The anti-inflammatory effect of both hBD3 and the mouse orthologue Defb14 19 was observed in mouse primary BM-derived Mϕ (BMDM), reducing the TNF-α response to LPS (Fig. 1E). hBD2 was not an effective suppressor of the selleck compound TNF-α response to LPS in mouse cells (Fig. 1E), whereas hBD3 was more effective than LL37 in all mouse strains tested (Fig. 1F). hBD2 has only approximately 30% amino acid similarity to hBD3, which may explain lack of anti-inflammatory effects. Conversely, Defb14, which is 64% identical to hBD3 20, did demonstrate anti-inflammatory activity. The anti-endotoxic effects of LL37 have been shown to be partly due to direct binding of LL37 to LPS 16, 21. It has previously been shown

that hBD3 does not inhibit endotoxin binding in a Limulus assay 22 and we confirmed this finding (Supporting Information) to demonstrate similar endotoxin Cobimetinib activity in the presence and absence of hBD3. However, the Limulus assay is not a direct measure of LPS-hBD3 binding; so we also investigated hBD3 effects after LPS stimulation of cells. Figure 2A shows that TNF-α levels were significantly reduced even when hBD3 was added to Mϕ 1 h after LPS. This suggests that even if hBD3 binds LPS to some

extent, most of the hBD3 inhibitory effect is occurring downstream of TLR4 activation by LPS. Further evidence that hBD3 is endowed with general anti-inflammatory properties is shown in Fig. 2B. Stimulation with IFN-γ and CD40L results in Mϕ activation and increased TNF-α, but here we show that hBD3 very inhibited this pro-inflammatory cytokine response in mouse BMDM. This effect was also

evident in C3H/HeJ Mϕ, which lack functional TLR4, demonstrating that hBD3 is not simply inhibiting stimulation by endotoxin contamination. The anti-inflammatory effect was not evident when cells were exposed to PAM3CSK4 a TLR1/2 agonist (Fig. 2C). This suggests that hBD3 has an effect on signalling molecules that are used by TLR4 and CD40 but not TLR1/2. This differs from LL-37, which has been shown to inhibit pro-inflammatory responses via both TLR4 and TLR1/2. 16. As TLR4 and TLR1/2 signalling both involve MyD88 it is possible that hBD3 is affecting components of the non-MyD88 pathway (such as TRAM and TRIF) downstream of TLR4. Next, we wished to see whether hBD3 could reduce the accumulation of TNF-α in mice following exposure to LPS. We injected 16 mg/kg LPS into male Balb/c mice with and without 10 μg of hBD3 and measured serum TNF-α levels 1 h later. We found that the group injected with hBD3 and LPS had significantly reduced levels of TNF-α compared with mice receiving LPS alone (Fig. 2D). This result demonstrates that hBD3 inhibits LPS-stimulated TNF-α production in vivo as well as in vitro. The extent of inhibition afforded by hBD3 was comparable to that conferred by 1 μg IL-10, which protects mice from endotoxic shock 23, so hBD3 may provide similar protection. hBD3 is a promiscuous ligand which interacts with CCR6 and another unknown Mϕ receptor 14, 24.

It has been suggested that apoptosis of infected macrophages is one way in which the host deals with intracellular pathogens and that M. tuberculosis can inhibit this process. To assess the relevance of this process for

human disease, we compared the expression of multiple genes involved in the activation of the extrinsic (“death receptor initiated”) pathway of apoptosis see more in 29 tuberculosis patients, 70 tuberculosis contacts and 27 community controls from Ethiopia. We found that there is a strong upregulation of genes for factors that promote apoptosis in PBMC from individuals with active disease, including TNF-α and its receptors, Fas and FasL and pro-Caspase 8. The anti-apoptotic factor FLIP, however, was also upregulated. A possible explanation for this dichotomy was given by fractionation of PBMC using CD14, which suggests that macrophage/monocytes may regulate several key molecules differently from non-monocytic cells (especially TNF-α and its receptors, a finding confirmed by protein ELISA) potentially reducing the sensitivity to apoptotic death of monocyte/macrophages – the primary host cell for M. tuberculosis. This may represent an important survival strategy for the pathogen. Despite vaccination and drug treatment campaigns, tuberculosis (TB) causes an estimated 8–9 million new cases and mortality of 2–3 million deaths annually 1. The TB epidemic is largely

