One other nutrient that has generated heaps of literature, including many controversies in rheumatology is vitamin D. Emerging evidence and consensus regarding its function have established it as a popular and economic therapeutic agent prescribed by many physicians and rheumatologists for a spectrum of disorders, but not without criticism. Careful and critical appraisal of such confusing and contradicting literature is needed to reach any cautious conclusion. There are also differing views on the cut-off value of vitamin D to label insufficiency and deficiency, but most agree on a value that keeps parathhormone (PTH) levels in the normal range. Keeping

Ku-0059436 datasheet this in mind, 25(OH)D levels more than 30 ng/mL (75 nmol/L) is considered normal, levels between 20 and 30 ng/mL (50–75 nmol/L) is defined as insufficiency and level less than 20 ng/mL (50 nmol/L) is called deficiency.[1] Vitamin D insufficiency and deficiency are global phenomena and sun exposure alone may not be the sole determinant for this. In spite of good sun exposure, vitamin D deficiency is prevalent from sub-Saharan Africa to south Asia and affects half the population

in this region, similar to that in Western countries with temperate climates.[2, 3] The fascinating molecule of vitamin D belongs to the class of secosteroids. It is different from other steroids by unfolding of two of its four rings. Its role as an anti-inflammatory, immunomodulatory and antineoplastic agent, as well as its Venetoclax solubility dmso role in preventing cardiovascular BCKDHA morbidity and mortality, are well known. It interacts with a large array of molecules, including vitamin D receptor (VDR), and much of it depends on vitamin D binding proteins. The role of VDR polymorphisms in the pathogenesis of autoimmune diseases has also been extensively studied.[4] As expected of a steroid, vitamin D’s anti-inflammatory actions are mediated by down regulation of dendritic cells, Th1 cells and B cells, many pro-inflammatory cytokines, and inhibition of micro-RNAs like MiRNA-155, and by inducing apoptosis.[5] Vitamin D is also capable of neutralizing interleukin (IL)-17A and IL-22 which are not achieved even by tumor necrosis factor (TNF) blockade; this action has far-reaching implications

in many systemic autoimmune diseases.[6] There are now studies showing enriched gene expression of vitamin D response elements (VDRE) in non-major histocompatibility loci associated with rheumatoid arthritis (RA) as well as modest association of variants of loci controlling vitamin D levels with RA.[7] These findings strongly support the theory that vitamin D plays an important role in the pathogenesis of RA. Prevalence of low vitamin D states in RA is reported from most populations,[8] including publications associating low vitamin D state with disease activity.[9, 10] Indeed, a recent meta-analysis of 215 757 participants proves these points beyond doubt.[11] Relatively fewer studies found no correlation between disease activity and low vitamin D state in RA.

These phenotypes differ from those observed in A. oryzae, as autophagy was slightly induced under starvation conditions in the ΔAoatg13 mutant, suggesting that AoAtg13 functions

as an amplifier or regulator of the signal from the A. oryzae Atg1 orthologue, resulting in a higher level of autophagy induction. Further studies are necessary to determine the first step of autophagy in A. oryzae; for example, by disrupting or overexpressing the A. oryzae ATG1 homologue. In S. cerevisiae, the delivery of Atg8 to PAS does not occur in Δatg4 cells (Suzuki et al., 2001), which indicates that the localization of Atg8 to PAS requires the prior lipidation of Atg8, allowing the PE conjugated form (Atg8-PE) to associate with PAS. The phenotype ABT-199 chemical structure of the ΔAoatg4 mutant appeared similar to that of the Aoatg8-deletion mutant, indicating a defect in autophagy. In the DA4EA8 strain, EGFP–AoAtg8 predominantly localized to dot-like structures, which seemed to be the PAS, although larger dot-like structures were also observed. These results

suggest that the localization of AoAtg8 might be independent of PE, and may be mediated by interaction with AoAtg proteins other than AoAtg4. We IBET762 speculate that the lipidation of AoAtg8 is required for the elongation of isolation membranes and formation of autophagosomes, and the larger dot-like structures was a result of the aggregation of EGFP–AoAtg8 in the ΔAoatg4 mutant. In the DA15EA8 strain, PAS-like structures, autophagosomes and autophagic bodies were observed, in addition to the Glutathione peroxidase accumulation of autophagic bodies in the lumen of vacuoles. These observations indicate that AoAtg15 is required for degradation of autophagic bodies, but not for the stages of autophagy involving dynamic membrane rearrangements for the uptake of intracellular components into vacuoles. Notably, the ΔAoatg15 strain displayed a more severe developmentally impaired phenotype. Colonies of the strain were significantly flatter

