel from one country to another

to infect patients has not been previously demonstrated and seems to be highly unlikely. Cysticercosis must be primarily buy MDV3100 considered as a disease transmitted from person to person, that is, from a taenia carrier.[3] Commenting on the other point raised by Joob and Wiwanitkit, what I meant by “reactivation of an infection that has previously been controlled by the host immune system” was that it may happen that the immune system of a given person infected Apoptosis inhibitor abroad, handled the infection without causing clinical manifestations. Then, several years later, the calcification that resulted from that successfully handled infection may become symptomatic when parasitic antigens (trapped within the calcified lesion) are liberated to the brain parenchyma and get exposed to the host immune system.[4] The resulting inflammatory response is responsible for the occurrence of seizures

(symptoms) and changes in neuroimaging studies that may resemble a fresh infection. Incorrect interpretation of imaging findings may lead the attending physician to believe that the patient has a cysticerci in the acute encephalitic phase (active neurocysticercosis).

“
“Background. Hajj, the pilgrimage to Mecca, is one of the obligatory religious duties of Islam. The travel clinic of the Public Health Service (PHS) Amsterdam administers vaccinations, including the required meningitis ACYW135 vaccine, and provides travelers with individual recommendations for all their travels. Methods. We extracted all data from the PHS database pertaining to Muslims who visited the clinic before travel to Mecca. From 2001 to 2009, PJ34 HCl the characteristics are described and trends are analyzed retrospectively. Acceptance of dTP vaccine was used as a proxy for acceptance of recommended vaccinations. For the years 2007 to 2009, predictive factors for the acceptance of advised vaccinations are analyzed. Results. From 2001 to 2009, significantly more women and people older than 50 years of age traveled to Mecca. Since 2007, only 527 of 2,156 (24%) of those who were advised to take vaccines accepted the recommendation. Independent factors for acceptance were being female, of younger age, and being less healthy. Specifically, Mecca travelers with heart disorders and with liver or gastrointestinal disorders accepted recommended vaccinations more often than those without. Conclusions. Only a quarter of Mecca travelers who visit the travel clinic for their mandatory meningitis vaccination also take other, recommended, vaccinations.

Bacterial strains and plasmids used in this study are listed in Supporting Information, Table S1. Photorhabdus luminescens TT01 was grown in Luria–Bertani (LB) medium at 28 °C, and strains of E. coli were grown in LB medium at 37 °C. Escherichia coli DH5α was used as the host Lumacaftor in vivo for recombinant DNA cloning. Escherichia coli BL21 (DE3) was used as the host for expression of binary toxin genes. Plasmid pET28a (Novagen) was used as expression vector in BL21 (DE3). Plasmid pETDuet-1 (Novagen) was used as co-expression vector in BL21 (DE3). Total DNA was

extracted from P. luminescens TT01 using the alkali lysis method. It was used as template for amplification of plu1961 and plu1962 (GenBank accession no. BX571865). Oligos used in this study were listed in Table S2. Oligo pair Plu1961-F/Plu1961-R was used to amplify plu1961, and Plu1962-F/Plu1962-R was used to amplify plu1962. Both PCR products were double-digested by EcoRI/SalI and cloned into pET28a to generate plasmids pET-plu1961 and pET-plu1962, respectively. For co-expression of Plu1961 and Plu1962 in BL21 (DE3), Co1961-F/Co1961-R and Co1962-F/Co1962-R were used to amplify plu1961 and plu1962, respectively. PCR products of plu1961 and plu1962 were double-digested

by PstI/SalI and NdeI/XhoI, respectively, and cloned into pETDuet-1 sequentially to generate co-expression plasmid pET-pluBi. All the plasmids were confirmed by DNA sequencing. Plasmids isocitrate dehydrogenase inhibitor pET-plu1961, pET-plu1962, and pET-pluBi were transformed into BL21 (DE3), and resultant strains were designated as BL21 (plu1961), BL21 (plu1962), and BL (Bi),

respectively. Recombinant strains were grown in LB medium with kanamycin (50 μg mL−1) or ampicillin (100 μg mL−1) at 37 °C to an OD600 between 0.6 and 0.8. Then, isopropyl-beta-d-thiogalactopyranoside (IPTG) was added at a final concentration of 1 mmol L−1. After IPTG induction for 4 h, ID-8 aliquots of 1 mL bacteria culture were sampled and harvested by centrifugation (10 000 g, 1 min). Pellets were washed three times with distilled water and suspended in 0.1 mL lysis buffer (50 mmol L−1 NaH2PO4, 300 mmol L−1 NaCl, 10 mmol L−1 imidazole, pH 8.0). Then, cells were lysed by sonication and centrifuged at 10 000 g for 2 min. The supernatant was collected, and 10 μL aliquots were taken for SDS-PAGE. Soluble binary toxins (Plu1961 and Plu1962) were directly purified on 1-mL HisTrapTM HP prepacked columns (GE Healthcare), using an AKTA Purifier system (GE Healthcare; flow rate 1 mL min−1). The column was equilibrated in His A buffer (20 mmol L−1 sodium phosphate, 0.5 mol L−1 NaCl, 20 mmol L−1 imidazole, pH 7.4). Proteins were eluted using a step gradient up to 0.5 mol L−1 imidazole in His A buffer. Fractions were analyzed by SDS-PAGE, and the protein content of the pools was determined using the Bio-Rad Bradford reagent. The purified proteins were dialyzed against PBS buffer prior to application.