confined to developing countries, and is particularly serious in Sub-Saharan Africa 2, where it is fanned by the HIV epidemic. Despite the FG-4592 nmr high mortality, most infected people do not immediately develop active disease, but become latently infected – though they may later reactivate their disease, if they become immunocompromised 3. It is thought that perhaps as much

as a third of the world’s population is latently infected, 4 complicating control Forskolin in vivo efforts by providing a reservoir from which new cases continually arise. Understanding immunity to Mycobacterium tuberculosis, so that more effective vaccines can be developed, is thus an international priority. The response to infection with M. tuberculosis is characterized by a strong inflammatory cell-mediated immune response, with elevated expression of both TNF-α 5–7 and IFN-γ 8–10. These two cytokines are essential for controlling mycobacterial infections 11–13 but in most cases, M. tuberculosis survives to establish a latent infection – which can rapidly reactivate if TNF-α production is blocked 14. The precise mechanisms involved in this process are still only poorly known. We and others have previously shown that a bias towards IL-4 expression is associated with elevated risk of disease 15 while a bias towards the IL-4 antagonist IL-4δ2, or towards IFN-γ, is associated with reduced pathology, a better prognosis after infection, recovery after treatment and with the ability to maintain the infection in a latent state 16–19. Thus, the immune response to M.

Although lyn–/–IL-21–/– mice lacked anti-DNA IgG, they still developed GN. The remaining IgG antibodies specific for non-DNA self-Ags have pathogenic potential since they recognize dissociated glomerular basement membrane and RNA-containing Ags. Indeed, IgG deposits were present in four of four lyn–/–IL-21–/– kidneys examined. Inflammation initiated by these non-DNA IgG autoantibodies could then be amplified by positive feedback loops between cytokine-producing T cells and CD11b+Gr1+CD11c− myeloid cells in the periphery [49, 50] and by elevated CD11b+

and CD8+ cells in the kidney, none of which are significantly altered by IL-21-deficiency. We find that the majority of splenic IL-21 mRNA is produced by CD4+ T cells in an IL-6-dependent manner in both WT and lyn–/– mice, consistent with previous reports [15-17, CH5424802 in vivo 39], IL-6 is required for expansion of Tfh cells and/or their expression of IL-21 upon chronic, but not acute, lymphocytic choriomeningitis

virus infection [56, 57]. These observations suggest that IL-6 maintains steady-state levels of IL-21 expression by T cells basally and during chronic infection or autoimmunity, while IL-6-independent events can induce IL-21 selleck chemicals during acute responses to certain pathogens or Ags. Kidney damage in lyn–/– mice is abrogated by deficiency of IL-6, but not IL-21 [11, 12]. Thus, IL-6 has both IL-21-dependent and -independent functions in the autoimmune phenotype of lyn–/– animals. There are several mechanisms by which IL-6 could drive MycoClean Mycoplasma Removal Kit the latter events. IL-6 promotes Th17-cell development and inhibits Treg-cell activity [58]. We observed a slight increase in Th17 cells among CD4+ T cells in lyn–/– mice (WT 0.34 ± 0.04%, n = 5 versus lyn–/– 1.25 ± 1.09%, n = 4), although this was not significant. Treg cells are present in lyn–/– mice but fail to suppress disease [53]. IL-6-deficiency also promotes myelopoiesis [59] and likely contributes to the increase in myeloid cells and their role in proinflammatory feedback loops in lyn–/– mice [12, 49, 50]. Finally, IL-6 acts on endothelial cells to alter