than the other gene-deletion mutants (Fig. 4). This phenotype might be due to defects in the lysis of lipid vesicles in vacuoles, including not only autophagic bodies, but also other lipid vesicles, such as those arising from the cytoplasm-to-vacuole (Cvt) pathway (Cvt bodies) (Klionsky & Ohsumi, 1999) and multivesicular body (MVB) pathway (MVB vesicles) (Epple et al., 2003), which have been described in S. cerevisiae. The Cvt pathway is morphologically similar to autophagy, and numerous components of this pathway overlap with Atg proteins (Harding et al., 1996; Scott et al., 1996; Wang & Klionsky, 2003). The MVB pathway also serves to transport Atg15 to vacuoles, and the breakdown of intravacuolar MVB vesicles is impaired in Δatg15 cells (Epple et al., 2003).

72; 95% CI Antidiabetic Compound Library 0.26, 1.99), CD4 T-cell count

was positively associated with incident HTN (HR 1.15 per 100 cells/μL; 95% CI 1.03, 1.28). Among physically active HIV-infected men, exposure to ARVs was negatively associated with incident HTN (HR 0.15; 95% CI 0.03, 0.78). HIV infection was not associated with incident HTN in older men or women. This study provides additional evidence supporting a causal relationship between immune function and incident HTN, which warrants further study. “
“The aim of the study was to assess the significance of low-level viraemia (LLV) and the timing of treatment change in low/middle-income country (L/MIC) compared with high-income country (HIC) settings. Patients with virological control following commencement of combination antiretroviral therapy (cART) were included in the study. LLV was defined as undetectable viral load (<50 HIV-1 RNA copies/mL) followed by confirmed detectable viral load < 1000 copies/mL. Virological failure was defined as viral load > 1000 copies/mL. Kaplan−Meier plots of time to virological failure by prior LLV and income category were generated. Regimen changes in

the setting of LLV were compared between sites. Sensitivity analysis of rates of LLV and virological failure by person-years and number of tests was conducted for differing LDK378 price definitions of LLV and virological failure. A total of 1748 patients from HICs and 823 patients from L/MICs were included in the study. One hundred and ninety-six (11.2%) HIC participants ASK1 and 36 (4.4%) L/MIC participants experienced at least one episode of LLV. Of the patients who underwent regimen switch in HIC settings, the majority changed from a nucleoside reverse transcriptase inhibitor (NRTI)/protease inhibitor (PI) regimen to an NRTI/nonnucleoside reverse transcriptase inhibitor (NNRTI) regimen (26.8%). Very few switches were made in L/MIC settings. Rates of LLV were significantly higher for HICs compared with L/MICs per 1000 person-years (28.6 and 9.9 per 1000 person-years,

respectively), but not in terms of the number of tests (9.4 and 7.2 per 1000 tests, respectively). Rates of virological failure per test were significantly higher for L/MICs compared with HICs (30.7 vs. 19.6 per 1000 tests, respectively; P < 0.001). LLV was a significant predictor of virological failure at 2 years in L/MICs [0.25; 95% confidence interval (CI) 0.11–0.50; P = 0.043] but not in HICs (0.13; 95% CI 0.08-0.22; P = 0.523). LLV is weakly predictive of virological failure at 2 years in L/MICs but not in HICs. This suggests that interventions targeted at subjects with LLV in L/MICs would help to improve treatment outcomes. "
“For the last 10 years there has been an epidemic of hepatitis C virus (HCV) infection in men who have sex with men (MSM) in Europe, North America and Australia. The majority of those infected are also HIV-positive and it is unclear to what extent HIV-negative MSM are also at increased risk of infection with HCV.

Over 300 TCSs are known to date regulating various activities such as metabolism, respiration, stress response and chemotaxis. Some TCSs have

been shown to be involved in virulence of some bacteria, such as the BvgA/S system in Bordetella pertussis and Bordetella bronchiseptica (Cotter & Miller, 1997; Williams & Cotter, 2007) and the OmpR–EnvZ system in Shigella flexneri (Bernardini et al., 1990). In this study, we carried out blast searches against the M. haemolytica A1 genome to identify its TCS(s). Out of the five putative TCSs, the NarQ/P system was chosen for further investigation. Mannheimia Trichostatin A haemolytica A1 strain SH1217 was obtained from Dr Sarah Highlander, Baylor College of Medicine. Escherichia coli strain DH5 is from our laboratory collection.

