Infectious hepatitis E virus is associated with the mature sperm head.

Hepatitis E virus (HEV) is the leading cause of acute viral hepatitis worldwide. HEV associated pregnancy mortality has been reported as up to 30% in humans. Recent findings suggest HEV may elicit effects directly in the reproductive system with HEV protein found in the testis, viral RNA in semen, and viral replication occurring in placental cell types. Using a natural host model for HEV infection, pigs, we demonstrate infectious HEV within the mature spermatozoa and altered sperm viability from HEV infected pigs. HEV isolated from sperm remained infectious suggesting a potential transmission route via sexual partners. Our findings suggest that HEV should be explored as a possible sexually transmittable disease. Our findings propose that infection routes outside of oral and intravenous infection need to be considered for their potential to contribute to higher mortality in HEV infections when pregnancy is involved and in HEV disease in general.

Effects of paternal overnutrition and interventions on future generations.

In the last two decades, evidence from human and animal studies suggests that paternal obesity around the time of conception can have adverse effects on offspring health through developmental programming. This may make significant contributions to the current epidemic of obesity and related metabolic and reproductive complications like diabetes, cardiovascular disease, and subfertility/infertility. To date, changes in seminal fluid composition, sperm DNA methylation, histone composition, small non-coding RNAs, and sperm DNA damage have been proposed as potential underpinning mechanism to program offspring health. In this review, we discuss current human and rodent evidence on the impact of paternal obesity/overnutrition on offspring health, followed by the proposed mechanisms, with a focus on sperm DNA damage underpinning paternal programming. We also summarize the different intervention strategies implemented to minimize effects of paternal obesity. Upon critical review of literature, we find that obesity-induced altered sperm quality in father is linked with compromised offspring health. Paternal exercise intervention before conception has been shown to improve metabolic health. Further work to explore the mechanisms underlying benefits of paternal exercise on offspring are warranted. Conversion to healthy diets and micronutrient supplementation during pre-conception have shown some positive impacts towards minimizing the impact of paternal obesity on offspring. Pharmacological approaches e.g., metformin are also being applied. Thus, interventions in the obese father may ameliorate the potential detrimental impacts of paternal obesity on offspring.

Ameliorating high-fat diet-induced sperm and testicular oxidative damage by micronutrient-based antioxidant intervention in rats.

PURPOSE: Emerging evidence from rodent studies suggests that high-fat-diet (HFD)-induced obesity is characterized by increased oxidative damage in sperm and testis. However, interventions using micronutrient supplementation to mitigate oxidative damage in obesity have not been extensively studied. This study aimed to investigate the effect of an antioxidant-based micronutrient supplement (added folate, vitamin B6, choline, betaine, and zinc) on sperm and testicular oxidative damage in HFD-fed male Sprague Dawley rats. METHODS: Rats (3-weeks-old, 12/group) were weaned onto control (C) or HFD (H) or these diets with micronutrient supplement (CS; HS); sperm and testis were harvested at 30.5 weeks. To assess oxidative stress and antioxidant capacity in testis, levels of malondialdehyde (MDA), glutathione (GSH), folate and susceptibility index (SI) of pro-oxidative damage, mRNA expression of Nrf2, NFκB-p65, IL-6, IL-10 and TNF-α, in addition to superoxide-dismutase (SOD), catalase and glutathione-peroxidase (GPx) activities were measured. 8-hydroxy-2-deoxyguanosine (8-OHdG) were assessed in both sperm and testis. RESULTS: HFD-fed rats had significantly increased 8-OHdG content in sperm and testis, increased testicular SI, decreased testicular weight, SOD and GPx activity compared to control. Strikingly, supplementation of HFD appeared to significantly reduce 8-OHdG in sperm and testis (22% and 24.3%, respectively), reduce testicular SI and MDA content (28% and 40%, respectively), increase testicular weight (24%), SOD and GPX activity (30% and 70%, respectively) and GSH content (19%). Moreover, supplementation had significant impact to increase testicular folate content regardless of diet. Furthermore, an overall effect of supplementation to increase testicular mRNA expression of Nrf2 was observed across groups. Interestingly, testicular SI was positively correlated with sperm and testicular 8-OHdG and MDA content, suggesting a critical role of testicular antioxidant activity to combat oxidative damage in sperm and testis. CONCLUSION: Our findings suggest that antioxidant-based micronutrient supplement has the potential to interrupt HFD-induced sperm and testicular oxidative damage by improving testicular antioxidant capacity.

