A topical vaginal microbicide preventing the HIV virus from estab

A topical vaginal microbicide preventing the HIV virus from establishing an infection through the female genital tract could be live saving for young women and other women at risk. With the recent evidence from the Caprisa004 trial showing a 39% reduction in HIV incidence among those using 1% tenofovir gel,7,8 we urgently need to strengthen and broaden the vaginal HIV prevention research by designing and developing more user-friendly formulations (such as vaginal rings) and more effective products, including the design of new chemicals that are not used for the treatment of HIV, thereby limiting the spread

of resistance to drugs that are part of critical combination treatments. Researchers from the Europrise consortium, representing CP-690550 supplier 14 projects funded by the European Commission, are now developing combined antiretroviral vaginal gel products, mucosal vaccines, and vaginal ring devices. Each of these new products will need to prove that they are safe and

efficacious through development pathway steps. Safety trials should selleck chemical be designed with the utmost care and specifically assess products for maintenance of healthy vaginal ecology and local mucosal immunity. Similarly, oral pre-exposure prophylaxis (PrEP) or an HIV vaccine, applied intramuscularly, nasally, subcutaneously or through any route should not negatively affect the local vaginal milieu. Of equal importance is the assessment of the presence or absence of protective humoral and cellular immunity in response to a vaccine whatever

the route of application. The cellular immunity (HIV-specific CD8 +  T cells) induced by the MRKAd5 HIV-1 gag/pol/nef vaccine in the Step trial did not provide protection from HIV. In this trial, an opportunity many was missed to evaluate the local mucosal immune responses to gain insight in the vaccine’s failure.9,10 The best way to assess safety and immune responses to products is by sampling the vaginal milieu; studying the local immune system before, during and after use of the products. A proven, well-documented and standardized sampling strategy will provide high quality data to be able to assess both safety and local immune response. The focus of this review is to critically assess the methods used for vaginal sampling in the context of clinical trials for vaginal products, and to highlight areas that need further exploration. At present, a wide range of clinical methods for sampling is used and new methods are being explored.

Animal models have been paramount in contributing to our knowledg

Animal models have been paramount in contributing to our knowledge and understanding of the consequences of vitamin D deficiency on brain development Dabrafenib concentration and its implications for adult psychiatric and neurological diseases. The conflation of in vitro, ex vivo, and animal model data provide compelling evidence that vitamin

D has a crucial role in proliferation, differentiation, neurotrophism, neuroprotection, neurotransmission, and neuroplasticity. Vitamin D exerts its biological function not only by influencing cellular processes directly, but also by influencing gene expression through vitamin D response elements. This review highlights the epidemiological, neuropathological, experimental and molecular genetic evidence implicating vitamin D as a candidate in influencing susceptibility to a number of psychiatric and neurological diseases. The strength of evidence varies for schizophrenia, autism, Parkinson’s disease, amyotrophic lateral sclerosis, Alzheimer’s disease, and is especially strong for multiple sclerosis. It is well established that the vitamin D endocrine system plays a critical role in calcium homeostasis and bone health; however, in recent decades, the broad range of physiological actions

of vitamin D has been increasingly recognized. In addition to its role in proliferation, differentiation and mTOR inhibitor immunomodulation, there is mounting evidence to support an intricate role of vitamin D in brain development and function in health and disease. The current review will summarize key concepts in vitamin D metabolism in the brain, and explore the relationship of vitamin D and brain development. A survey of the role of vitamin D in several psychiatric and neurological disorders including schizophrenia, autism, Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), and multiple sclerosis (MS) will be presented. Tolmetin Vitamin D is a seco-steroid hormone that comes in two major forms depending on the source, vitamin D2 (ergocalceiferol) of plant origin, and vitamin D3 (cholecalciferol) of

animal origin. Vitamin D3 can be either ingested or produced photochemically in the epidermis by action of ultraviolet light (UVB) on 7-dehydrocholesterol. In both instances, vitamin D2 and D3 are biologically inert and require two separate hydroxylations by 25-hydroxylase (liver) and 1-α-hydroxylase (primarily in the kidney) to give rise to the active form (1,25-dihydroxyvitamin D2 and 1,25-dihydroxyvitamin D3 or calcitriol, respectively) [1] (Figure 1). The potential role of 1,25-dihydroxyvitamin D3 in the brain was first suggested by the discovery of high affinity calcitriol receptors in the pituitary [2], and later in the forebrain, hindbrain, and spinal cord [3] of rats. The presence of vitamin D metabolites in the cerebrospinal fluid of healthy patients further implied a role for vitamin D in the brain [4].