Mannheimia haemolytica A1 was cultured in brain heart infusion broth (BHIB) at 37 °C, supplemented with chloramphenicol (5 mg L−1), ampicillin (25 mg L−1), or streptomycin (100 mg L−1) where necessary. To examine the response to the addition of nitrate, BHIB was supplemented with 2.5 mM NaNO3. This concentration was chosen through a titration experiment in search for the minimum concentration selleck chemical of NaNO3 to elicit a response in SH1217 (data not shown). When necessary, M. haemolytica was grown under a semi-anaerobic condition by growing the liquid cultures in a sealed container without shaking (modified from Browning et al., 2006). Escherichia coli cultures were grown in Luria–Bertani + thymidine (50 mg L−1) broth at 37 °C, supplemented with ampicillin (100 mg L−1) where necessary. Multiple bioinformatics tools were used to search for putative TCS homologs in the M. haemolytica

A1 genome (accession number: AASA00000000). A consensus sequence of the RR regulatory domain (GAADY) was used to perform a blastp search against the M. haemolytica A1 genome sequence at Baylor College of Medicine (http://www.hgsc.bcm.tmc.edu). The nucleotide sequences of the contigs that contain significant hits were retrieved and analyzed with the ‘sequence analysis’ software (Informagen Biotechnology Information Resource; http://www.informagen.com/SA/) to identify the ORFs containing the putative RRs. Amino acid sequences Aspartate of the putative RRs were then analyzed by a blastp search against the NCBI sequence database. The putative RR homologs were used to perform blastp against the M. haemolytica A1 genome to search for more RR homologs. Multiple rounds of the analyses were performed until no more additional hits were obtained. After the putative RR homologs were identified, consensus sequences for their cognate HKs were retrieved from the NCBI database. These HK sequences were used to perform blastp against the M. haemolytica A1 genome. The search results were analyzed as above. Again, multiple rounds of searches and analyses were performed until no new hits were obtained.

Over 300 TCSs are known to date regulating various activities such as metabolism, respiration, stress response and chemotaxis. Some TCSs have

been shown to be involved in virulence of some bacteria, such as the BvgA/S system in Bordetella pertussis and Bordetella bronchiseptica (Cotter & Miller, 1997; Williams & Cotter, 2007) and the OmpR–EnvZ system in Shigella flexneri (Bernardini et al., 1990). In this study, we carried out blast searches against the M. haemolytica A1 genome to identify its TCS(s). Out of the five putative TCSs, the NarQ/P system was chosen for further investigation. Mannheimia VX 809 haemolytica A1 strain SH1217 was obtained from Dr Sarah Highlander, Baylor College of Medicine. Escherichia coli strain DH5 is from our laboratory collection.

Mannheimia haemolytica A1 was cultured in brain heart infusion broth (BHIB) at 37 °C, supplemented with chloramphenicol (5 mg L−1), ampicillin (25 mg L−1), or streptomycin (100 mg L−1) where necessary. To examine the response to the addition of nitrate, BHIB was supplemented with 2.5 mM NaNO3. This concentration was chosen through a titration experiment in search for the minimum concentration Epigenetics Compound Library in vitro of NaNO3 to elicit a response in SH1217 (data not shown). When necessary, M. haemolytica was grown under a semi-anaerobic condition by growing the liquid cultures in a sealed container without shaking (modified from Browning et al., 2006). Escherichia coli cultures were grown in Luria–Bertani + thymidine (50 mg L−1) broth at 37 °C, supplemented with ampicillin (100 mg L−1) where necessary. Multiple bioinformatics tools were used to search for putative TCS homologs in the M. haemolytica

A1 genome (accession number: AASA00000000). A consensus sequence of the RR regulatory domain (GAADY) was used to perform a blastp search against the M. haemolytica A1 genome sequence at Baylor College of Medicine (http://www.hgsc.bcm.tmc.edu). The nucleotide sequences of the contigs that contain significant hits were retrieved and analyzed with the ‘sequence analysis’ software (Informagen Biotechnology Information Resource; http://www.informagen.com/SA/) to identify the ORFs containing the putative RRs. Amino acid sequences Ribonucleotide reductase of the putative RRs were then analyzed by a blastp search against the NCBI sequence database. The putative RR homologs were used to perform blastp against the M. haemolytica A1 genome to search for more RR homologs. Multiple rounds of the analyses were performed until no more additional hits were obtained. After the putative RR homologs were identified, consensus sequences for their cognate HKs were retrieved from the NCBI database. These HK sequences were used to perform blastp against the M. haemolytica A1 genome. The search results were analyzed as above. Again, multiple rounds of searches and analyses were performed until no new hits were obtained.

