3c) on both crystalline and amorphous cellulose as well as complex cellulosic substrates, for example, alfalfa cell walls, wheat straw and banana fruit stem. Both recombinant CBM3s underwent partial cleavage by E. coli native proteases during the purification procedure. Nevertheless, the full-length recombinant CBM3 of Cthe_0059 bound strongly to all of the cellulosic target substrates; the recombinant CBM3 of Cthe_0404 showed much weaker binding characteristics to the various substrates, particularly to amorphous cellulose and alfalfa cell

walls, perhaps indicating the different recognition properties of the two CBM3 variants. The cellulose-degradation process commences with the binding of the cellulolytic enzymes and/or the entire organism to the cellulosic substrate, mediated by a separate cellulosome-borne component, the CBM3 (Poole et al., 1992; Bayer et al., 1996; Tormo et al., 1996). CBMs can serve as targeting agents for the catalytic modules of free cellulases GSK-3 inhibition or can act as a separate

find more targeting module, for example, as part of the noncatalytic scaffoldin subunit of the cellulosome (Bayer et al., 1998). The C. thermocellum genome contains 20 genes encoding proteins, which carry 23 CBM3s. The CBM3s are known to either bind strongly to crystalline cellulose, thus playing a substrate-targeting role, or serve to modulate the apparent mode of action of the parent cellulase. Thirteen of these proteins are GHs and other enzymes involved in polysaccharide degradation; one is the main cellulosomal structural protein (scaffoldin CipA), and six others are hypothetical proteins of unknown function. All in all, the functional Pregnenolone connection between carbohydrate-active proteins and the huge majority

of genes encoding for CBM3-containing proteins could be accounted for, with the notable exception of Cthe_0059, Cthe_267 and Cthe_404. This anomaly deserved further attention (Lamed, 2010), and upon meticulous bioinformatic examination, we discovered that the N-terminal portions of the latter hypothetical proteins bore tenuous homology to the B. subtilisσI-modulating protein RsgI (Fig. S1). Systematic analysis of the C. thermocellum genome revealed another six hypothetical proteins whose N-terminal regions also exhibited homology to those of the abovementioned CBM3-containing proteins and, hence, also shared a relationship with the B. subtilis RsgI. Intriguingly, the C-terminal regions of additional proteins contained other types of carbohydrate-active modules, i.e., CBM42, PA14 and GH10 (Fig. 1). Moreover, in each case, a gene located immediately upstream of the rsgI-like ORF encoded a putative alternative σ factor resembling B. subtilisσI (Fig. 2). Such an operon-like organization of the B. subtilis and C. thermocellum sigI and rsgI genes matches perfectly one of the main criteria for the ECF σ factors (Helmann, 2002). Preliminary analysis of putative σI-related promoter sequences of the C.

There are no direct comparisons of the boosted PIs in second-line treatment after first-line failure on an NNRTI-based regimen and choice would be individualized to the patient. Sequencing from an EFV or NVP-based regimen to ETV is not recommended [35] although it remains an option when switched as part of a new combination when only K103N is present. Switching to RAL

or MVC with two active NRTIs is an option but is also not recommended in a patient with historical or selleck existing RT mutations/previous NRTI virological failure [36]. Less than 1% of patients harbour viruses with primary PI mutations and 10–20% NRTI mutations at 48 weeks, with 75% having WT virus [24, 27-29, 37, 38]. There are currently limited data regarding the efficacy of switching to another PI/r, NNRTI, MVC or RAL-based regimen and again the decision is individualized to the patient. However, switching to RAL, MVC or NNRTI in a patient with historical or existing RT mutations is not recommended because of an increased risk of virological failure and further emergence of resistance [36]. By contrast, because

of the high genetic barrier of PI/r, sequencing to a regimen that includes a new PI/r is unlikely to lead to further emergent resistance and is recommended. Where PI/r mutations exist, DRV/r is the preferred agent unless resistance is likely. Up to one-half of patients harbour viruses with primary integrase mutations Tyrosine-protein kinase BLK and 25% NRTI mutations at 48 weeks: approximately half have WT virus [26, 33, 37, 39]. Again, there BMS-777607 are no data supporting a switch to PI/r, NNRTI or MVC but sequencing to a new regimen that includes PI/r is unlikely to lead to further emergent resistance and is recommended. Switching to NNRTI or MVC with two active NRTIs is an option but is also

