These were analysed as a total group, by gender, and by glycaemic

These were analysed as a total group, by gender, and by glycaemic control (initial HbA1c over or below 64mmol/mol [8.0%]). Mean age was 41±8 years, diabetes duration 19±9 years, 58% were male, and mean HbA1c was 75±17mmol/mol (9.0±1.6%). Over the study period there was a small improvement in total population mean HbA1c (75±17 to 72±16mmol/mol [9.0±1.6 to 8.7±1.5%], p=0.003). This was accounted for by improvements in male (74±17 to 70±15mmol/mol [8.9±1.6

to 8.6±1.4%], p=0.005) and poorly-controlled (HbA1c ≥65mmol/mol [8.1%]) patients (79±15 to 75±15mmol/mol [9.4±1.4 to 9.0±1.4%], p=0.002). Female and well-controlled (HbA1c ≤64mmol/mol [8.0%]) patients showed no change in mean glycaemia. Most patients maintained closely similar HbA1c levels over time. NVP-LDE225 in vitro Interventions in type 1 diabetes may be more usefully aimed at risk factors rather than glycaemia. Copyright © 2013 John Wiley & Sons. “
“Mucormycosis is an unusual but serious fungal infection that most commonly affects people with diabetes mellitus. A defining characteristic is the rapidity at which it develops and the devastation which it can cause. Copyright © 2014 John Wiley & Sons. Mucormycosis is a serious fungal Crenolanib infection that most commonly affects people

with diabetes. A defining characteristic is the pugnacious rapidity at which it develops and attacks. Saprophytic aerobic fungi of the Phycomycetes class, which are common in the environment, can be transmitted though the inhalation of airborne spores, colonising the oral and nasal mucosa, paranasal sinuses and throat. In the normal host, there is a phagocytic response that destroys fungal reproduction, halting the infectious process. However, in those with impaired immunity the response to this type of fungal attack is weakened. The majority of patients who contract mucormycosis have diabetes, often poorly controlled. Where there is a glucose rich, acidotic, ketotic environment together with weakened cellular immunity, the circumstances are ripe for the proliferation and spread of fungi throughout the nose.

Other immunocompromised individuals are also susceptible; including those with haematological malignancies and patients undergoing chemotherapy or on other Olopatadine immunosuppressive therapies.1,2 Phycomycetes can grow extremely quickly when provided with the right conditions and fewer than 4% of cases occur without a recognised underlying cause.3,4 To aid its advance in vivo, the Mucor fungus has a predilection for lymphatics, arteries and nerves, the invasion of which causes the most serious consequences. Damage to cartilage, erosion of bone through the walls of the sinuses, spread into the orbit, retro-orbital area, along cranial nerves and via the meninges enable intracranial extension of disease. Occasionally, cerebral vascular infringement may lead to haematogenous dissemination of the infection, with or without development of mycotic aneurysms throughout the body.

Finally, a meta-analysis showed that patients with HIV-1/HCV coin

Finally, a meta-analysis showed that patients with HIV-1/HCV coinfection had less immune reconstitution, as determined NVP-BEZ235 mw by CD4 cell count after 48 weeks of ART, than did patients with HCV infection alone [13]. Few studies have analysed the apoptosis of CD4 cells in this setting. One suggested that HCV coinfection sensitizes CD4 cells towards apoptosis in untreated HIV-1-positive patients, but that this effect is rapidly lost under effective ART [39]. Another study similarly found that apoptosis in naïve CD4 cells and in naïve and memory

CD8 cells was significantly higher in HIV-1/HCV-coinfected than in monoinfected patients who were not receiving ART [40]. In our series, we did not find any of the multiple HCV-related factors to be independently associated with CD4 cell count in ART-treated or untreated patients. Regarding virological responses, there is general agreement that HCV does not influence HIV-1 viral load in ART-treated patients [4–8,25,31–34]. Although a single study found a trend towards higher HIV-1 viral load in coinfected patients, significant differences were not observed [25]. This is not unexpected considering that ART has a dramatic effect on HIV-1 viral load that could not be compensated by any possible effect of