Lastly, genetic factors may play a role. Such were also considered when a higher TD incidence rate among British travelers was found.21 Three kinds of selection bias might limit our study: Travelers consulting for pre-travel health advice might have been either somewhat hypochondriac or represent a subpopulation with special health literacy skills, as 51.3% of our customers reported a university degree. The latter would result in an underestimation of the IBS risk when compared to travelers with

a different educational background, whereas for the former higher TD rates as well as a higher rate of IBS would be expected. Actually, we found C59 wnt purchase a higher TD incidence rate when compared with the nonresponders’ TD rate, which might indicate an overestimation of our IBS incidence rate. Third, although attracting millions of visitors, some popular tourist destinations, such as Turkey, North Africa, and the Caribbean were underrepresented as travelers to those countries rarely consult for pre-travel health advice.28 Diarrhea is a risk factor for IBS whether it occurred at home or abroad. Evidence shows that an infectious agent may trigger new onset Enzalutamide solubility dmso of IBS and of other long-term sequelae,

such as, eg, reactive arthritis.29,30 Thereby, the severity and duration of IBS illness are important risk factors23; however, it remains unknown whether the type of the pathogen, the inoculum, and the time interval between diarrheal attacks play a role.31 Notably, it appears that multiple diarrheal episodes would raise the IBS risk. This might support the hypothesis of IBS being associated with increased epithelial barrier permeability and/or altered gut flora.4 The results of the sensitivity analyses validate

our risk estimates. For a more detailed subgroup analysis a different study design would be more appropriate. Such data would be needed to assess factors and syndromes associated with other low-grade inflammatory and immunological processes, such as, eg, atopy32 or antibiotic Tau-protein kinase treatment14 which were supposed to be associated with IBS. The reported threefold increased IBS risk following the experience of a recent adverse life event corresponds to the relative risk of 2.0 found previously for IBS.33 Contrary to some reports, female gender and smoking were not found to be significant independent risk factors for IBS. IBS patients are often reluctant to request thorough medical evaluation. Accordingly, most of our IBS patients managed their symptoms themselves. The consulting physicians rated the severity of IBS as “mild.” At the beginning of the symptoms the Rome III-based case definition seemed to be prone to misclassification. In about one third of our IBS cases, who had visited a physician, the medical doctors’ diagnosis did not confirm the IBS assessment to full extent because another diagnosis was found.

Limited studies on the relationship between tablet shape, Crizotinib size and the splitter model and the accuracy of splitting. In this

work, divisibility of tablets with various shapes and sizes for medicines normally split was studied using a kitchen knife and four tablet splitter models. Results demonstrated deviation in tablet fragments weight changes with tablet shape, size and splitter model. The tablets-related factors (shape and size) and the splitter model are critical parameters in splitting of tablets. Splitting of tablets into halves and quarters to obtain a suitable unit dose is frequently done using a variety of methods.1 A significant deviation in weight from the theoretical value for tablet halves and quarters on splitting using scissors, hands and one tablet splitter model.2 In this work, a kitchen knife and four tablet splitter models were tested for splitting of tablets having different shapes and sizes for medicines normally split. Tablets from furosemide 40 mg (circular shape, unscored), captopril 50 mg (square shape, bisected both sides), spirolactone 100 mg (circular shape, scored), enalpril 10 mg (heart shape,

scored) and paracetamol 500 mg (caplet, scored) were first assessed for diameter/length, thickness and hardness. From each medicine, ten randomly selected tables were individually weight using a sensitive balance, split into halves and into quarters using a kitchen knife and splitter Selumetinib models; Pillmate (P), Fortuna (F), Safe Sound (S) and Health Care (H). The weight variation for 10 intact tablets, 20 halves and 40 quarters for each medicine was calculated using United States Pharmacopoeia (USP) criteria for intact tablets. Weight loss was determined by subtracting the weight of the two tablet halves