, 2006). Next, the β-Gal activities from WK074 cells expressing either

wild-type His-Irr or mutant His-Irr proteins were compared. The β-Gal activities obtained were normalized to those from WK074 harbouring the pBBR vector (100% β-Gal activity, Lapatinib cell line no repression of mbfA-lacZ) (Fig. 2a). WK074 cells expressing wild-type His-Irr (pHIRR) had 1.99% β-Gal activity (Fig. 2a). A single mutation in His-Irr proteins at H38, D86, H92, H93 or D105 could repress mbfA-lacZ as effectively as wild-type His-Irr (1.39, 1.04, 0.97, 1.29 and 0.94% β-Gal activity, respectively) (Fig. 2a). A single mutation at H45, H65 or H127 in the protein caused a slight defect in the ability of the protein to repress mbfA-lacZ compared with wild-type His-Irr, as indicated by the increase http://www.selleckchem.com/products/cobimetinib-gdc-0973-rg7420.html in β-Gal activities (3.83%, 4.77% and 8.96% β-Gal activity, respectively) (Fig. 2a).

The H94 mutation caused the greatest reduction in the repressor function of His-Irr (17.23% β-Gal activity) as compared with the mutations at the other H residues (Fig. 2a). A double mutation at residues H45 and H65 of His-Irr (corresponding to the second haem-binding site of IrrRl) caused a small defect (H45H65, 11% β-Gal activity). Triple mutation in the HHH motif of His-Irr (H92, H93 and H94) caused a large defect in the repressor function of the protein (HHH, 63% β-Gal activity) but did not completely abolish protein function (Fig. 2b). Based on this, it is likely that amino acid residues outside

of the HHH motif also contribute to the repressor function of His-Irr. The plasmids containing the mutated HHH motif in combination with the mutation of other residues, including H38, H45, H65, D86, D105 or H127, were constructed to produce the mutant His-Irr proteins HHH38, HHH45, HHH65, HHH86, HHH105 and HHH127, respectively. Additional mutations at H45, H65 or H127 together with the HHH motif mutation led to the complete loss of His-Irr function (HHH45, HHH65 and HHH127: 103%, 101% and 99% β-Gal activity, crotamiton respectively) (Fig. 2b). Although the mutant His-Irr proteins HHH38 and HHH105 both showed an additive effect compared to HHH, the mutant proteins did not lose function completely (76% and 85% β-Gal activity, respectively) (Fig. 2b). Unexpectedly, an additional mutation at D86 could fully reverse the defect caused by the HHH mutation (HHH86, 0.87% β-Gal activity) (Fig. 2b). The experiments were repeated using the plasmid pIRR to express wild-type IrrAt that encodes the native protein without the 6× His tag. As previously described, the results from the mutagenesis of His-Irr (Fig. 2) showed that H45, H65, D86, H94, the HHH motif and H127 influence the function of Irr.

A significant number of these modulators are involved in the adaptation to nutritional stimuli (Guillouard et al., 2002). Others are involved in the response of bacterial cells to environmental outputs, such as stress (Lahiri et al., 2008) or quorum sensing (Cao et al., 2001; Kim et al., 2004). Some of them are of special interest due to their implication in virulence (Axler-Diperte et al., 2006; Heroven & Dersch, 2006). A recent

report has shown that Salmonella encodes 44 LTTRs. To date, the target genes of just 16 of them have been characterized (Lahiri et al., 2009). We present here preliminary characterization of GSK-3 beta phosphorylation YfeR (referred as STM2424 by Lahiri et al., 2009). Evidence that this modulator belonging to the LTTR family comes from the facts that YfeR (1) exhibits sequence and structure similarities to members of the LTTR, (2) binds specifically to the intergenic yfeR/yfeH region and (3) autoregulates its own transcription. An outstanding feature of YfeR is the fact that

its expression is sensitive to the osmolarity of the medium, and it is induced when cells grow at low osmolarity. MAPK Inhibitor Library Apart this report, low osmotic stress increasing the expression of a LTTR has only been described for the Anabaena regulator RbcR1 (Mori et al., 2002). A global transcriptomic analysis of Yersinia pestis showed three osmolarity-regulated LTTRs (upregulated by high-salinity stress; Han et al., 2005). Interestingly, expression of the putative Na+-dependent transporter YfeH appears to be governed by a complex network, rather than by YfeR alone. It is apparent that, rather than osmolarity, the main factor influencing YfeH expression is the stationary phase. Expression of yfeH increases in yfeR mutants only when cultures grown at high osmolarity enter the stationary mafosfamide phase. Whereas this suggests that YfeR is a repressor of yfeH transcription, it is also apparent that factors other than YfeR modulate

YfeH expression. In turn, this strongly suggests that, as has been shown for other LTTRs, YfeR targets genes other than to those adjacent to it, and that may be required for optimal growth under low osmolarity conditions. The global transcriptomic analysis performed in this work supports this assumption. Interestingly, whereas several upregulated genes in the yfeR mutant encode envelope proteins, downregulated genes encode proteins related to amino acid transport and metabolism. These results suggest that, when growing under low osmolarity conditions, YfeR, either directly or indirectly, represses some envelope proteins and induces specific amino acid metabolic pathways. These factors may contribute to the adaptive response of Salmonella to low osmolarity conditions. Whereas in the recent past LTTRs appeared to specifically modulate transcription of their adjacent gene, increasing experimental evidence shows that both modulators and the modulated genes are related to more complex regulatory networks (Lehnen et al.