HCV. However, in one study, no significant association was found between HCV infection and HIV-1 RNA titre, regardless of ART status [8]. Similarly, another study reported that, following interruption of ART, plasma HIV-1 viral load did not differ between HIV-1-monoinfected and coinfected patients [34]. buy Veliparib Our series supports these findings, as we observed that neither active or past HCV infection nor any other HCV-related parameter influenced HIV-1 viral load in ART-treated or untreated patients. Regarding HCV genotypes, a study found that genotype 3, as opposed to genotype 1, was associated with HIV-1 disease progression in long-term nonprogressors [11]. However,

another study found that multiple combined genotypes accelerated clinical and immunological HIV-1 Florfenicol progression, and that genotype 1 was associated with faster immunological progression [41]. The latter study also found that the effect of HCV genotype on HIV-1 progression was greater in the pre-highly active ART era, suggesting to the authors that the effectiveness of ART may diminish the effect of HCV genotype on HIV-1 disease progression. However, we failed to confirm these results, as no significant effect of HCV genotype on immunological or virological outcomes was found either in the whole study group or in the subgroup of ART-untreated patients. Although many studies have analysed the possible effect of HCV on HIV-1 outcomes, there is a noteworthy lack of studies also analysing its effects on the liver, that is, hepatic fibrosis.

Conclusions  The pharmacist-driven osteoporosis pathway at The Qu

Conclusions  The pharmacist-driven osteoporosis pathway at The Queen Elizabeth Hospital

has sustained the rate of prescription for osteoporosis therapy over a prolonged period of time. “
“The aims of the study were to (i) quantify the sales of over-the-counter (OTC) ophthalmic chloramphenicol from all community pharmacies in Wales and investigate the impact on primary care prescriptions up to 5 years after reclassification and (ii) click here investigate the temporal relationship between items supplied OTC and on NHS primary care prescriptions. Primary care prescription data (2004–2010) and OTC sales data (2005–2010) for ophthalmic chloramphenicol were obtained. The quantity sold OTC was calculated from pharmacy wholesale records and sales data from a large pharmacy multiple. Spearman’s rank correlation for prescription and OTC supplies of ophthalmic

chloramphenicol was calculated for data from January 2008 to December 2010. OTC supply of chloramphenicol eye drops and ointment were both highest in 2007–2008 and represented 68% (57 708/84 304) and 48% (22 875/47 192) of the corresponding prescription volume, respectively. Selumetinib There was a steady year-on-year increase in the combined supply of OTC ophthalmic chloramphenicol and that dispensed on prescription from 144 367 items in 2004–2005 to 210 589 in 2007–2008 before stabilising in 2008–2009 and 2009–2010. A significant positive correlation was observed between prescription items and OTC sales of chloramphenicol eye drops and ointment combined (r = 0.7, P < 0.001). OTC availability increased the total quantity of ophthalmic chloramphenicol supplied in primary care compared to that seen prior to reclassification. Although growth in the sales of ophthalmic chloramphenicol OTC has stabilised and the supply pattern mirrors primary care prescribers, further work is required to investigate whether use is appropriate and whether the publication of updated practice guidance has changed this. There are three categories for human medicines in the UK, namely Buspirone HCl prescription-only medicines (POMs),

pharmacy-only (P) medicines and general sales list (GSL) medicines. POMs are only available on prescription whereas P medicines can be sold from a pharmacy under the supervision of a pharmacist. In contrast, GSL medicines can be sold from most retail outlets.[1, 2] Over-the-counter (OTC) medicines is a collective term used to describe P and/or GSL medicines that can be purchased without a prescription, although in this paper it is used exclusively to indicate supply from a community pharmacy. The main determinant of a medicine’s legal status is its safety, although factors such as side effects, monitoring requirements, route of administration, liability to misuse and risk to human health are also considered.[2] When a medicine is ‘switched’ from one legal category to another this is termed reclassification.

They secrete proteins such as tPAI-1, tumour necrosis factor (TNF

They secrete proteins such as tPAI-1, tumour necrosis factor (TNF)-α, interleukin (IL)-6, adiponectin, resistin, and leptin [11]. An excess or deficiency of these adipokines in cases of obesity or lipoatrophy is thought to play an important

role in the development of IR, positive energy balance, endothelial dysfunction and abnormal fibrinolysis [11,22]. Serum leptin concentrations reflect body fat content and are associated with IR [11]. Increases in leptin may also be explained by so-called leptin resistance [23]. Furthermore, the increase in circulating resistin levels may reflect fat redistribution, as it has been found to correlate with the amount of visceral fat [24]. However, we did not find an association of leptin or resistin with lipodystrophy

or HOMA values, which only increased during the TAM Receptor inhibitor Venetoclax mw first year on HAART. This lack of an association of leptin or resistin with lipodystrophy or HOMA values may be attributable to the increase in adiponectin levels, which happened at the same time as increases in leptin levels because of a compensatory mechanism for IR [3,25]. The possibility that the follow-up time in our study was not long enough to show adipokine levels to be associated with lipodystrophy should also not be excluded. A previous report on HIV noninfected children showed that leptin and BMI values increased over the 3-year follow-up period [26], while our data show an increase in plasma leptin levels in HIV-infected children on HAART despite a lack of change in BMI. Finally, leptin regulates proinflammatory immune responses because leptin is capable of controlling TNF-α production and macrophage activation