S Wain-Hobson (Paris)

S. Wain-Hobson (Paris) selleck products discussed the contribution of the APOBECs, a class of cytidine deaminases, in tumorigenesis. A.

Gori (Monza) closed the session with a special lecture discussing what infectiologists could learn from immunologists in order to better understand clinical situations of viral infection, paying special attention to HIV. First of all, we apologize to all those scientists who are not quoted in this non-exhaustive report. We were very satisfied with the high quality of the scientific presentations, the interesting discussions, and the number of young scientists who presented their work in Riccione. The linkage “in equilibrium” between an exciting immunological conference and an intense social program created new collaborations and close friendships among

the participants of both Societies. Considering that, last but not least, the financial side looks very promising, a similar experiment asks to be repeated. “
“Over the past decade, a growing recognition of the importance of neutralizing antibodies Belnacasan clinical trial in host defense combined with the success of B-cell depletion therapies in treating auto-immune disorders has led to an increased focus on better understanding the pathways underpinning B-cell antibody production. In general, B cells require cognate interaction with T helper cells in the germinal center of lymphoid follicles to generate protective antibodies. However, recent evidence shows that B cells receive additional help from invariant natural killer T cells, dendritic cells, and various granulocytes, including neutrophils, eosinophils, and basophils. These innate immune cells enhance T-cell-dependent antibody responses by delivering B-cell helper signals both in the germinal center and

at postgerminal center lymphoid sites such as the bone marrow. In addition to enhancing and complementing the B-cell helper activity of canonical T cells, invariant natural killer T cells, dendritic cells, and granulocytes can deliver T cell-independent B-cell helper signals at the mucosal interface and in the marginal zone of the spleen to initiate rapid innate-like antibody responses. Fossariinae Here, we discuss recent advances in the role of adaptive and innate B-cell helper signals in antibody diversification and production. The mammalian immune system comprises of innate and adaptive branches that mount integrated protective responses against intruding microbes. The innate immune system includes dendritic cells (DCs), macrophages, granulocytes, and natural killer (NK) cells that mediate fast but nonspecific responses after recognizing generic microbial structures through invariant germline gene-encoded receptors often referred to as pattern recognition receptors, including Toll-like receptors (TLRs) (reviewed in [[1]]).

The age-specific prevalence of patients with ESKD was estimated u

The age-specific prevalence of patients with ESKD was estimated using a logistic regression model with generalized estimating

equation based on the data of high-income countries. The ratio between number Crizotinib of RRT and estimated number of ESKD (RRT/ESKD ratio) \ were computed for all countries on the basis of gross national income levels for each country. Results: The number of patients with ESKD was estimated to be 7.8 million, of which 2.3 million (30%) had access to RRT, leading to 5.5 million preventable deaths. The proportion of patients who did not received RRT among patients with ESKD was greater in lower income countries. The largest differences in the number of patients with ESKD and those receiving RRT were observed in Asia, Africa and Latin America. Global use of RRT is estimated to increase up to 5.2 million over next two decades, with most growth in Asia. Conclusion: Globally, ESKD continues to cause many premature deaths, mainly in developing regions. The prevalence

of ESKD as well as RRT is projected to increase over next two decades, mainly in Asia, but a similar number of people will continue to die due to lack of access to treatment. Effective prevention and management of CKD, coupled with the development of affordable dialysis and kidney transplant services for ESKD should be priorities for the renal community. PERIYASAMY MUTHUKUMAR, THANIGACHALAM DINESHKUMAR, NATARAJAN GOPALAKRISHNAN, JEYACHANDRAN DHANAPRIYA, RAMANATHAN SAKTHIRAJAN, T BALASUBRAMANIAM Madras Medical College Introduction: Rheumatoid arthritis (RA), a chronic crippling disease can affect all check details components of the kidney. Renal involvement may be due to disease or drugs used to treat the condition. We intend to study the renal lesions in RA and its clinic o pathologic correlations. Methods: Prospective observational study click here was conducted at department of nephrology, Rajivgandhi Government general Hospital, Chennai, India between 2010 to 2013. RA patients with abnormal urine sediments (>3 RBC, s or RBC cast), proteinuria (>0.3 gms/day) or eGFR (<80 ml/min) were included in the study. Those with normal renal parameters were