not recommended in a patient with historical or existing RT mutations/previous NRTI virological failure. Patients experiencing virological failure on RAL should switch to a new regimen as soon as possible to reduce the risk of accumulating resistance mutations that may affect susceptibility to newer INIs such as dolutegravir. We recommend patients with persistent viraemia and with limited options to construct a fully suppressive regimen are discussed/referred for expert advice (or through virtual clinic referral) (GPP). We recommend patients with triple-class resistance switch to a new ART regimen containing at least two and preferably three fully active agents with at least one active PI/r such as DRV/r or TPV/r and one agent with a novel mechanism (CCR5 receptor antagonist or integrase/fusion inhibitor) with ETV an option based on viral susceptibility (1C). Risk of development of triple-class virological failure is relatively low at about 9% at 9 years from start of ART [40].

Titles and abstracts were assessed by two review authors [Arathi Papineni (AP) and Paul Ashley (PA)] for inclusion in the review. Data extraction was carried out using a specially designed form independently by two of the review authors (AP and PA). Any disagreements were resolved by discussion. Review authors were not blinded to the journal of publication or the author’s names on the papers. The descriptive data recorded is shown in Figure 4. These were characterised under the following headings (see tables 13.2a and b in the Cochrane

Handbook for more details[12]): whether there was an intervention; how groups were created; which parts of the study were prospective if any. Risk of bias was assessed by ranking studies according to a hierarchy of evidence. Across studies, a summary assessment was rated as low risk of bias when most information was from studies at low risk of bias, unclear risk of bias when most information this website was from studies at low or unclear risk of bias, and high risk of bias when the proportion of information was from studies at high risk of bias sufficient to affect the Acalabrutinib purchase interpretation of the results. Data from individual studies were presented; where possible, data from studies were to be pooled to allow some estimate of the number of adverse effects overall. Ideally, dichotomous or continuous outcome variables with means and standard deviations were to be recorded where

available. To further evaluate side effects following use of oral midazolam for behaviour management in paediatric dentistry, the following subgroup analyses were also proposed if data were available: age; dose. Randomised controlled clinical trials of effectiveness and randomised controlled clinical trials looking at side effects There were no RCTs found looking

at side effects alone. After combining the results from Medline and Embase searches and removing papers that did not meet the criteria, 16 papers were included[13-28]. Data from these papers are summarised in Table 1. Only the numbers of subjects receiving oral midazolam are described. Summary data are at the bottom of the table; only simple summary measures could be calculated due to the limited data available from some studies. n = 30 4.6 (0.77) Crossover n = 25 5.36 (1.7) Parallel Hypoxaemia, Telomerase or disinhibition (n = 6) Vomiting and nausea (n = 2) Vertigo, vomiting, speaking disability (n = 3) Euphoria, hypoxaemia, disinhibition and headache (n = 1) Vertigo, disinhibition and nausea, salivation, speaking disability (n = 2) Nb – hypoxaemia not defined, assumed to be minor n = 16 (unclear) Age range = 4–10 years Parallel 7.5 mg midazolam vs Placebo n = 23 6.8 Crossover Minor visual disturbances: one diplopia and a mild hallucination (n = 2) Ataxia (n = 1) n = 31 4.7 Crossover Transient desaturation (n = 4) Vomiting (n = 1) Confrontational/defiant behaviour (n = 2) n = 20 Younger than 4 years old Parallel n = 20 No age given Parallel n = 11 3.

TraB is a hexameric pore-forming ATPase that resembles the chromosome segregator protein FtsK buy Venetoclax and translocates DNA by recognizing specific 8-bp repeats present in the plasmid clt locus. Mobilization of chromosomal genes does not require integration of the plasmid, because TraB also recognizes clt-like sequences distributed all over the chromosome. Mycelium-forming actinomycetes

do not divide by binary fission but grow by apical tip extension and undergo a complex life cycle ending in sporulation (Flardh & Buttner, 2009). They are well known for the production of antibiotics, a feature probably developed to inhibit competitors in the soil community (Allen et al., 2010). During evolution of the antibiotic biosynthetic gene clusters, they also evolved specific resistance