or four quarters from the weight of intact Methocarbamol tablet. Statistical analysis of data was performed using t-test at P value less than 0.05 as significant. The average diameter/length, thickness and hardness of tablets were (8, 10, 9.6, 8 and 17.7 mm), (2, 4, 4, 4 and 5 mm) and (7, 11, 9, 10 and 8 Kp) for furosemide, captopril, spirolactone, enalpril and paracetamol. The relative standard deviation (RSD) values of weight were between 1.0–1.6, 8.4–15.2 and 17. 2–26.7% for intact tablets, halves and quarters respectively after splitting using a kitchen knife and tablet splitter models (P, F, S and H). Tablet fragments deviated in weight by more than 15% from the theoretical values were 10, 20, 37, 22 and 4% for halves and 35, 48, 53, 58 and 35% for quarters. The associated tablet weight loss ranges were 0.5–1, 1–7, 0–5, 0–3 and 0–2% after halving and 2–3, 2–9, 1–12, 1–5 and 1–4% after splitting into quarters.

Limited studies on the relationship between tablet shape, CAL-101 price size and the splitter model and the accuracy of splitting. In this

work, divisibility of tablets with various shapes and sizes for medicines normally split was studied using a kitchen knife and four tablet splitter models. Results demonstrated deviation in tablet fragments weight changes with tablet shape, size and splitter model. The tablets-related factors (shape and size) and the splitter model are critical parameters in splitting of tablets. Splitting of tablets into halves and quarters to obtain a suitable unit dose is frequently done using a variety of methods.1 A significant deviation in weight from the theoretical value for tablet halves and quarters on splitting using scissors, hands and one tablet splitter model.2 In this work, a kitchen knife and four tablet splitter models were tested for splitting of tablets having different shapes and sizes for medicines normally split. Tablets from furosemide 40 mg (circular shape, unscored), captopril 50 mg (square shape, bisected both sides), spirolactone 100 mg (circular shape, scored), enalpril 10 mg (heart shape,

scored) and paracetamol 500 mg (caplet, scored) were first assessed for diameter/length, thickness and hardness. From each medicine, ten randomly selected tables were individually weight using a sensitive balance, split into halves and into quarters using a kitchen knife and splitter GKT137831 nmr models; Pillmate (P), Fortuna (F), Safe Sound (S) and Health Care (H). The weight variation for 10 intact tablets, 20 halves and 40 quarters for each medicine was calculated using United States Pharmacopoeia (USP) criteria for intact tablets. Weight loss was determined by subtracting the weight of the two tablet halves

or four quarters from the weight of intact Racecadotril tablet. Statistical analysis of data was performed using t-test at P value less than 0.05 as significant. The average diameter/length, thickness and hardness of tablets were (8, 10, 9.6, 8 and 17.7 mm), (2, 4, 4, 4 and 5 mm) and (7, 11, 9, 10 and 8 Kp) for furosemide, captopril, spirolactone, enalpril and paracetamol. The relative standard deviation (RSD) values of weight were between 1.0–1.6, 8.4–15.2 and 17. 2–26.7% for intact tablets, halves and quarters respectively after splitting using a kitchen knife and tablet splitter models (P, F, S and H). Tablet fragments deviated in weight by more than 15% from the theoretical values were 10, 20, 37, 22 and 4% for halves and 35, 48, 53, 58 and 35% for quarters. The associated tablet weight loss ranges were 0.5–1, 1–7, 0–5, 0–3 and 0–2% after halving and 2–3, 2–9, 1–12, 1–5 and 1–4% after splitting into quarters.

9 A prospective observational study over a period of 10 years (1991–2000) Nivolumab order from Mumbai, western India, included 153 pregnant women with TB (133 pulmonary and 20 extrapulmonary cases).10 This study revealed that maternal TB was associated with a high incidence of LBW neonates, which was primarily attributed to fetal growth restriction. Although there was some improvement of perinatal outcomes in the latter half of the study, the problems of LBW and late fetal death remained unabated. Because of sparse literature on perinatal effects of