Biofilm and metallo beta-lactamase production among the strains of Pseudomonas aeruginosa and Acinetobacter spp. at a Tertiary Care Hospital in Kathmandu, Nepal.

INTRODUCTION: Pseudomonas aeruginosa and Acinetobacter spp. are found to be associated with biofilm and metallo-ß-lactamase production and are the common causes of serious infections mainly in hospitalized patients. So, the main aims of this study were to determine the rates of biofilm production and metallo beta-lactamase production (MBL) among the strains of Pseudomonas aeruginosa and Acinetobacter spp. isolated from hospitalized patients. METHODS: A total of 85 P. aeruginosa isolates and 50 Acinetobacter spp. isolates isolated from different clinical specimens from patients admitted to Shree Birendra Hospital, Kathmandu, Nepal from July 2013 to May 2014 were included in this study. The bacterial isolates were identified with the help of biochemical tests. Modified Kirby-Bauer disc diffusion technique was used for antimicrobial susceptibility testing. Combined disc diffusion technique was used for the detection of MBL production, while Congo red agar method and tube adherence method were used for detection of biofilm production. RESULTS: Around 16.4% of P. aeruginosa isolates and 22% of the strains of Acinetobacter spp. were metallo ß-lactamase producers. Out of 85 P. aeruginosa isolates, 23 (27.05%) were biofilm producers according to tube adherence test while, only 13 (15.29%) were biofilm producers as per Congo red agar method. Similarly, out of 50 Acinetobacter spp. 7 (14%) isolates were biofilm producers on the basis of tube adherence test, while only 5 (10%) were positive for biofilm production by Congo red agar method. Highest rates of susceptibility of P. aeruginosa as well as Acinetobacter spp. were seen toward colistin. CONCLUSION: In our study, biofilm production and metallo beta-lactamase production were observed among Pseudomonas aeruginosa and Acinetobacter spp. However, no statistically significant association could be established between biofilm production and metallo beta-lactamase production.

Thyroid dysfunction and dyslipidemia in chronic kidney disease patients.

BACKGROUND: Chronic kidney disease (CKD) is becoming a serious health problem; the number of people with impaired renal function is rapidly rising. Progression of CKD is associated with having a number of complications, including thyroid dysfunction, dyslipidemia and cardiovascular diseases. This study was conducted to investigate thyroid function and lipid profile in CKD patients. METHODS: A cross-sectional study was conducted among 360 chronic kidney disease patients at B P Koirala Institute of Health Sciences, Dharan, Nepal. Demographic features (age and sex) and medical history of diabetes mellitus, hypertension and cardiovascular diseases of each patient were noted, and blood samples (5 ml) were analyzed for serum urea, creatinine, glucose, free triiodothyronine (T3), free thyroxine (T4), thyroid stimulating hormone (TSH), total cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride. RESULTS: Thyroid dysfunction was found in 38.6 % CKD patients, the most common being subclinical hypothyroidism (27.2 %), followed by overt hypothyroidism (8.1 %) and subclinical hyperthyroidism (3.3 %). Hypercholesterolemia, low HDL cholesterol, undesirable LDL cholesterol and hypertriglyceridemia were observed in 34.4, 34.1, 35 and 36.6 % patients respectively. Stage 4 and 5 CKD patients had significantly higher risk of having thyroid dysfunction as compared to stage 3 patients. Significant risk factors for cardiovascular disease in CKD patients included presence of diabetes mellitus, hypercholesterolemia, undesirable LDL cholesterol and being in stage 4 and 5 (as compared to stage 3). CONCLUSIONS: Thyroid dysfunction, hypercholesterolemia, low HDL cholesterol, undesirable LDL cholesterol and hypertriglyceridemia are common in CKD patients. Progression of CKD is accompanied by rise in hypothyroidism and cardiovascular disease.