genes as a part of the cluster to protect themselves from their own compounds. Because a typical Streptomyces strain contains 10–20 different gene clusters for the production of antibiotics and other bioactive secondary metabolites (Bentley et al., 2002; Medema et al., 2011), streptomycetes form a huge reservoir of antibiotic resistance genes in the soil, which can be passed to other bacteria by horizontal gene transfer (D’Costa et al., 2006; Allen et al., 2010). Therefore, the antibiotic Selleck Pifithrin�� producers not only compete with other organisms by the production of antimicrobial compounds but they also provide resistance genes that can help others to survive. In Streptomyces and related actinomycetes, even small multi-copy plasmids of < 10 kb in size are normally self-transmissible and able to mobilize chromosomal resistance genes and auxotrophic markers (Kieser et al., 1982; Kataoka et al., 1991; Servin-Gonzalez et al., 1995). These plasmids are normally cryptic and do not confer phenotypic traits (Hopwood

& Kieser, 1993; Vogelmann et al., 2011a). Efficiency of transfer reaches nearly 100% and between 0.1% and 1% of U0126 manufacturer the transconjugants obtain chromosomal fragments during mating (Kieser et al., 1982). DNA transfer takes place only on solid surfaces in the early growth phase of the life cycle, when Streptomyces grows as substrate mycelium (Pettis & Cohen, 1996; Possoz et al., 2001). The transfer determinants of many Streptomyces plasmids were initially identified as killing functions (kilA, traB), which could only be subcloned in the presence of the corresponding killing override (korA, traR) region (Kendall & Cohen, 1987; Hagege et al., 1993; Reuther et al., 2006a). Probably due to the toxic effects of the transfer determinants, plasmid transfer is associated with the formation of so-called pock structures having a diameter of 1–3 mm. Pocks are formed when donor spores germinate on a lawn of a plasmid-free recipient. Pocks represent temporally retarded growth inhibition zones and indicate the area, where the recipient mycelium has obtained a plasmid by conjugation (Fig. 1).

Subjects were predominantly male (64%) and from countries of low (<0.5%) HIV prevalence (84%). The median age was 30 years (range 14–87 years). Fifty per cent of subjects did not http://www.selleckchem.com/products/wnt-c59-c59.html belong to any known risk groups for HIV infection. The other 50% consisted of clients of commercial sex workers (16%), MSM (15%), IDUs (6%) and commercial sex workers (3%). Housekeepers,

who frequently sought care after injuries from needles left in trash bags, and police officers, who were exposed to infectious body fluids during violent arrests, accounted for 2 and 3% of the subjects, respectively. Four per cent were stable partners of HIV-infected persons. Excluded subjects differed from those included in the analysis in the following ways: they were more likely to be older than 40 years, more likely to be exposed through nonsexual routes, and less likely to be IDUs and clients of commercial sex workers but more likely to be exposed as housekeepers. Of 734 sexual exposures, 527 (72%) involved heterosexual contact and 132 (18%) homosexual contact (see

Table Fulvestrant molecular weight 1). Proportions of anonymous sexual contacts were similar in heterosexual and homosexual subjects (62 and 61%, respectively). Fifty-eight sexual assaults were also registered. The majority of the 179 nonsexual events were related to needlestick injuries (37%) and IDU equipment sharing (25%). In 208 episodes (23% of 910 eligible requests), the source was reported to be HIV positive, and in 187 episodes the Anidulafungin (LY303366) HIV-positive status could be confirmed. Among those for whom information was available, more than half were not under ART and had a detectable viral load at the time of exposure. In 702 events (77%), the HIV status of the source subjects was unknown. In these cases, 298 (42%) source persons could be tested and 11 new HIV infections were diagnosed (see Table 2). The likelihood of being able to contact and test the source varied significantly across risk categories. Police officers were more likely to have

their source found and tested compared with non-police officer subjects (57 vs. 32%; P<0.001). Conversely, IDUs, MSM and housekeepers were less likely to have their source tested than non-IDUs (4 vs. 34%; P<0.001), non-MSM (24 vs. 34%; P=0.02) and nonhousekeepers (10 vs. 33%; P=0.02), respectively. No difference was seen for commercial sex workers (27% of sources tested) and clients of commercial sex workers (32%). Heterosexual subjects had their contacts tested more often than did MSM (38 vs. 24%; P=0.001). The median time to consultation was 17 h after the exposure. Five hundred and forty-seven participants (60%) sought care within 24 h and 747 (82%) within 48 h. Among 910 eligible events for nPEP, it was received in 710 cases (78%) (Fig. 1). Twenty-six persons received nPEP twice during the study time, while five patients had three nPEP courses.