excluded. Results: Three hundred patients with RA were screened. Mean follow up was 23 months. 52 patients found to have renal disease. Mean age was 45 years (range 18–67). 60 % patients were female. (Male: female ratio 1.5:1). Mean duration of illness was 8.5 years. 30% had odema, 4% had macrohaematuria, 52% were asymptomatic. The common renal syndromes observed in our study were chronic kidney disease (CKD-44%) Hypertension (20%), nephrotic syndrome(13%), acute kidney injury(4%). 29 patients (56%) underwent renal biopsy. The common histological pattern of renal biopsy observed were mesangial proliferation (10), focal endocapillary proliferation(5), IgA nephropathy(3), minimal change disease(2), membranous (2) and Amyloidosis(2).

Diagnostic guidelines should also depend on the medical history o

Diagnostic guidelines should also depend on the medical history of the patient, the anatomic site of infection, and even the primary organism. For

example, P. aeruginosa may occur deeper in the tissues than staphylococci (Kirketerp-Møller et al., 2008; Fazli et al., 2009), and diagnostic criteria for wound infections are also specific to the type of wound (Cutting & White, 2004). IE also illustrates that determining the anatomic site is important, because in this infection, biofilm bacteria colonizing the endocardium are localized on the heart valves (Parsek & Singh, 2003; Mallmann et al., 2009; Moter et al., FDA approved Drug Library price 2010). Characteristically, IE, although frequently associated with bacteria that exhibit antibiotic susceptibility in the microbiology lab, requires prolonged (2–6 weeks) antibiotic treatment. Thus, chronicity or recurrence and documentation of antibiotic recalcitrance are important clues for BAI (Hall-Stoodley & Stoodley, 2009). As specific biofilm markers along with definitive signs and symptom criteria for occult or suspected deep biofilm

infections are currently lacking, detection at the site of infection may include advanced imaging techniques such as whole body 18F fluorodeoxyglucose positron emission tomography (PET/CT) (Makis & Stern, 2010; Bensimhon et al., 2011). If such imaging techniques or other signs of occult or foreign body-associated biofilm infection are convincing, then guided (ultrasound or X-ray or surgery), aseptically obtained diagnostic biopsies are, in most cases, selleck inhibitor necessary unless bacteria

MYO10 are released from the biofilm to the blood (endocarditis) or secretions such as sputum. Microscopy (indicating microbial aggregates), culture (aerobic and anaerobic on differential media and for 1–2 weeks), and culture-independent broad spectrum methods (PCR) should then be used to detect any bacteria or fungi. Contaminants such as CoNS from skin may also cause biofilm infections on foreign bodies such as intravenous catheters and other implantable devices. Ultimately, indirect methods such as antibody detection can only be used, if their predictive diagnostic value has been proven in clinical studies (Pressler et al., 2009). Similar problems in diagnosing and classifying patients with IE lead to the Duke criteria (Durack et al., 1994) and later modified Duke criteria (Fournier et al., 1996; Li et al., 2000), which have been developed to facilitate and standardize the diagnostic process. A combination of major and minor criteria including echocardiography, microbiological, clinical, and histological findings results in a score, which indicates the probability of IE. However, although the Duke criteria may be helpful and provide a starting point for a BAI algorithm, it must be noted that they are used for one disease, in one organ, whereas biofilm infections are much more diverse.

7 Likewise, some miRNAs are found less expressed in choriocarcino

7 Likewise, some miRNAs are found less expressed in choriocarcinoma cells than in normal trophoblast, which

suggests a role in carcinogenesis.8 We focused on five miRNAs previously published to correlate with tumor grade, to be implicated in pregnancy, or to be related with members of the signaling intracellular cascade of LIF. For instance, miR-141, belonging to the miR-200 cluster, is found upregulated in nasopharyngeal and ovarian carcinomas in comparison with normal tissues and correlates with poor prognosis.9,10 As biological marker, levels of miR-141 are increased in plasma from pregnant women.11 Also, expression Selleck Wnt inhibitor of miR-9 may serve as a biomarker, which correlates with tumor grade and metastatic status in breast and cervical cancer.12,13 Its inhibition results in increased levels of phospho-STAT3 in embryonic stem cells.14 Among the miRNAs selected for the present investigation, to date, miR-21 is the most extensively studied. Because of its over-expression in at least six different solid cancers (lung, stomach, prostate, colon, pancreas, and