Anemia among school children in eastern Nepal.

Anemia is one of the most common public health problems in developing countries like Nepal. This study was done to find the prevalence of anemia among the children aged 4-13 years in eastern Nepal. A cross-sectional study was conducted in 2012 in four districts (Morang, Udayapur, Bhojpur and Ilam) of eastern Nepal to find the prevalence of anemia among the school children of eastern Nepal. Children aged 4-13 years were selected randomly from different schools of above districts and 618 venous blood samples were collected. Hemoglobin level was estimated by using cyanmethemoglobin method. The mean hemoglobin level was 12.2 ± 1.82 gm/dl. About 37.9% (n = 234) children were found anemic. Anemia prevalence was 42.4% (n = 78), 31.6% (n = 60), 45.3% (n = 48) and 34.8% (n = 48) among school children of Morang, Udayapur, Bhojpur and Ilam district, respectively. The study finds anemia as a significant health problem among the school children of eastern Nepal.

Development of fatty liver disease model using high cholesterol and low choline diet in white leghorn chickens.

Nonalcoholic fatty liver disease (NAFLD), which shows similar symptoms as fatty liver hemorrhage syndrome (FLHS) in chickens, is the most common cause of chronic liver disease and cancer in humans. NAFLD patients and FLHS in chickens have demonstrated severe liver disorders when infected by emerging strains of human hepatitis E virus (HEV) and avian HEV, respectively. We sought to develop a fatty liver disease chicken model by altering the diet of 3-week-old white leghorn chickens. The high cholesterol, and low choline (HCLC) diet included 7.6% fat with additional 2% cholesterol and 800 mg/kg choline in comparison to 5.3% fat, and 1,300 mg/kg choline in the regular diet. Our diet induced fatty liver avian model successfully recapitulates the clinical features seen during NAFLD in humans and FLHS in chickens, including hyperlipidemia and hepatic steatosis, as indicated by significantly higher serum triglycerides, serum cholesterol, liver triglycerides, cholesterol, and fatty acids. By developing this chicken model, we expect to provide a platform to explore the role of lipids in the liver pathology linked with viral infections and contribute to the development of prophylactic interventions.

Prevalence of drug resistant Enterobacteriaceae in a Nepalese tertiary care hospital.

Antimicrobial resistance in Enterobacteriaceae is an emerging global public health problem. Numerous studies have reported community-acquired AmpC beta-lactamase and extended spectrum beta-lactamase (ESBL) producing Enterobacteriaceae in Nepal. However, there are limited data on community-acquired Metallo-beta-lactamase (MBL) producing Enterobacteriaceae. A hospital-based descriptive cross-sectional study was conducted using 294 Enterobacteriaceae isolates from a total of 2,345 different clinical specimens collected from patients attending a tertiary care hospital in Nepal. Bacteria were isolated using standard microbiological growth media and identified using biochemical tests. For antimicrobial susceptibility testing, Kirby-Bauer disc diffusion technique was used. AmpC, ESBL, and MBL productions were detected by using combined disc method. AmpC, ESBL, and MBL productions were detected in 19.4%, 29.6%, and 8.5% of total Enterobacteriaceae isolates respectively. Higher rates of beta-lactamases production were seen among the isolates from in-patients in comparison with those from out-patients. However, 11.6%, 25%, and 3.7% of the total isolates from out-patients were AmpC, ESBL, and MBL producers respectively. The co-production of the beta-lactamases was also detected, with two Klebsiella pneumoniae isolates producing all three beta-lactamases. One MBL producing Proteus vulgaris isolate that was pan-resistant with no remaining treatment options was also isolated. Prevalence of drug resistant Enterobacteriaceae in our study was very high. Detection of AmpC, ESBL, and MBL positive isolates from out-patients, who did not have recent history of hospital visit, indicated the community dissemination of the drug resistant bacteria. This is a matter of great concern and an immediate attention to formulate strategies to prevent further development and spread of antibiotic resistance is required.