[27]. Moreover, it appears that TNF-α Methocarbamol and IL-6 are capable of stimulating adipocyte leptin production [27]. Alternatively, an increase in leptin levels might be a manifestation of a chronic activation process observed with increasing tPAI-1, an important inhibitor of fibrinolysis, which is increased in metabolic syndrome and lipodystrophy and has been shown to be an independent risk factor for cardiovascular disease [11,22]. We observed a significant increase in tPAI-1 after patients started HAART, which may be associated with dysregulation of the TNF system, decreased fibrinolysis and increased coagulability [28], and thus represent an additional risk factor for cardiovascular disease in this patient group [29]. Furthermore, we did not find a significant increase in cholesterol or triglyceride levels, and only a few children in our study had significant hyperlipidaemia during follow-up. It is possible that plasma lipid levels in the peripheral blood do not show a close correlation with chronic immune activation, metabolic disorders or endothelial disease in HIV-infected children. Adiponectin has been found to be inversely associated with components of metabolic syndrome such as obesity, IR and type II diabetes [11].

, 2001) C/EBP β, especially LAP1 and LAP2, can be phosphorylated

, 2001). C/EBP β, especially LAP1 and LAP2, can be phosphorylated at several sites by many different protein kinases, such as mitogen-activated ZD1839 supplier protein kinases, protein kinase A, protein kinase C, glycogen synthase kinase 3, and calcium/calmodulin-dependent protein kinases, with different effects on its transcriptional activity, depending on the phosphorylation site (Mahoney et al., 1992; Wegner et al., 1992; Trautwein et al., 1993, 1994; Piwien-Pilipuk et al., 2001, 2002). In particular, whereas phosphorylation

of rat C/EBP β by protein kinase A, protein kinase C or glycogen synthase kinase 3 on Ser240, which is located in the DNA-binding domain, has been reported to attenuate DNA binding and induce nuclear export, Ser105 phosphorylation of LAP isoforms is a key determinant of its transactivation capacity (Trautwein et al., 1993, 1994; Buck et al., 1999; Piwien-Pilipuk et al., 2001, ALK inhibitor 2002). We therefore evaluated C/EBP β phosphorylation on Ser105 as a marker of transcriptional activity for this transcription factor. By using an antibody that specifically recognizes C/EBP β phosphorylated on Ser105, we observed that LAP1 is phosphorylated on Ser105 only in the nuclear compartment, implying

its transcriptional activation. From our co-immunoprecipitation experiments, we determined that LAP1 is essentially present in CGNs in its sumoylated form, both in the cytoplasm and in the nucleus, MYO10 and that the phosphorylated form is only nuclear and is only detected when neurons are kept in pro-survival conditions. The SUMOs serve as modifiers, exerting their effect by becoming conjugated to target proteins and stabilizing them (reviewed

by Lieberman, 2004). Sumoylation provides a rapid and efficient way to modulate the subcellular localization, activity and stability of a wide variety of protein substrates (Dorval & Fraser, 2007). C/EBPs, including C/EBP β, are well-known targets of SUMOs, which control their transcriptional activity by releasing, in rats, the inhibitory action of a conserved inhibitory domain that is a target for lysine sumoylation (Kim et al., 2002). Concerning C/EBP β isoforms, both LAP1 and LAP2 are potential targets of SUMO-2/3, but only LAP1 has been demonstrated to be conjugated to SUMO-2/3, as confirmed by our present results in CGNs. C/EBP β sumoylation has been shown to regulate its transcriptional activity, without influencing its subcellular localization (Eaton & Sealy, 2003). When CGNs were shifted to K5 medium to induce apoptosis, we observed a decrease in the LAP1 level and an increase in the LIP level in the nuclear compartment, and a decrease in the LAP2 level in the cytosolic fraction. Concomitantly, p-(Ser105)-LAP1 disappeared from the nuclear fraction.