Various approaches have been used to define the population structure of P. aeruginosa and to identify an association between strain types and environmental origin or particular types of infection. Using a combined analysis of amplified

fragment length polymorphism (AFLP), serotype, pyoverdine type and antibiograms, Pirnay et al. (2005) concluded that population diversity in river water reflected the wider population diversity of P. aeruginosa and that environmental and clinical isolates are indistinguishable (Pirnay et al., 2005). A combination of phenotypic and genotypic characteristics used in a larger survey reached similar conclusions (Pirnay et al., 2009). In contrast, a study using multilocus sequence typing (MLST) indicated that C59 wnt purchase oceanic isolates were divergent from the general Kinase Inhibitor Library P. aeruginosa population (Khan et al., 2008). AT genotyping has been applied to collections of isolates of clinical relevance, particularly in chronic infections associated with cystic fibrosis (CF; Mainz et al., 2009; Fothergill et al., 2010) and chronic obstructive pulmonary disorder (COPD; Rakhimova et al., 2009). Although dominant clones are a feature

in these populations, evidence for an association between a subgroup of P. aeruginosa clones and a specific type of infection has only been reported in our previous study AT genotyping of keratitis isolates (Stewart et al., 2011). To determine whether this association of a clonal subgroup with disease was a unique occurrence among UK keratitis isolates collected between 2003 and 2004 rather than an inherent feature of isolates associated with this disease, we replicated the study on a further set of 60 isolates obtained 5 years later from the same contributing hospitals. Our results

show that there was a similar cluster to that observed previously, revealing that a subgroup of keratitis-associated P. aeruginosa strains was a feature of both collections when analysed separately or when combined (n = 123). There were some minor variations between the two time points. Differences were observed in the dominant clone types (type A in 2009–2010 vs. type D in 2003–2004). There was also a reduction in the proportion of keratitis isolates falling within the core keratits cluster (cluster 1) between the time points (40% in 2009–2010 vs. 48% in Florfenicol 2003–2004). However, overall 71% of keratitis isolates belonged to a core keratitis cluster (cluster 1; Fig. 2). Although the carriage of the exoU/S was not included in the eBURST analysis, all of the exoU-positive keratitis isolates (66 of 123) belonged to cluster 1. This cluster also includes 19 isolates carrying the exoS gene. However, 35 of the 36 keratitis isolates not within cluster 1 carry the exoS gene. In our previous study, we identified RODs between keratitis isolate 039016 (AT clone type D; serotype O11; poor clinical outcome) and strain PAO1 (Stewart et al., 2011).

The murine intravenous model of disseminated C. albicans infection is a well-characterized and reproducible infection model (Louria et al., 1963; Papadimitriou & Ashman, 1986; MacCallum & Odds, 2005). Fungal cells are injected intravenously via the lateral tail vein, spreading rapidly throughout the body. In this model, infection is controlled in most organs, but progresses in the kidneys and, at higher inoculum levels, in the brain (MacCallum & Odds, 2005), with sepsis the eventual cause of death (Spellberg et al., 2005). This

model mimics infection development after fungal cells have entered the bloodstream from the gut, and can include immunosuppression regimens to model those severely immunosuppressed patients at particular risk

of disseminated infection. Gastrointestinal colonization and dissemination models require colonization of the mouse gastrointestinal Sotrastaurin molecular weight tract with C. albicans, either in infant mice or after antifungal/antibacterial treatment of adults, which is followed JAK inhibitor by dissemination. In the infant mouse model, C. albicans cells rapidly disseminate from the gut to the liver and, less frequently, to the kidneys and spleen (Pope et al., 1979; Field et al., 1981). Where dissemination does not occur and mice survive, there is persistent colonization of the gastrointestinal tract. In the adult mouse colonization and dissemination model, adult mice are infected with C. albicans in the chow, drinking water or by gavage. Fungal colonization is highest in the stomach, caecum and small intestine (Sandovsky-Losica et al., 1992; those Mellado et al., 2000; Clemons