maternal TB, it may be worthwhile extrapolating the experience from a comparative study carried out in Mexico, which also showed increased risk of perinatal morbidity and mortality among 35 women with pulmonary or extrapulmonary TB: prematurity (RR 2.1; 95%CI 1–4.3), LBW neonates (RR 2.2; 95%CI 1.1–4.9), neonatal complications (RR 2.1; 95%CI 1.1–3.9) and perinatal death (RR 3.1; 95%CI 1.6–6).13 Approximately twofold increase

in prematurity and fetal growth restriction was responsible for most neonatal complications.13 In this study, pulmonary localization of TB and late start of treatment were two major factors which determined poor perinatal outcome Doxorubicin clinical trial in maternal TB.12,13 Furthermore, by stratified analysis, the authors inferred that anti-TB treatment early in pregnancy can reverse these complications.12 This is in contrast to a recent comparative study from Taiwan, which showed an increased risk of LBW (odds ratio [OR] 1.35; 95%CI 1.01–1.81) and SGA (OR 1.22; 95%CI 1.00–1.49) babies born to mothers who started

anti-TB drugs even before conception.22 Although several case series from developed countries reaffirmed potential perinatal dangers of maternal TB,14,21,48 the others reported satisfactory pregnancy outcomes.49–51 Pregnancy outcome among women Inositol monophosphatase 1 with TB is often influenced by poverty, which is a multidimensional phenomenon.32,52,53 In South Asian countries, poverty, hunger and undernutrition are widespread.2 There is a close link between TB and poverty.32,52 It is very important to understand the potential effects of this combination on maternal and perinatal health, especially in low-income South Asian countries, where the health-care system is relatively dysfunctional and barriers to care are substantial.27 Pervasive poverty, inequitable economic growth, political instability and widespread corruption are major roadblocks to most public health measures in the South Asian region.2,54 It is well known that nutritional status, chronic disease like TB and pregnancy events are influenced by each other.7,8,32,52 These factors are synergistically modulated by the socioeconomic factors that include education, income and occupation of couples, demographic features of home, access to quality food and health-care practices.

9 A prospective observational study over a period of 10 years (1991–2000) learn more from Mumbai, western India, included 153 pregnant women with TB (133 pulmonary and 20 extrapulmonary cases).10 This study revealed that maternal TB was associated with a high incidence of LBW neonates, which was primarily attributed to fetal growth restriction. Although there was some improvement of perinatal outcomes in the latter half of the study, the problems of LBW and late fetal death remained unabated. Because of sparse literature on perinatal effects of

maternal TB, it may be worthwhile extrapolating the experience from a comparative study carried out in Mexico, which also showed increased risk of perinatal morbidity and mortality among 35 women with pulmonary or extrapulmonary TB: prematurity (RR 2.1; 95%CI 1–4.3), LBW neonates (RR 2.2; 95%CI 1.1–4.9), neonatal complications (RR 2.1; 95%CI 1.1–3.9) and perinatal death (RR 3.1; 95%CI 1.6–6).13 Approximately twofold increase

in prematurity and fetal growth restriction was responsible for most neonatal complications.13 In this study, pulmonary localization of TB and late start of treatment were two major factors which determined poor perinatal outcome find more in maternal TB.12,13 Furthermore, by stratified analysis, the authors inferred that anti-TB treatment early in pregnancy can reverse these complications.12 This is in contrast to a recent comparative study from Taiwan, which showed an increased risk of LBW (odds ratio [OR] 1.35; 95%CI 1.01–1.81) and SGA (OR 1.22; 95%CI 1.00–1.49) babies born to mothers who started

anti-TB drugs even before conception.22 Although several case series from developed countries reaffirmed potential perinatal dangers of maternal TB,14,21,48 the others reported satisfactory pregnancy outcomes.49–51 Pregnancy outcome among women 5-Fluoracil purchase with TB is often influenced by poverty, which is a multidimensional phenomenon.32,52,53 In South Asian countries, poverty, hunger and undernutrition are widespread.2 There is a close link between TB and poverty.32,52 It is very important to understand the potential effects of this combination on maternal and perinatal health, especially in low-income South Asian countries, where the health-care system is relatively dysfunctional and barriers to care are substantial.27 Pervasive poverty, inequitable economic growth, political instability and widespread corruption are major roadblocks to most public health measures in the South Asian region.2,54 It is well known that nutritional status, chronic disease like TB and pregnancy events are influenced by each other.7,8,32,52 These factors are synergistically modulated by the socioeconomic factors that include education, income and occupation of couples, demographic features of home, access to quality food and health-care practices.