homing of leukocytes to sites of inflammation [60]. This may contribute to kidney damage in lyn–/– mice. Disruption of IL-21 signaling also prevents IgG autoantibody production and reduces ICOS+CXCR5− T cells in BXSB.Yaa [31] and MRL.lpr mice [33, 34]. However, a more profound effect on other aspects of the autoimmune phenotype was observed in BXSB.Yaa and MRL.lpr mice lacking the IL-21R than was seen in lyn–/–IL-21–/– mice [31, 34] In contrast, IgG autoantibody production is independent of IL-21 in Roquinsan/san mice [46], despite increased Tfh cells and IL-21 overexpression. This varying dependence of autoimmune phenotypes on IL-21 signaling may be explained by different disease mechanisms in each model.

IL-17A level was significantly higher in patients with MS; whereas no statistically significant changes in glutamate concentrations were found. There was a direct correlation between IL-17A and glutamate levels; IL-17A levels were also associated with the neutrophil expansion in CSF and blood–brain barrier disruption. However, IL-17A level and the number

of neutrophils tended to fall with disease duration. The results suggest that Th17 cells might enhance and use glutamate excitotoxicity as an effector mechanism in the MS pathogenesis. Furthermore, Th17 immune response, as well as neutrophils, could be more important for MS onset rather than further disease development and progression, what could explain why some MS clinical trials, targeting Th17 cells in the later stage of the disease, failed to provide any clinical benefit. “
“The pathogenic isoform (PrPSc) of the host-encoded normal NVP-AUY922 price cellular prion protein (PrPC) is believed to be the infectious agent of transmissible spongiform encephalopathies. Spontaneous conversion of α-helix-rich recombinant PrP into the PrPSc-like β-sheet-rich form or aggregation of cytosolic PrP has been found to be accelerated under reducing conditions. However, the effect of reducing conditions

on PrPSc-mediated conversion of PrPC into PrPSc has remained unknown. In this study, the effect of reducing conditions on the binding of bacterial recombinant mouse PrP (MoPrP) with PrPSc and the conversion of MoPrP ABC294640 research buy into proteinase K-resistant PrP (PrPres) using a cell-free conversion assay was investigated. High concentrations of dithiothreitol did not inhibit either the binding or conversion reactions of PrPSc from five prion strains. Indeed, dithiothreitol significantly accelerated mouse-adapted BSE-seeded conversion. These data suggest that conversion of PrPSc derived from a subset of prion strains is accelerated under reducing

conditions, as has previously been shown for spontaneous conversion. Furthermore, the five prion strains Oxymatrine used could be classified into three groups according to their efficiency at binding and conversion of MoPrP and cysteine-less mutants under both reducing and nonreducing conditions. The resulting classification is similar to that derived from biological and biochemical strain-specific features. Transmissible spongiform encephalopathies are infectious and fatal neurodegenerative diseases of humans and other animals. The conversion of normal host-encoded, PK-sensitive, prion protein (PrPC) into the partially PK-resistant PrPSc pathological form represents the central event in TSE pathogenesis (1). Direct interaction between PrPC and PrPSc is crucial for formation of additional PrPSc from PrPC (2, 3). However, the molecular mechanisms involved remain poorly understood.

These sequences were submitted to GenBank and were assigned the accession numbers HM773966–HM775073. One hundred and sixty-two IgG1 sequences were also amplified from Australian samples. A number of VDJ sequences were found that aligned to a recently identified germline IGHV3 gene (HM855939). The IGHV3-NL1*01 gene was seen in seven VDJ rearrangements (accession numbers HM773984, HM774108, HM774124, HM774201, HM774302, HM774729, and HM774738). One of these

is an IgG3 sequence (HM774124) that contains no somatic point mutations. Alignments were also seen to 12 other recently identified IGHV allelic variants, including IGHV1-8*02 (HM855457), IGHV1-18*03 (HM855463), IGHV3-7*03 check details (HM855666), IGHV3-9*02 (HM855577), IGHV3-11*06 (HM855329), IGHV3-21*03 (HM855323), IGHV3-21*04 (HM855688), IGHV3-33*06 (HM855436), IGHV3-48*04 (HM855336), IGHV3-53*04 (HM855453), IGHV4-59*11 (HM855471) and IGHV7-4-1*04 (HM855485).