Iodine status after iodized salt supplementation in schoolchildren of eastern Nepal.

This study was designed to assess the urinary iodine concentrations of schoolchildren at baseline and after iodized salt supplementation in eastern region of Nepal. A cross sectional study was conducted from August 2009 to July 2011 among schoolchildren of three eastern districts of Nepal: Sunsari, Dhankuta, and Tehrathum. A sample of 828 school age children from the three districts was chosen for the study after obtaining written consent from their guardians. The schoolchildren treatment group (n=300) was provided with a supplement of iodized salt for six months. Urinary iodine concentration was estimated by ammonium persulfate digestion microplate method at baseline and after supplementation. Urinary iodine controls L1, L2 (Seronorm, Norway) were analyzed to obtain intra-assay CVs (L1 = 7.4%, L2 = 3.3%) and inter assay CVs (L1=23.5%, L2=11.26%). Median interquartile range urinary iodine concentration in the three districts: Sunsari, Dhankuta and Tehrathum at baseline versus intervention were 272.0 (131.5-473.0) microg/l versus 294.0 (265.0-304.0) microg/l (p=0.379), 247.0 (144.5-332.32) versus 361.0 (225.66-456.52) microg/l (p<0.001), and 349.5 (203.75-458.09) microg/l versus 268.76 (165.30-331.67) microg/l (p<0.001), respectively. This study indicated improved iodine status and increased median urinary iodine concentration after iodized salt supplementation. Regular monitoring of population urinary iodine concentration at national and regional levels should be performed to ensure that all individuals have optimal delivery of iodine nutrition.

Unveiling the complex relationship between gut microbiota and liver cancer: opportunities for novel therapeutic interventions.

Hepatocellular carcinoma (HCC) has been linked to the gut microbiota, with recent studies revealing the potential of gut-generated responses to influence several arms of the immune responses relevant to HCC formation. The pro- or anti-tumor effects of specific bacterial strains or gut microbiota-related metabolites, such as bile acids and short-chain fatty acids, have been highlighted in many human and animal studies. The critical role of the gut microbiota in HCC development has spurred interest in modulating the gut microbiota through dietary interventions, probiotics, and fecal microbiota transplantation as a potential strategy to improve liver cancer outcomes. Encouragingly, preclinical and clinical studies have demonstrated that modulation of the gut microbiota can ameliorate liver function, reduce inflammation, and inhibit liver tumor growth, underscoring the potential of this approach to improve HCC outcomes. As research continues to unravel the complex and dynamic mechanisms underlying the gut-liver axis, the development of safe and effective interventions to target this pathway for liver cancer prevention and treatment appears to be on the horizon, heralding a significant advance in our ongoing efforts to combat this devastating disease.

Modulation of the Gut Microbiome to Improve Clinical Outcomes in Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related mortality worldwide. Recently, the gut microbiota has been shown to be closely linked to modulation of the immune and inflammatory responses, hence its potential as a therapeutic target. Although still under intense investigation, there exists a 'gut-liver axis' that links changes in the gut to the liver. In this regard, composition of gut microbiota and related metabolites, such as bile acids and short-chain fatty acids, have been shown to orchestrate key immune-metabolic events in liver disease and liver cancer. As hepatic immune cells are important determinants of antitumor responses, it is now increasingly recognized that the gut-liver axis plays a key role in influencing the intrahepatic immune response in HCC to favor a pro- or antitumor immune milieu. Hence, modulation of gut microbiota is potentially an attractive option to reinvigorate the antitumor responses. In this regard, promising evidence from melanoma preclinical and clinical studies has demonstrated the efficacy of gut-based intervention in reinvigorating the antitumor responses and improving responses to immunotherapy. However, the role of gut-based interventions as a therapeutic option in HCC remains to be elucidated. This review details how the gut microbiota and bacterial metabolites affect gut barrier function and ultimately immune response in HCC and raises the question of the potential of gut-based interventions as an adjunct therapy for patients with HCC receiving immunotherapy.