breast), it has been considered an oncomir (reviewed in15). MiR-21 can be induced by STAT3.7 Mir-93 seems to be related with the trophoblast response FLT3 inhibitor to hypoxia as it is upregulated in hypoxic trophoblast cells.16 MiR-93 shares some features with miR-141 and miR-21 as they all are expressed in human embryonic stem cells, but their effects in cell maintenance or differentiation seem to be dissimilar. While miR-93 expression remains similar also in adult tissue, miR-141 attenuates differentiation and miR-21 expression intensifies it.17–20 Finally, we selected let-7g, a member of one of the currently most important miRNA families (let-7), which is aberrantly expressed in human cancer.21 Let-7g and also miR-21 were expressed in vitro as well as in vivo via STAT3 activation after IL-6 stimulation.22 Although the LIF-induced STAT3 activation in trophoblastic cells seems to be crucial for many cell functions, thus far, the LIF-induced miRNA expression in these cells has not yet been investigated.

Therefore, in the present study, we aim to analyze the kinetics of the expression Etomidate of miR-9, miR-21, miR-93, miR-141, and let-7g after LIF treatment in JEG-3 cells. Being the most affected, influence of miR-141 on proliferation has been analyzed by its experimental over-expression and silencing. JEG-3 (DSMZ, Braunschweig, Germany) is an adherent human choriocarcinoma cell line preserving several trophoblast-like capacities including production of pregnancy-related hormones and cytokines. JEG-3 cells cultures were performed at 106 cells/175 cm2 flask and maintained under standard conditions (37°C, 5% CO2, humid atmosphere) in Ham’s F-12 Nutrient Mixture with l-glutamine (Gibco, Paisley, UK) supplemented with 10% heat-inactivated fetal calf serum (FCS; Gibco) and 1% penicillin/streptomycin antibiotic solution (Gibco).

This article is protected by copyright All rights reserved “

This article is protected by copyright. All rights reserved. “
“Activation of Toll-like receptors (TLRs) triggers rapid inflammatory cytokine production in various cell types. The exogenous product of growth-arrest-specific gene 6 (Gas6) and Protein S (ProS) inhibit the TLR-triggered inflammatory responses through the activation of Tyro3, Axl and Mer (TAM) receptors. However, regulation of the Gas6/ProS-TAM system remains largely unknown. In the current study, mouse macrophages are shown to constitutively express Gas6 and

ProS, which synergistically suppress the basal and TLR-triggered production of inflammatory cytokines, including those of tumour necrosis factor-α, interleukin-6 and interleukin-1β, by the macrophages in an autocrine manner. Notably, TLR signalling markedly decreases LBH589 ic50 Gas6 and ProS expression in macrophages through the activation of the nuclear factor-κB. Further,

the down-regulation of Gas6 and ProS by TLR signalling facilitates the TLR-mediated inflammatory cytokine see more production in mouse macrophages. These results describe a self-regulatory mechanism of TLR signalling through the suppression of Gas6 and ProS expression. Toll-like receptors (TLRs) are crucial triggers of innate immunity through the recognition of pathogen-associated molecular patterns.1 To date, 11 distinct TLRs have been found in humans, and 13 in mice.2 The ligands of most TLRs have been identified.3 For example, TLR4 recognizes the lipopolysaccharides (LPS) of Gram-negative bacteria;4 TLR3 recognizes the double-stranded RNA (dsRNA) produced by many viruses during replication, and is also activated by a synthetic dsRNA analogue, polyinosinic-polycytidylic acid [poly(I:C)],5 and TLR9 can be activated by CpG DNA motifs of both bacteria and viruses.6 Activation

of TLR triggers two signalling pathways:3 the MyD88-dependent (D) pathway, which uses the adaptor molecule MyD88, leading to the activation of the nuclear factor-κB HAS1 (NF-κB) and mitogen-activated protein kinases (MAPKs); and the MyD88-independent (I) pathway through the recruitment of Toll/interleukin-1 receptor domain-containing adaptor inducing interferon-β, resulting in the activation of NF-κB and interferon-regulating factor-3 (IRF3). With the exception of TLR3 and TLR4, all other TLRs trigger immune response exclusively through the D pathway. TLR3 signals exclusively through the I pathway,7 whereas TLR4 initiates both the D and I pathways.8 The TLR pathway-mediated activation of NF-κB and MAPKs induces the production of numerous pro-inflammatory cytokines including interleukin-1β (IL-1β), IL-6 and tumour necrosis factor-α (TNF-α). The I pathway-mediated IRF3 activation leads to the induction of type 1 interferons (IFN-α and IFN-β).