In total, alignments were seen to 91 different IGHV genes and allelic variants. Despite the use of primers specific for the Talazoparib VH1, VH3 and VH4 gene families, many sequences were also amplified that utilized the IGHV5 family genes. In fact, the IGHV5 family genes as well as IGHV1-69 alleles were over-represented in all data sets, when compared with previously reported rearrangement frequencies [21]. Analysis of the VDJ junctions showed the mean CDR3 lengths of PNG IgG sequences to vary between 14.9 (IgG2) and 16.6 amino acids (IgG3), while the IgE sequences had a mean length of 15.4. These differences were not statistically www.selleck.co.jp/products/Neratinib(HKI-272).html significant. Within the junctions, all previously reported functional IGHD genes were observed. Alignments were also seen to one or more allele of each IGHJ gene, including both IGHJ3*01 and IGHJ3*02. IGHJ3*01 was originally reported as part of a haplotype that includes IGHJ4*01 and IGHJ5*01. In an earlier bioinformatic study of VDJ rearrangements, we failed to find convincing evidence for the existence of these three alleles [24]. The alignments seen in this study confirm the existence of IGHJ3*01, although no convincing alignments were observed to IGHJ4*01 or IGHJ5*01.

In the PNG data sets, 64 sets of clonally related sequences were seen, involving a total of 175 sequences. Forty-four sets contained two sequences, 12 sets contained 3 sequences, 3 sets contained 4 sequences, 2 sets contained 5 sequences and 3 additional sets contained 6, 7 and 16 sequences, respectively. Seven sets contained clonally related sequences from different isotypes, including three sets of mixed IgG1/IgG2 sequences, three set of IgG1/IgG4 sequences and one set of IgG1/IgE sequences. Clonally related sequences were particularly common amongst the IgG4 sequences. Of the 154 IgG4 sequences, 55 (35.7%) sequences were related to other IgG4 or IgG1 sequences. In contrast, only 69 of the 482 IgG1 sequences, 23 of the 288 IgG2, 16 of the 59 IgG3 and 12 of the 125 IgE sequences were members of clonally related sets.

05). In contrast, both ligands increased the VEGF levels (Fig. 3D). Previous studies have suggested high throughput screening assay the possible involvement of Gal-3 in diverse physiological and pathological processes, including pre-mRNA splicing, neoplastic transformation and immune response [18]. Gal-3 is also reported to play a negative role in T-cell activation, a process that requires clustering of a threshold number of T-cell receptor at the site of antigen presentation [19, 20]. Based on these early findings, we investigated the potential effect of Gal-3 gene silencing in MSC on T-cell proliferation to alloantigens. To identify

effective siRNA against Gal-3, we visually examined the sequence of Gal-3 mRNA and selected 3 targeting sites. The silencing potency of the designed siRNA was tested in freshly isolated human monocytes (Fig. 4A). All the 3 siRNA inhibited Gal-3 expression with siRNA-3 being the most effective. At a concentration of 2 μg, the silencing efficiency was around 99% when compared to control cells. Having demonstrated that siRNA-3 is effective in human monocytes, next we assessed its silencing potency in MSC (Fig. 4B and C). The designed siRNA resulted in nearly 94% (±3%) reduction in intracellular protein levels, and around 95% (±4%) reduction in the secreted protein when compared to cells transfected with control siRNA. In contrast, depletion of Gal-3 has no