Refining a Protocol for Faecal Microbiota Engraftment in Animal Models After Successful Antibiotic-Induced Gut Decontamination.

BACKGROUND: There is mounting evidence for the therapeutic use of faecal microbiota transplant (FMT) in numerous chronic inflammatory diseases. Germ free mice are not always accessible for FMT research and hence alternative approaches using antibiotic depletion prior to FMT in animal studies are often used. Hence, there is a need for standardising gut microbiota depletion and FMT methodologies in animal studies. The aim of this study was to refine gut decontamination protocols prior to FMT engraftment and determine efficiency and stability of FMT engraftment over time. METHODS: Male C57BL/6J mice received an antibiotic cocktail consisting of ampicillin, vancomycin, neomycin, and metronidazole in drinking water for 21 days ad libitum. After antibiotic treatment, animals received either FMT or saline by weekly oral gavage for 3 weeks (FMT group or Sham group, respectively), and followed up for a further 5 weeks. At multiple timepoints throughout the model, stool samples were collected and subjected to bacterial culture, qPCR of bacterial DNA, and fluorescent in-situ hybridisation (FISH) to determine bacterial presence and load. Additionally, 16S rRNA sequencing of stool was used to confirm gut decontamination and subsequent FMT engraftment. RESULTS: Antibiotic treatment for 7 days was most effective in gut decontamination, as evidenced by absence of bacteria observed in culture, and reduced bacterial concentration, as determined by FISH as well as qPCR. Continued antibiotic administration had no further efficacy on gut decontamination from days 7 to 21. Following gut decontamination, 3 weekly doses of FMT was sufficient for the successful engraftment of donor microbiota in animals. The recolonised animal gut microbiota was similar in composition to the donor sample, and significantly different from the Sham controls as assessed by 16S rRNA sequencing. Importantly, this similarity in composition to the donor sample persisted for 5 weeks following the final FMT dose. CONCLUSIONS: Our results showed that 7 days of broad-spectrum antibiotics in drinking water followed by 3 weekly doses of FMT provides a simple, reliable, and cost-effective methodology for FMT in animal research.

A Mechanistic Link Between Selenium and Coronavirus Disease 2019 (COVID-19).

PURPOSE OF REVIEW: Coronavirus disease 2019 (COVID-19) is a rapidly emerging disease caused by a highly contagious virus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and this disease has affected millions of people across the world and led to hundreds of thousands of deaths worldwide. Nutrition is a key factor related to this disease, and nutritional status may determine the risk and outcomes of SARS-CoV-2 infection. Selenium is one of the major trace elements required for redox functions and has significant roles in viral infections. The purpose of this review was to examine the current evidence on the role of selenium in COVID-19. We reviewed studies on selenium and COVID-19, and other relevant studies to understand how selenium status can modify the risk of SARS-CoV-2 infection, and how selenium status might affect a person post-infection. RECENT FINDINGS: We found that oxidative stress is a characteristic feature of COVID-19 disease, which is linked with the immunopathological disorder observed in individuals with severe COVID-19. Selenium plays a key role in strengthening immunity, reducing oxidative stress, preventing viral infections and supporting critical illness. Moreover, selenium deficiency is related to oxidative stress and hyperinflammation seen in critical illness, and selenium deficiency is found to be associated with the severity of COVID-19 disease. Selenium supplementation at an appropriate dose may act as supportive therapy in COVID-19. Future studies in large cohorts of COVID-19 are warranted to verify the benefits of selenium supplementation for reducing risk and severity of COVID-19.

Effects of Micronutrient Supplementation on Glucose and Hepatic Lipid Metabolism in a Rat Model of Diet Induced Obesity.