aureus cells Biological approaches have great potential in allev

aureus cells. Biological approaches have great potential in alleviating microbial attachments. Microbial species coexist and interact extensively with each other in natural biofilms. The competition for substrates serves as one of the major evolutionary driving forces in these multiple-species biofilms (Xavier & Foster, 2007; Xavier et al., 2009). Thus, many bacteria are capable of synthesizing and excreting chemicals that inhibit biofilm formation by other species.

For example, biosurfactants are synthesized selleck products and excreted by many bacteria, which inhibit attachment by their competitors (Zeraik & Nitschke, 2010; Luna et al., 2011). Thus, biosurfactants producing probiotic bacteria are proposed as potential biofilm control agents (Rodrigues et al., 2004; Falagas & Makris, 2009). Biological buy Cisplatin approaches for controlling biofilms are well studied in dental plaque biofilms. The oral microbial flora contains many beneficial species that are able to halt the progression of oral disease. Probiotic strain Lactobacillus acidophilus was shown to reduce the biofilm formation of Streptococcus mutans,

one of primary dental cariogen, through inhibiting attachment (Tahmourespour & Kermanshahi, 2011). The early dental plaque colonizer Streptococcus gordonii secretes proteases that reduce subsequent colonization of S. mutans by inactivating its competence-stimulating peptide signalling system (Wang et al., 2010). In a recent study, Ogawa et al. (2011) identified exo-beta-d-fructosidase from the culture supernatants of Streptococcus salivarius as an active substance to inhibit S. mutans biofilm formation (Ogawa et al., 2011). Young biofilms are often more susceptible to antimicrobial agents than mature biofilms (Drenkard & Ausubel, 2002; Mukherjee et al., 2003; Allesen-Holm et al., 2006; Ito et al., 2009). The large amounts of EPS in the mature biofilms can act as a diffusion barrier to antimicrobial agents (Hoyle et al., 1992; Souli & Giamarellou, 1998; Anderl et al., 2000). The high cell density in the mature biofilms can induce cell-to-cell communication

PIK3C2G (quorum sensing) systems, which up-regulate expression of genes contributing to antibiotic resistance (De Kievit et al., 2001; Bjarnsholt et al., 2005) and release of protecting DNA (Hunt et al., 1995; Allesen-Holm et al., 2006). Also, competition for nutrients can lead to subpopulation differentiation and spatial physiological heterogeneity in the mature biofilms, which further cause antibiotic resistance (Xu et al., 1998; Walters et al., 2003). Thus, strategies for interfering structure development and differentiation of biofilms are being developed by many research groups. Enzymatically and chemically disrupting biofilm EPS matrix is proved to be an efficient approach to arrest biofilm structure development. Longhi et al.

Thus, the data from ablation models cannot be interpreted without

Thus, the data from ablation models cannot be interpreted without also taking into account the actual rather than predicted ablation patterns, the kinetics of deletion and regeneration, the effect on the remaining DC compartment and the role the depleted cell populations may play in immune homeostasis in the steady state. Models in which MHC alleles required for specific antigen presentation are expressed only by a defined DC

subset would overcome most, if not all, of the problems associated with DC immunization, Dinaciclib antibody targeting and ablation strategies. By retaining the entire complement of DC subsets with their normal transcriptional and biochemical programme, these models have the potential

to define DC biology in a physiological context. So far, this aim has been achieved only for radioresistant DC subsets, namely LCs. A number of published models have studied responses to LCs in MHC-disparate bone marrow (BM) chimeras in which LCs remain of host origin, whereas the majority of DDCs and cDCs are replaced [6, 8, 80-82]. The functional capacity of LCs can then be assessed using well-characterized TCR transgenic T cells whose specificity is restricted by an MHC allele encoded within the radioresistant host genome. MHC I-restricted models have made use of the fact that the Kbm1 mutant allele does not allow presentation of the ovalbumin (OVA) epitope to CD8+ OT-I TCR-transgenic T cells. In these models, OT-I stimulation capacity is restricted to LCs and radioresistant stromal cells of the H-2k host reconstituted with H-2Kbm1 BM [82]. click here The preservation of deletion of OT-I cells in response to skin-derived antigen has been interpreted as indicating that LCs can induce CD8+ T cell deletion in vivo, but the possibility that the effect was mediated via MHC I-expressing LN stromal Endonuclease cells cannot be excluded [82]. In contrast, MHC II-dependent skin responses are effectively restricted only to LCs in MHC II-disparate chimeras,