et al., 2006). Colonization can be maintained by continuous antibiotic therapy and can be monitored noninvasively by faecal fungal counts. Subsequent treatment with immunosuppressive and/or mucosa-damaging agents leads to dissemination of fungal cells to the liver, kidneys and spleen (Sandovsky-Losica et al., 1992; Clemons et al., 2006; Koh et al., 2008). This model has been used to monitor dissemination of both C. albicans and C. tropicalis; however, C. parapsilosis was found to be unable to disseminate from the gut (Mellado et al., 2000). This model is probably a more accurate reflection of how infection can initiate in some human patients, with the dissemination of commensal organisms occurring when defects in the immune system and mucosal barriers are no longer effective in preventing fungal gut translocation (Koh et al., 2008). It is interesting to note that, similar to the at-risk patient population, there remains a considerable variation in the number of animals that develop disseminated infection, requiring increased numbers of animals to obtain statistically significant results (Sandovsky-Losica et al., 1992; Clemons et al., 2006; Koh et al., 2008). One important point to bear in mind, when modelling Candida infection in mice, is that C.

The murine intravenous model of disseminated C. albicans infection is a well-characterized and reproducible infection model (Louria et al., 1963; Papadimitriou & Ashman, 1986; MacCallum & Odds, 2005). Fungal cells are injected intravenously via the lateral tail vein, spreading rapidly throughout the body. In this model, infection is controlled in most organs, but progresses in the kidneys and, at higher inoculum levels, in the brain (MacCallum & Odds, 2005), with sepsis the eventual cause of death (Spellberg et al., 2005). This

model mimics infection development after fungal cells have entered the bloodstream from the gut, and can include immunosuppression regimens to model those severely immunosuppressed patients at particular risk

of disseminated infection. Gastrointestinal colonization and dissemination models require colonization of the mouse gastrointestinal Enzalutamide clinical trial tract with C. albicans, either in infant mice or after antifungal/antibacterial treatment of adults, which is followed selleck products by dissemination. In the infant mouse model, C. albicans cells rapidly disseminate from the gut to the liver and, less frequently, to the kidneys and spleen (Pope et al., 1979; Field et al., 1981). Where dissemination does not occur and mice survive, there is persistent colonization of the gastrointestinal tract. In the adult mouse colonization and dissemination model, adult mice are infected with C. albicans in the chow, drinking water or by gavage. Fungal colonization is highest in the stomach, caecum and small intestine (Sandovsky-Losica et al., 1992; Dichloromethane dehalogenase Mellado et al., 2000; Clemons

et al., 2006). Colonization can be maintained by continuous antibiotic therapy and can be monitored noninvasively by faecal fungal counts. Subsequent treatment with immunosuppressive and/or mucosa-damaging agents leads to dissemination of fungal cells to the liver, kidneys and spleen (Sandovsky-Losica et al., 1992; Clemons et al., 2006; Koh et al., 2008). This model has been used to monitor dissemination of both C. albicans and C. tropicalis; however, C. parapsilosis was found to be unable to disseminate from the gut (Mellado et al., 2000). This model is probably a more accurate reflection of how infection can initiate in some human patients, with the dissemination of commensal organisms occurring when defects in the immune system and mucosal barriers are no longer effective in preventing fungal gut translocation (Koh et al., 2008). It is interesting to note that, similar to the at-risk patient population, there remains a considerable variation in the number of animals that develop disseminated infection, requiring increased numbers of animals to obtain statistically significant results (Sandovsky-Losica et al., 1992; Clemons et al., 2006; Koh et al., 2008). One important point to bear in mind, when modelling Candida infection in mice, is that C.

Mean age of the patients in the study was 47 ± 13.4 years. Rheumatoid factor (RF) was positive in 63%, anticyclic citrullinated peptide antibody (anti-CCP) in 71% and both of them were positive in 49% of cases. A very small group of patients had greater than six tender joints (6%) and swollen joints (9%); moreover there was no significant differences in number

of tender and swollen joint counts across different populations. Mean DAS28 erythrocyte sedimentation rate (ESR) was 2.91 ± 1.02 and there were no statistically Obeticholic Acid molecular weight significant differences between the study groups. Almost half of the patients (49%) were in remission (DAS28 < 2.6) and one-third (36%) were in active disease (DAS28 > 3.2). However, a minority of patients selleck inhibitor (15%) were in low disease activity (DAS28 2.6–3.2). The mean HAQ score was 1.02 (± 0.60). X-rays of hand and feet were performed on 65% of patients, of whom 11% were found to have erosions. Sixty-six percent of our patients were on