Obesity increases the risk of metabolic disorders, partly through increased oxidative stress. Here, we examined the effects of a dietary micronutrient supplement (consisting of folate, vitamin B6, choline, betaine, and zinc) with antioxidant and methyl donor activities. Male Sprague Dawley rats (3 weeks old, 17/group) were weaned onto control (C) or high-fat diet (HFD) or same diets with added micronutrient supplement (CS; HS). At 14.5 weeks of age, body composition was measured by magnetic resonance imaging. At 21 weeks of age, respiratory quotient and energy expenditure was measured using Comprehensive Lab Animal Monitoring System. At 22 weeks of age, an oral glucose tolerance test (OGTT) was performed, and using fasting glucose and insulin values, Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) was calculated as a surrogate measure of insulin resistance. At 30.5 weeks of age, blood and liver tissues were harvested. Liver antioxidant capacity, lipids and expression of genes involved in lipid metabolism (Cd36, Fabp1, Acaca, Fasn, Cpt1a, Srebf1) were measured. HFD increased adiposity (p < 0.001) and body weight (p < 0.001), both of which did not occur in the HS group. The animals fed HFD developed impaired fasting glucose, impaired glucose tolerance, and fasting hyperinsulinemia compared to control fed animals. Interestingly, HS animals demonstrated an improvement in fasting glucose and fasting insulin. Based on insulin release during OGTT and HOMA-IR, the supplement appeared to reduce the insulin resistance developed by HFD feeding. Supplementation increased hepatic glutathione content (p < 0.05) and reduced hepatic triglyceride accumulation (p < 0.001) regardless of diet; this was accompanied by altered gene expression (particularly of CPT-1). Our findings show that dietary micronutrient supplementation can reduce weight gain and adiposity, improve glucose metabolism, and improve hepatic antioxidant capacity and lipid metabolism in response to HFD intake.

Diagnostic Accuracy of Serum Cystatin C for Early Recognition of Nephropathy in Type 2 Diabetes Mellitus.

OBJECTIVES: Diabetic nephropathy is one of the major complications that develop over time in type 2 diabetes mellitus (T2DM). This prospective study was conducted to assess the diagnostic accuracy of serum cystatin C in detecting diabetic nephropathy at earlier stages. MATERIALS AND METHODS: This study was undertaken on 50 cases of T2DM and 50 healthy subjects as controls. Demographic and anthropometric data and blood and urine samples were collected. The concentration of serum cystatin C (index test) and traditional markers of diabetic nephropathy, serum creatinine, and urinary microalbumin (the reference standard) were estimated. Similarly, blood glucose, glycated haemoglobin (HbA1c), triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, and urinary creatine were measured. RESULTS: The mean ± SD serum cystatin C was significantly higher in T2DM as compared to control (1.07 ± 0.38 and 0.86 ± 0.12 mg/dl, respectively, p < 0.001). The mean ± SD bodyweight, BMI, W : H ratio, pulse, SBP, and DBP were 66.4 ± 12.6 kg, 26.2 ± 5.6 kg/m2, 1.03 ± 0.09, 78 ± 7, 125 ± 16 mm of Hg, and 77 ± 9 mm of Hg, respectively, in cases. A significant difference in HDL cholesterol (p=0.018) and serum cystatin C (p < 0.001) was observed among different grades of nephropathy. Cystatin C had a significant positive correlation with age (r = 0.323, p=0.022), duration of T2DM (r = 0.326, p=0.021), and UACR (r = 0.528, p < 0.001) and a significant negative correlation with eGFR CKD-EPI cystatin C (r = -0.925, p < 0.001). The area under ROC curve for serum cystatin C (0.611, 95% CI: 0.450-0.772) was greater than for serum creatinine (0.429, 95% CI: 0.265-0.593) though nonsignificant. CONCLUSION: Serum cystatin C concentration increases with the progression of nephropathy and duration of diabetes in Nepalese T2DM patients suggesting cystatin C as a potential marker of renal impairment in T2DM patients.