significant selleck Vildagliptin effect on either β actin or VEGF expression, thus confirming the specificity of the designed siRNA-3. To uncover the potential effects of Gal-3 knockdown on MSC function, we asked whether MSC-expressing Gal-3 could have an effect on the proliferation of lymphocytes in response to alloantigens. To this end, we first determined the cell concentration that gave a significant inhibition and found that suppression can be achieved after the addition of approximately 10–50 000 MSC to mixed lymphocyte cultures. Second, we tested lymphocyte response in the presence of 30 000 allogeneic MSC that have been transfected with either siRNA-3 against Gal-3

or control siRNA. In these experiments, peripheral blood mononuclear cells from donor 1 (PBMC1) were incubated with PBMC from a responder donor 2 (PBMC2) in the absence or presence of irradiated “third-party” MSC. In contrast to Gal-3 expressing MSC, knockdown of Gal-3 resulted in less immunosuppressive effect on T-cell proliferation (Fig. 4D, P < 0.05, as a representative example). In addition to the expression of certain TLR, this study shows that MSC also express NOD-1. Unlike TLR, NLR consist of soluble proteins that survey the cytoplasm for signs that advertise the presence of intracellular invaders [15]. By screening the expression profiles in response to NOD-1 and TLR-2 synthetic ligands, we have identified a set of genes that were altered subsequent to overnight activation of MSC.

9 and 7.0 pg mL−1, respectively. Secretions of IFN-γ and IL-10 in response to a given antigen were considered positive when absolute concentrations were ≥100 and ≥29 pg mL−1, respectively, and E/C was ≥2 (Brock et al., 2004; Moura et al., 2004; Al-Attiyah & Mustafa, 2008). A positive response for both cytokines was considered strong

at ≥60%, moderate at 40% to <60% and weak at <40% (Mustafa, 2009a, b). The ratios of IFN-γ : IL-10 were calculated to determine Th1 vs. anti-inflammatory biases in response to Con A, complex mycobacterial antigens and peptides of RD1 and RD15. The ratios of ≥2 were considered to be Th1, <0.5 to be anti-inflammatory and 0.5 to <2 to be neither Th1 nor anti-inflammatory. Moreover, Th1 responses were considered strong, moderate and weak with IFN-γ : IL-10 ratios of >20, 5–20 and 2 to <5, respectively. The antigen-induced cell proliferation and IFN-γ secretion results click here with Con A, complex

mycobacterial antigens and peptide pools were statistically analyzed for significant differences between TB patients and healthy subjects using the nonparametric Mann–Whitney U-test for two independent samples. P-values of <0.05 were considered significant. In lymphocyte proliferation assays, Con A and the complex mycobacterial antigens were strong stimulators of PBMC from TB patients and healthy subjects, as indicated by high percentages of positive responders (83–100%) (Fig. 1a and Erlotinib molecular weight b). Furthermore, the proliferation of PBMC

from TB patients was strong in response to RD1 peptide pool (70% positive responders) and weak in response to peptide pools of RD15 and all of its ORFs (<40% positive responders) (Fig. 1c). In healthy subjects, the RD1 peptide pool induced moderate responses (47% positive responders), whereas the peptide pool of RD15 and 1502 induced strong responses (70% and 63% positive responders, respectively), and RD1501, RD1504 and RD1505 induce moderate responses (40%, 43% and 43% positive responders, respectively) (Fig. 1d). Peptide pools of other ORFs of RD15 induced weak proliferation of PBMC (<40% positive responders) (Fig. 1d). Statistical analysis of the results showed that positive responses induced by RD15 and RD1502 were significantly higher (P<0.05) in healthy L-gulonolactone oxidase subjects than in TB patients (Fig. 1c and d). To further determine the secretion of Th1 and anti-inflammatory cytokines and their ratios in response to complex mycobacterial antigens and peptides of RD1 and RD15, we studied secretion of Th1 cytokine IFN-γ and the anti-inflammatory cytokine IL-10 with PBMC from 20 TB patients and 12 healthy subjects using FlowCytomix assays. The results showed that PBMC from both TB patients and healthy subjects secreted high concentrations of IFN-γ (median values=6727–10 986 pg mL−1) with strong responses to complex mycobacterial antigens (positive responders =92–100%) (Fig. 2a and b).