, 2001) C/EBP β, especially LAP1 and LAP2, can be phosphorylated

, 2001). C/EBP β, especially LAP1 and LAP2, can be phosphorylated at several sites by many different protein kinases, such as mitogen-activated MDV3100 protein kinases, protein kinase A, protein kinase C, glycogen synthase kinase 3, and calcium/calmodulin-dependent protein kinases, with different effects on its transcriptional activity, depending on the phosphorylation site (Mahoney et al., 1992; Wegner et al., 1992; Trautwein et al., 1993, 1994; Piwien-Pilipuk et al., 2001, 2002). In particular, whereas phosphorylation

of rat C/EBP β by protein kinase A, protein kinase C or glycogen synthase kinase 3 on Ser240, which is located in the DNA-binding domain, has been reported to attenuate DNA binding and induce nuclear export, Ser105 phosphorylation of LAP isoforms is a key determinant of its transactivation capacity (Trautwein et al., 1993, 1994; Buck et al., 1999; Piwien-Pilipuk et al., 2001, click here 2002). We therefore evaluated C/EBP β phosphorylation on Ser105 as a marker of transcriptional activity for this transcription factor. By using an antibody that specifically recognizes C/EBP β phosphorylated on Ser105, we observed that LAP1 is phosphorylated on Ser105 only in the nuclear compartment, implying

its transcriptional activation. From our co-immunoprecipitation experiments, we determined that LAP1 is essentially present in CGNs in its sumoylated form, both in the cytoplasm and in the nucleus, Tacrolimus (FK506) and that the phosphorylated form is only nuclear and is only detected when neurons are kept in pro-survival conditions. The SUMOs serve as modifiers, exerting their effect by becoming conjugated to target proteins and stabilizing them (reviewed

by Lieberman, 2004). Sumoylation provides a rapid and efficient way to modulate the subcellular localization, activity and stability of a wide variety of protein substrates (Dorval & Fraser, 2007). C/EBPs, including C/EBP β, are well-known targets of SUMOs, which control their transcriptional activity by releasing, in rats, the inhibitory action of a conserved inhibitory domain that is a target for lysine sumoylation (Kim et al., 2002). Concerning C/EBP β isoforms, both LAP1 and LAP2 are potential targets of SUMO-2/3, but only LAP1 has been demonstrated to be conjugated to SUMO-2/3, as confirmed by our present results in CGNs. C/EBP β sumoylation has been shown to regulate its transcriptional activity, without influencing its subcellular localization (Eaton & Sealy, 2003). When CGNs were shifted to K5 medium to induce apoptosis, we observed a decrease in the LAP1 level and an increase in the LIP level in the nuclear compartment, and a decrease in the LAP2 level in the cytosolic fraction. Concomitantly, p-(Ser105)-LAP1 disappeared from the nuclear fraction.

In a reciprocal manner, adipocytes and their precursors interact

In a reciprocal manner, adipocytes and their precursors interact with the immune system through the release of various cytokines, potentially linking fat and inflammation [2]. Interleukin-17A (IL-17A) is a recently discovered cytokine produced primarily in T-helper 17 (Th17) cells which play a role in a variety of inflammatory conditions [3] and HIV infection [4]. In adipose tissue, IL-17A is

an important regulator of adipogenesis in murine models, and in vitro it acts on preadipocytes and adipocytes to inhibit adipogenesis [5, 6]. However, the relevance of IL-17 to human obesity remains to be established. The pathway regulating the association between IL-17A and obesity remains controversial, and the association between Th17 cells and adipose tissue inflammation remains to be determined. There are no data on the role of IL-17A Enzalutamide molecular weight in adipogenesis or obesity in HIV-1-infected subjects. The aim of the study was to assess the correlation between IL-7A plasma level and visceral obesity in HIV-1-infected patients. Eighty-four patients between 18 and 70 years of age with a chronic HIV-1 infection, who had been

on highly active antiretroviral therapy (HAART) for more than 6 months, were consecutively recruited. An in-depth assessment was performed, including HIV disease history, duration of HAART and infection, viral load, metabolic parameters, BMI, abdominal waist circumference, smoking status and blood Compound C chemical structure pressure. Subjects were excluded from participating if they had any of the following clinical conditions: active AIDS-defining illness, active drug abuse or alcohol abuse. HIV-1-infected patients were divided into two groups. The first group comprised patients with a diagnosis of visceral obesity. The second group included patients for whom a diagnosis of visceral obesity had been excluded. Forty-six subjects (23 with visceral obesity and 23 without) Nintedanib (BIBF 1120) negative for HIV infection were also selected to match HIV-positive patients in terms of age range and gender distribution as a control