Lung microbiome and coronavirus disease 2019 (COVID-19): Possible link and implications.

Coronavirus disease 2019 (COVID-19) is a rapidly emerging disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease begins as an infection of lungs, which is self-limiting in the majority of infections; however, some develop severe respiratory distress and organ failures. Lung microbiome, though neglected previously have received interest recently because of its association with several respiratory diseases and immunity. Lung microbiome can modify the risk and consequences of COVID-19 disease by activating an innate and adaptive immune response. In this review, we examine the current evidence on COVID-19 disease and lung microbiome, and how lung microbiome can affect SARS-CoV-2 infection and the outcomes of this disease. To date there is no direct evidence from human or animal studies on the role of lung microbiome in modifying COVID-19 disease; however, related studies support that microbiome can play an essential role in developing immunity against viral infections. Future studies need to be undertaken to find the relationship between lung microbiome and COVID-19 disease.

Hepatitis C virus genotype and its correlation with viral load in patients from Kathmandu, Nepal.

INTRODUCTION: Knowledge about the distribution of hepatitis C virus (HCV) genotype and its correlation with viral load are important for the decision of treatment and the prediction of disease progression, however such information is very limited in Nepal. Here, we investigated the distribution of HCV genotypes and viral load for HCV-infected patients from Kathmandu, Nepal. METHODOLOGY: Ninety-six patients with HCV infection and not on antiviral therapy were enrolled from three different medical centers in Kathmandu valley, Nepal. Demographics were recorded and blood samples were collected. Plasma was separated and HCV RNA was extracted. Reverse transcriptase PCR (RT-PCR) was performed to measure the viral load, and virus genotype was determined. RESULTS: Genotype 3a (n = 53, 55.2%) was the most prevalent, followed by 1b (n = 19, 19.8%), 1a (n = 18, 18.8%), 5a (n = 3, 3.1%), and mix types (n = 3, 3.1%). The median viral load for HCV genotype 1a was 770,942 IU/mL (IQR, 215,268-3,720,075), 1b was 700,000 IU/mL (IQR, 431,560-919,000), 3a was 1,060,000 IU/mL (IQR, 641,050-6,063,500), 5a was 673,400 IU/mL, and mixed was 6,428,000 IU/mL. A correlation between genotype and viral load was observed (p = 0.02), of which genotype 3a showed a high viral load. CONCLUSIONS: HCV genotypes 1a, 1b, 3a, and 5a were identified in Kathmandu, Nepal, and mixed genotype patients were observed in the patients studied. HCV genotype showed a correlation with viral load in patient plasma. This finding may contribute to the treatment and prevention of hepatitis C in Kathmandu, Nepal.

Nutritional assessment and factors associated with malnutrition among the elderly population of Nepal: a cross-sectional study.

OBJECTIVES: This study aimed at assessing the nutritional status among the elderly population and factors associated with malnutrition in the community setting in rural Nepal. RESULTS: Out of 339 participants, 24.8% (95% CI 20.21-29.30) fell into the normal nutritional status range; 49.6% (95% CI 44.29-54.91) were at risk for malnutrition while 24.8% (95% CI 20.21-29.30) were in the malnourished range, based on Mini Nutritional Assessment scores. Our findings revealed that belonging to a Dalit community, being unemployed, having experience of any form of mistreatment, lack of physical exercise, experiencing problems with concentration in past 30 days and taking medication for more than one co-morbidity was significantly associated with the malnutrition status of the elderly.

Association of antithyroglobulin antibody with iodine nutrition and thyroid dysfunction in Nepalese children.