837. On behalf of the British Neuropathological Society, the editorial team and our publishers, Wiley-Blackwell, I would like to thank Dr Wharton for all of his hard work leading to these achievements. We both appreciate the vital role that the editorial team and reviewers have played in this success and extend our gratitude to all those who have contributed to these activities. The constant professional support of our publishers, https://www.selleckchem.com/products/BIBW2992.html Wiley-Blackwell; in particular, Ms Elizabeth Whelan and her team, has been invaluable. Neuropathology and Applied Neurobiology, the Journal of the British Neuropathological Society, was established in 1975, 25 years after

the founding of the Society, under the editorship of Professor John Cavanagh who served in this position until 1989. The Journal was subsequently under the energetic leadership of Professors Roy Weller and James Lowe who have

continued to play an active part in recent years. The influence and work of Professor Cavanagh has been honoured by the Society with the foundation of the Cavanagh Prize, awarded every two years to a young neuroscientist who has made a significant contribution to the field of neuropathology. In his opening editorial Professor Cavanagh commented that the discussions of the Society ‘are in the forum of the world’. I believe that this message remains as important today as it was 38 years ago; that the goal of Neuropathology and Applied Neurobiology is to further our understanding of neuropathology see more and underlying disease mechanisms by publishing high quality scientific research 4-Aminobutyrate aminotransferase and to be in the forefront of scientific discussion in this field. Neuropathology and Applied Neurobiology plays an important role in the British Neuropathological Society, of which I have been an active member for many years. I look forward to working with the President, Professor Seth Love, and his successors to maintain the mutual

support between the Society and the Journal. Together we aim to continue the approach of sponsoring lectures at meetings including the International Society of Neuropathology and the European Confederation of Neuropathological Societies, to promote neuropathology on the international stage. Looking forward I will continue to develop the international profile of Neuropathology and Applied Neurobiology. The readily available measure of the impact factor is clearly important for all authors and journals but I believe that there are other markers of quality. Service to our authors and adherence to ethical standards in publishing should be paramount. For authors it is important to have an efficient and fair review process with rapid indexing and availability on-line after acceptance. I will work with the editorial team and publishers to facilitate this.

Three of the five ‘classical’ HIES patients

had known STAT3 mutations (R382W twice and V463del) [5] (Table 1). Two of the patients with ‘classical’ HIES had no STAT3 mutation. To investigate the immunological functional properties Roxadustat with respect to Th17 responses in HIES patients with different mutations, PBMC from healthy volunteers, ‘classical’ HIES patients and three members from a HIES family with ‘variant’ HIES were assessed for the capacity to mount IL-17 responses. We have developed a new methodology of Th17 generation using human PBMC stimulated with whole microbial stimuli relevant for HIES: S. aureus and C. albicans[18]. HIES patients had a defective response to C. albicans, although IL-17 was measurable in all patients (Fig. 2a). Interestingly, IL-17 production was completely absent in PBMC stimulated with S. aureus in all ‘classical’ HIES patients (Fig. 2b). In contrast, PBMC isolated from the variant HIES patients, bearing the STAT3 mutations in the linker domain, were able to produce IL-17 in response to S. aureus, albeit at lower concentrations when compared to healthy volunteers (Fig. 2b and c). IFN-γ production was distorted in HIES patients when compared to healthy controls, while IL-10 was found to be elevated in HIES patients when stimulated with