group. The diagnosis of central obesity was confirmed by measurement of visceral fat thickness based on ultrasound measurement of the PRFD/BMI ratio according to previously published data [7-9]. For ultrasound measurement, a Logiq 5 ultrasound scanner (General Electric Medical Systems, Wallingford, CT) equipped with a 3.75-MHz convex probe was used. Sonographic evaluation of visceral obesity was performed by a single trained sonographer blinded to the patients’ data. For each subject, an aliquot of serum sample was collected and stored at −80°C. Serum IL-17 was measured by enzyme-linked immunosorbent assay (ELISA; R&D Systems, Abingdon, UK) in duplicate, adding 100 μL of serum per well following the manufacturer’s recommendations.

In addition, two flavin-binding monooxygenases were found to be u

In addition, two flavin-binding monooxygenases were found to be upregulated during growth on alkanes indicative of two novel pathways likely to be involved in alkane degradation by A. borkumensis (ABO_0282, ABO_1097, Table 1). this website Moreover, we detected the up-expression of two genes similar to the ones involved in the degradation of halogenated alkanes in other bacteria, namely haloacid dehalogenase-like hydrolase dhlA (ABO_1537, Table 1) and haloalkane dehalogenase dhmA (ABO_2415,

Table 1). If the first enzyme is known to convert haloalkanes to corresponding alcohols and halides, the second one catalyzes hydrolytic cleavage of carbon-halogen bonds in halogenated aliphatic compounds, leading to the formation of primary alcohols, halide ions, and protons. Alkane-induced coexpression of these enzymes mediating the breakdown of haloalkanes, alongside the induction of enzymes degrading aliphatic alkanes, signifies unspecific upregulation of expression, probably reflecting the presence of halogenated alkanes in sea water. Additionally, we found alkane-induced

expression of aldehyde reductase (ABO_2414, Table 1). This gene is predicted to be involved in the metabolic activation of polycyclic aromatic hydrocarbons (PAHs), as shown recently for human aldehyde reductase AKR1A1 (Palackal et al., 2001). However, as yet, A. borkumensis has not been shown to either degrade or transform PAHs, and thus requires further experimentation to explore what coexpression ABT-737 clinical trial of this gene alongside those mediating the degradation of aliphatic alkanes may signify for the degradation of alkanes or petroleum. These data allow us to update the list of enzymatic systems shown before by our proteomic study to be potentially involved in the initial terminal oxidation of alkanes by A. borkumensis (Figs 1 and 2). Attachment of A. borkumensis to hydrocarbons and its molecular mechanisms have not yet been studied, although such abilities are likely to form part of the specific ecological adaptation of this bacterium. EM observation of Alcanivorax SK2 indeed indicates that this organism forms biofilm-supporting structures during growth on alkanes (Fig.

Immune system 3). Cells grown on alkane seem to more connect to each other rather than to the solid surface of the carrier slide, and they are shorter and rounder, and produce considerable amount of extracellular polymeric substances (EPS), which appears to support the three-dimensional structure of a biofilm. After 10 days of growth, alkane-grown cells develop a biofilm, which exhibits a pronounced three-dimensional architecture supported by extracellular matrix (Fig. 3). The argument of an alkane-induced formation of EPS is supported by alkane-induced up-expression of gmhA (ABO_0584). GmhA encodes a phosphoheptose isomerases that mediates the synthesis of heptose, a conserved component of outer membrane lipopolysaccharide, that for example in Yersinia, was shown to contribute to the formation of biofilms (Darby et al., 2005).

We used data from the HIV Research Network

(HIVRN), a con

We used data from the HIV Research Network

(HIVRN), a consortium of sites (see Appendix) that provide primary and subspecialty care to HIV-infected patients in 14 cities throughout the USA. To participate in the HIVRN, a site had to have a minimum data set including the patients’ age, sex, race, HIV transmission risk factor, AIDS-defining illnesses, CD4 Nutlin-3a order cell count, HIV-1 RNA level and use of antiretroviral medication. Eleven HIVRN sites that treated adult HIV-infected patients, nine with academic affiliations, also collected data on resource utilization and in-patient ICD-9 codes. Data from 10 of these sites, located in the Northeastern (six sites), Western (two), Midwestern (one) and Southern (one) USA, were included in the analysis. One nonacademic site discontinued participation in the HIVRN during this period and was excluded from analyses. All adult HIV-infected patients (≥18 years old) at these 10 sites with at least one out-patient visit between 2000 and 2008 were eligible for inclusion in the study. Each site abstracted the data elements described above from electronic or paper