BACKGROUND: Aberrant iodine intake and thyroid autoimmunity affect thyroid function. Deficiencies of iodine including thyroid disorders have serious impact on child physical and mental development. This study was conducted to investigate iodine nutrition, thyroid function and thyroid autoimmunity in the Nepalese children, and explore the association of thyroidal autoimmunity with iodine nutrition and thyroid dysfunction. METHODS: Five schools from Udayapur district of eastern Nepal were selected for the study. A total of 213 school children aged 6-12 years were enrolled, and anthropometric data, urine samples and blood samples were collected. Urinary iodine concentration (UIC), free triiodothyronine (fT3), free thyroxine (fT4), thyroid stimulating hormone (TSH), and antithyroglobulin antibody (TgAb) was measured. Independent T test, Man-Whitney test, Chi-square test and Fisher's Exact test were used for testing statistical significance. Spearman's correlation analysis was done to find association between variables. RESULTS: The median UIC with IQR, mean ± SD fT3, mean ± SD fT4, median TSH and TgAb with IQR was 150.0 µg/L (102.8; 204.0), 2.49 ± 0.83 pg/ml, 1.33 ± 0.42 ng/dl, 2.49 mIU/L (1.58; 4.29), and 21.40 IU/ml (15.54; 31.20) respectively. Elvated TgAb (≥30 IU/ml, thyroid autoimmune condition) was seen in 25.8% (n = 55) children. UIC was less than 100 µg/L in 17.4% (n = 37) of the children. Subclinical hypothyroidism, overt hypothyroidism and sublinical hyperthyroidism was seen in 1.4% (n = 3), 3.3% (n = 7) and 3.8% (n = 8) children respectively. A strong association of TgAb with UIC (r = - 0.210, p = 0.002) and thyroid hormones; fT3 (r = - 0.160, p = 0.019), fT4 (r = - 0.275, p < 0.001), and TSH (r = 0.296, p < 0.001) was seen. The relative risk for thyroid autoimmunity in children with UIC less than 100 µg/L was 1.784 (95% CI: 1.108-2.871, p = 0.024). Similarly, children with thyroid autoimmunity had higher relative risk [7.469 (95% CI: 2.790-19.995, p < 0.001)] for thyroid dysfunction. CONCLUSIONS: School children of eastern Nepal have adequate iodine nutrition. Thyroid autoimmunity is very common, while thyroid dysfunction is sparse in children. An association of thyroid autoimmunity with iodine nutrition and thyroid dysfunction was seen in children.

Iodine and Thyroid Function Status, and Anti-thyroid Peroxidase Antibody among Pregnant Women in Eastern Nepal.

BACKGROUND: Iodine deficiency, thyroid dysfunction and development of thyroid autoimmunity during pregnancy may affect mother and the developing fetus. This study was carried out to find iodine status, thyroid dysfunction and thyroid autoimmunity among pregnant women. METHODS: Ninety two pregnant women from three districts of eastern Nepal (Sunsari, Morang and Jhapa) were enrolled for the study, and urine and blood samples were collected. Urinary iodine concentration (UIC), free thyroxine (free T4), thyroid stimulating hormone (TSH), thyroglobulin and anti-thyroid peroxidase (TPO) antibody levels were estimated. RESULTS: The median UIC, mean free T4 and TSH, median thyroglobulin and anti-TPO antibody in the pregnant women were 282.2 (158.42-376) µg/L, 1.14±0.41 ng/dL, 4.57±2.56 IU/mL, 6.5 (4.0-11.0) ng/mL, 1.52 (0.97-2.23) IU/mL respectively. In sufficient (<150 µg/L), adequate (150-249 µg/L) and above requirements (250-499 µg/L) iodine intake was observed in 17 (18.5%), 22 (23.9%) and 53 (57.6%) women respectively. Subclinical hypothyroidism and overt hypothyroidism were seen in 18 (19.5%) and 1(1.1%) women, respectively. Elevated thyroglobulin (>40 ng/mL) and positive anti-TPO antibody was observed in three (3.26%) women for both. CONCLUSIONS: Iodine intake was sufficient among pregnant women recently, however, chronic iodine deficiency persisted in small fraction of pregnant women. Mild thyroid dysfunction was common, and thyroid autoimmunity was present in small portion of Nepalese pregnant women population.