both S. aureus and C. albicans. The in vitro stimulations described above suggest that HIES patients have a significant defect in the generation of Th17 cells. This was Hydroxychloroquine in vitro indeed the case for the patients with ‘classical’ HIES, either bearing STAT3 mutations or not (Fig. 3). Surprisingly, when the familial variant HIES patients were challenged with disease-related microorganisms, they showed a clear induction

of single IL-17-positive and IL-17/IFN-γ-positive CD4+ cells compared to normal controls (Fig. 3). IL-6 augmented IL-17 production induced by Immune system C. albicans and S. aureus in cells isolated from healthy controls (Fig. 4a). No effect was apparent in the HIES patients, independently of the type of STA3 mutation. In contrast to IL-6, IL-10 reduced the amount of IL-17, and this effect was observed both in healthy controls and HIES patients (Fig. 4b). Mutations in the SH2 and DNA-binding domain of STAT3 have been reported to be the cause of disease in a large proportion of HIES patients [4]. These mutations function as dominant-negative mutations [4] and result in a defective Th17 response in these patients [9,10], explaining many of the clinical features of HIES. In the present study we confirm, on one hand, the relationship between HIES and defective Th17 responses; on the other hand, we also refine this notion to include the relationships between the type of STAT3 mutation, immunological response to relevant microbial stimulation and clinical phenotype of the patients.

This study aimed to clarify the effect of sodium restriction on prolonging the duration between the time when eGFR is 15 mL/min/1.73 m2 check details to hemodialysis (HD) induction (G5 spans). Methods: Seventy-seven type 2 DKD patients (61 men and 16 women, mean age 58.6 ± 11.2 years) were recruited. All patients underwent frequent nutritional therapy and 24-h urine collection. Sodium intake was calculated using the 24-h urine collection. Patients

were divided into the following 2 groups: adequate group (AG: n = 39) defined as patients with sodium intake < 8.0 g/day, and over-intake group (OG: n = 32) defined as sodium intake ≧ 8.0 g/day. We retrospectively evaluated the G5 span between the 2 groups. Results: The SB203580 price glycated hemoglobin value was 6.4 ± 1.8% when eGFR was firstly 15 mL/min/1.73 m2. In all patients, the G5 span was 556 ± 372 days, and the sodium intake was 7.9 ± 3.2 g/day. The G5 was significantly

longer in AG than in OG (660 ± 403 days vs. 487 ± 314 days, p < 0.05). Conclusion: Sodium restriction ameliorates the progression of renal dysfunction in type 2 advanced DKD patients (CKD stage G5). RAVI RAMA1,2, RAVI RAJALAKSHMI1,2, KURIEN ABRAHAM1,2, NAIR SANJEEV1,2, YUVARAJ ANAND1,2, ABRAHAM GEORGI1,2, RAVICHANDRAN SANGEETHA2, PANDIAN DEVI1,2 1Madras Medical Mission; 2Tamilnad Kidney Research Foundation Introduction: The current scenario of global burden of diseases comprise of a triple burden of diseases of which non communicable diseases form a huge proportion. Among the non communicable diseases, chronic kidney disease has emerged a major threat in terms of complications, accessibility and availability of treatment, especially in developing countries like India. There are a few studies done on prevalence of kidney disease and our programme targets early detection of kidney disease in the form of awareness and screening programmes directed at different segments of the society. Methods: The awareness programme

comprises of powerpoint presentation on basics of kidney functions and symptoms for early detection of kidney disease. The screening programme consists of brief history of medical illness, followed by measurement Clomifene of body mass index and blood pressure and urine examination to look for proteinuria. Results: We have so far conducted a total of 447 programmes of which 93.5% of the programmes were targeted to urban areas and we covered 79.2% of students through our awareness programmes. Our programme identified prehypertension in 38.7% of the population screened and 24.% were identified with proteinuria. Individuals who were above 45 years of age, and those with proteinuria were found to be significantly associated with abnormal serum creatinine and eGFR.