as LN stromal cells do not express MHC II [8]. Two groups have published results from such models. Allen et al. used wild-type hosts reconstituted with MHC II-knock-out (H2-Ab1–/–) BM and concluded that LCs were unable to support CD4+ T cell proliferation [80]. However, reconstitution with MHC II-knock-out BM would generate an immune system in which tonic MHC II-dependent TCR signalling was deficient due to a lack of MHC II expression by the vast majority of DCs [83-86]. Such tonic TCR signalling is known to be critical for the maintenance of TCR sensitivity and responsiveness to activation, motility and memory generation within the CD4+ T cell compartment [87-90]. Thus the lack of CD4+ T cell response may have been due to the failure of most DCs to express MHC II, rather than an inability of LCs to support T cell proliferation under physiological conditions.

004; OR: 2 73(1 33–5 29) for DN] There is no difference in the f

004; OR: 2.73(1.33–5.29) for DN]. There is no difference in the frequency

between DM and DN subjects. Conclusion: Subjects with T2DM show higher frequency of the 6L-6L leucine repeat in CNDP1 gene compared to non-diabetics. There is no association, however with development of nephropathy. LOH PT1, TOH MPHS2, MOLINA JAD2, VATHSALA A1 1Division of Nephrology, Department of Medicine, National University Hospital. Singapore; 2Health Services and Outcomes Research, National Healthcare Group, Singapore Introduction: Diabetic Nephropathy (DN) is the leading cause of End Stage Renal Disease in Singapore and its incidence is increasing in relation Paclitaxel order to increasing prevalence of Type 2 diabetes mellitus (T2DM). While measures to prevent diabetes and its early detection are important, optimal diabetes and blood pressure control, early detection of DN and its early treatment at the primary care setting are crucial to ameliorate the course of DN. We aimed to evaluate the prevalence of DN in a primary care cluster and identify the risk factors for its occurrence in a multi ethnic Asian population. Methods: 57,594 PLX4032 purchase T2DM patients on follow-up at the National Healthcare Group Polyclinics with eGFR and at least two urine Albumin/Creatinine Ratio (UACR) measurements were stratified into DN stages:

Normoalbuminuria (NI, UACR <30 mg/g), Microalbuminuria (MI, UACR 30–299 mg/g), Macroalbuminuria (MA, >300 mg/g)

and Renal Impairment Idoxuridine (RI, eGFR <60 mL/min/1·73 m2). Risk factors for DN stages were evaluated through multivariate analysis. Results: The study population was 71% Chinese, 56% Female with mean age: 66 years, duration of diabetes of 8 years, HbA1c of 7·5% and Body Mass Index (BMI) of 26·5 kg/m2; 81% has hypertension and 73% were on Angiotensin-Converting-Enzyme-Inhibitor or Angiotensin-Receptor-Blocker. Prevalence of DN, including MI, MA or RI in this primary healthcare cluster was high at 52·5%; 32·1% had MI, 5·3% had MA, while 15·1% had RI. DN prevalence among the ethnic subpopulations was different: 52·2% of Chinese, 60·4% of Malays and 45·3% of Indians had DN respectively, p < 0·0001 (Table 1). After regression analysis, the odds ratio for DN in Malays was 1·42 (95% CI, 1·35–1·51) while in Indians was 0·86 (95%CI, 0·81–0·91). Other independent risk factors for DN prevalence were age, female gender, duration of diabetes and hypertension, HbA1c and BMI (Table 2). While Malays had the shortest duration of diabetes but highest BMI, Indians had the poorest control of diabetes whereas Chinese were older and had the longest duration of hypertension. Conclusion: The high prevalence of DN and its inter-ethnic differences suggest the need for additional measures to optimise the care of T2DM at the primary care setting so as to mitigate its progression.