records. After removal of identifying information, the sites sent the abstracted data Buparlisib chemical structure to a data co-ordinating centre in an electronic format. For this analysis, data collection encompassed the period from 1 January 2000 to 31 December 2008, as recorded by the date of encounter, not the date of billing or claim payment. Development, maintenance and use

of the database are approved by the Institutional Review Board of the Johns Hopkins University School of Medicine, which serves as the data co-ordinating centre, as well as the Institutional Review Boards of each of the participating institutions. Because bacteraemia is nearly always treated in in-patient settings, we focused on hospital admissions data recorded at each study site. Each Celecoxib HIVRN site reported dates of admission and discharge and all ICD-9 codes associated with an in-patient episode. Any text descriptions were translated to ICD-9 codes. All in-patient episodes were reviewed, starting from 1 January 2000 or the patient’s first recorded out-patient visit to the HIV clinic, whichever came later, and ending at date of death or 31 December 2008, whichever came first. ICD-9 codes were examined to identify all in-patient cases of bacteraemia or septicaemia during the study period. The ICD-9 code for septicaemia (038.XX) intrinsically includes the organism of interest whereas the ICD-9 code for bacteraemia (790.7) does not include an organism. Therefore, in these cases we used the second ICD-9 code (041.XX), which indicates the organism causing bacteraemia. Table 1 shows the classification of bacteraemia/septicaemia episodes in terms of types of organisms and their mapping to ICD-9 codes. In addition, analyses also included a small number of episodes associated with Salmonella (003.1) and Listeriosis (027.0).

Primer extension analysis revealed that the cfaB gene in P putid

Primer extension analysis revealed that the cfaB gene in P. putida KT2440 is expressed from a single promoter, and that its expression does not occur in an RpoS-deficient background, confirming the total dependence of cfaB expression on the alternative sigma-factor, σ38. Much of the knowledge regarding CFA synthase gene expression comes from studies in E. coli, in which its expression is driven by two promoters: one σ70-dependent and the other σ38-dependent (Wang & Cronan, 1994). Furthermore,

check details in Pseudomonas, two enzymes, the CTI and the CFA synthase, use the same substrate (the cis-UFAs) while CTI has not been found in E. coli. Because of these differences from the E. coli paradigm, we became interested in the regulation and formation of CFAs in P. putida. The cfaB promoter of P. putida KT2440 has a sequence that is very similar to the RpoS recognition consensus sequence of E. coli (Fig. 3a; Espinosa-Urgel et al., 1996; Lee & Gralla, 2001; Weber et al., 2005), with six out of seven nucleotides being conserved. RpoS recognition sequences have been thoughtfully investigated in E. coli and several studies Natural Product Library high throughput have indicated that the −13C, −12T, −11A and −7T nucleotides are essential for maximum expression of the RpoS-dependent transcription

(Hiratsu et al., 1995; Bordes et al., 2000; Lee & Gralla, 2001) and that these four positions are highly conserved (Weber et al., 2005). In the P. putida KT2440 cfaB promoter, changes in −14C, −13T and −12A ( correspond to

Acyl CoA dehydrogenase −13C, −12T and −11A in the E. coli consensus sequence) were also found to be essential for the cfaB promoter expression, in agreement with the results mentioned above. Mutation in −8T, critical in E. coli (−7T), did not lead to a significant decrease in promoter activity in the P. putida KT2440 cfaB promoter. This position was also pointed out as critical in the recognition of σ32 and σ38 in the Pm promoter that controls the expression of the meta operon in the pWW0 toluene degradation pathway (Domínguez-Cuevas et al., 2005) of P. putida mt-2. However, these experiments were performed in E. coli and the importance of this position in promoter recognition by σ-factors in Pseudomonas may be different from that in E. coli. Position −10 in Pm was relevant for recognition by the σ factor, and when we mutated the equivalent position in the cfaB promoter (−11C), a 3.5-fold reduction in expression was observed. Interestingly, nucleotide −9C in the cfaB promoter was critical for activity. This position is conserved in 70% of the RpoS-dependent promoters in E. coli (Weber et al., 2005), but was not previously found to be essential for RpoS recognition. The CFA content in Pseudomonas membranes is tightly regulated such that they are only produced during the stationary phase of bacterial growth and they never represent more than 20–30% of the total fatty acids.