one synthetic DMARD in the last 2 months before being involved in the study, 27% were on two synthetic DMARDs and 7% were not on synthetic DMARDs. Synthetic DMARDs were mostly used in the Asian group (74.8%). Methotrexate was the most commonly used DMARD (75%). It was used alone in 31% or in combination with other synthetic or biologic DMARDs (44%). Biologic DMARDs were used in 29%: 11% on rituximab, 8% on tocilizumab, 9% on anti-tumor necrosis factor and one patient was on abatacept. Use of biologics was more in the Qatari population (65.2%) and least in Asians (15.3%). Glucocorticoids were used in 51% of patients with dose range of 5–10 mg\day. In this cross-sectional study we described the characteristics

of RA in Qatar managed on an outpatient base and analyzed the severity and activity of the disease. Our study showed that the majority of patients was female (67%) and they were more frequently Qataris (91.3%) compared with Asians (52.5%) which reflects Casein kinase 1 the pattern of the Qatar population (most Asians are male). Among all patients, RF was positive in 63%, anti-CCP in 71% and both were positive in 49% which is close to that reported from Kuwait 60%.[4] A comparative study of RA in British and Malaysian patients showed that RF was positive in 65% in each group of patients which is similar to our study.[7] In our study 64% of patients were either in remission (49% with DAS28 < 2.6) or in low disease activity (15% with DAS28 < 3.2) while mean DAS28-ESR was 2.85 ± 1.047. This is in contrast to a UAE study which showed that only a few patients (15%) were in low disease activity and most of them had high disease activity with mean DAS of 5.2.[6] However, 36% of our patients had moderate to high disease activity with DAS28 > 3.2. The majority of our patients (93%) were being treated with DMARDs over the last 2 months before enrolment in the study, 66% on one synthetic DMARD and 27% on two.

Mean age of the patients in the study was 47 ± 13.4 years. Rheumatoid factor (RF) was positive in 63%, anticyclic citrullinated peptide antibody (anti-CCP) in 71% and both of them were positive in 49% of cases. A very small group of patients had greater than six tender joints (6%) and swollen joints (9%); moreover there was no significant differences in number

of tender and swollen joint counts across different populations. Mean DAS28 erythrocyte sedimentation rate (ESR) was 2.91 ± 1.02 and there were no statistically selleck screening library significant differences between the study groups. Almost half of the patients (49%) were in remission (DAS28 < 2.6) and one-third (36%) were in active disease (DAS28 > 3.2). However, a minority of patients find more (15%) were in low disease activity (DAS28 2.6–3.2). The mean HAQ score was 1.02 (± 0.60). X-rays of hand and feet were performed on 65% of patients, of whom 11% were found to have erosions. Sixty-six percent of our patients were on

one synthetic DMARD in the last 2 months before being involved in the study, 27% were on two synthetic DMARDs and 7% were not on synthetic DMARDs. Synthetic DMARDs were mostly used in the Asian group (74.8%). Methotrexate was the most commonly used DMARD (75%). It was used alone in 31% or in combination with other synthetic or biologic DMARDs (44%). Biologic DMARDs were used in 29%: 11% on rituximab, 8% on tocilizumab, 9% on anti-tumor necrosis factor and one patient was on abatacept. Use of biologics was more in the Qatari population (65.2%) and least in Asians (15.3%). Glucocorticoids were used in 51% of patients with dose range of 5–10 mg\day. In this cross-sectional study we described the characteristics

of RA in Qatar managed on an outpatient base and analyzed the severity and activity of the disease. Our study showed that the majority of patients was female (67%) and they were more frequently Qataris (91.3%) compared with Asians (52.5%) which reflects MG-132 in vivo the pattern of the Qatar population (most Asians are male). Among all patients, RF was positive in 63%, anti-CCP in 71% and both were positive in 49% which is close to that reported from Kuwait 60%.[4] A comparative study of RA in British and Malaysian patients showed that RF was positive in 65% in each group of patients which is similar to our study.[7] In our study 64% of patients were either in remission (49% with DAS28 < 2.6) or in low disease activity (15% with DAS28 < 3.2) while mean DAS28-ESR was 2.85 ± 1.047. This is in contrast to a UAE study which showed that only a few patients (15%) were in low disease activity and most of them had high disease activity with mean DAS of 5.2.[6] However, 36% of our patients had moderate to high disease activity with DAS28 > 3.2. The majority of our patients (93%) were being treated with DMARDs over the last 2 months before enrolment in the study, 66% on one synthetic DMARD and 27% on two.