Explore the vast range of titles available.

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.

Heat stress (HS) is one of the most important stressors in chickens, and its adverse effects are primarily caused by disturbing the redox homeostasis. An increase in electron leakage from the mitochondrial electron transport chain is the major source of free radical production under HS, which triggers other enzymatic systems to generate more radicals. As a defense mechanism, cells have enzymatic and non-enzymatic antioxidant systems that work cooperatively against free radicals. The generation of free radicals, particularly the reactive oxygen species (ROS) and reactive nitrogen species (RNS), under HS condition outweighs the cellular antioxidant capacity, resulting in oxidative damage to macromolecules, including lipids, carbohydrates, proteins, and DNA. Understanding these detrimental oxidative processes and protective defense mechanisms is important in developing mitigation strategies against HS. This review summarizes the current understanding of major oxidative and antioxidant systems and their molecular mechanisms in generating or neutralizing the ROS/RNS. Importantly, this review explores the potential mechanisms that lead to the development of oxidative stress in heat-stressed chickens, highlighting their unique behavioral and physiological responses against thermal stress. Further, we summarize the major findings associated with these oxidative and antioxidant mechanisms in chickens.

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.

Background Escherichia coli is the most predominant causative agent of urinary tract infection (UTI). Recently, increase in drug resistance among the uropathogenic bacteria has caused great problem in treatment of UTI. The main objective of this research is to determine the correlation between biofilm formation and resistance toward different commonly used antibiotics along with extended spectrum beta lactamase production in uropathogenic Escherichia coli . Methods The urine samples collected from the patients suspected of urinary tract infections (visiting Shree Birendra Hospital, Chhauni, Kathmandu, Nepal between July to December 2013) were cultured in cystine lactose electrolyte deficient (CLED) agar by using semi quantitative culture technique. Extended spectrum beta lactamase (ESBL) production was detected by combined disc diffusion technique and biofilm formation was detected by Congo red agar method. Chi-square test was applied and p -value < 0.05 was considered statistically significant. Results Out of 1480 urine samples, E. Coli was isolated from 208 (14.1 %) samples. Of total 69 (33.2 %) ESBL producing uropathogenic strains of E. coli , 20 (29 %) were strong biofilm producers, 22 (31.9 %) were moderate biofilm producers, 11 (15.9 %) were weak biofilm producers and 16 (23.2 %) were biofilm non producers. Whereas among 139 ESBL non producing E. coli , 22 (15.8 %) were strong biofilm producers, 20 (14.4 %) were moderate biofilm producers, 13 (9.4 %) were weak biofilm producers and 84 (60.4 %) were biofilm non producers. Among total 108 biofilm producing E. coli , maximum resistance was observed toward cephalexin followed by amoxicillin and highest susceptibility was seen toward amikacin. Conclusion The ability of biofilm formation was found to be significantly higher in ESBL producing strains of E. coli than that in ESBL non producing strains ( p  < 0.05). There was higher resistance rate to antimicrobial agents among biofilm producing strains of E. coli than that in biofilm non producing strains. According to our antimicrobial susceptibility pattern for E. coli , to start preliminary treatment for UTI in Nepal, we recommend to use amikacin or nitrofurantoin. Further, for the treatment of the UTI, the antibiotics should be selected on the basis of the urine culture and sensitivity report.

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.

Background/Objectives: African swine fever virus (ASFV), the causative agent of African swine fever (ASF), is a highly contagious virus affecting both domestic and feral pig populations with mortality rates approaching 100% within one week of infection. Currently, there are limited treatments or vaccines available to control the disease. Although ASF is endemic in sub-Saharan Africa, the virus has also spread widely, reaching regions of the European Union, Russia, China, Southeast Asia, and, more recently, to the Dominican Republic and Haiti, bringing the threat closer to the United States (U.S.). ASF introduction to the U.S. would have severe consequences for swine producers and the national pork industry. Consequently, there is an urgent need to develop effective vaccine strategies to manage ongoing outbreaks abroad and mitigate the risk of future ASF incursions. Recent efforts have identified several ASFV epitopes and evaluated them in experimental vaccine trials. However, these vaccine candidates have elicited limited protective immune responses and have not demonstrated full protective efficacy. Methods: In this study, we employed in silico modeling and epitope prediction tools to design a synthetic multiepitope ASF protein incorporating key immunogenic regions of ASFV. The goal was to generate a single-antigen construct capable of inducing broad and robust immune responses when formulated with an established nanoparticle-based vaccine platform. The multiepitope ASF protein was subsequently expressed and entrapped into mannose-conjugated chitosan (M-CS) nanoparticles for vaccine formulation. The candidate vaccine, formulated with M-CS nanoparticle-entrapped adjuvant (ADU S100), was administered intramuscularly to pigs, and both T- and B-cell responses were assessed following the primary (DPV 22) and booster (DPV 42) doses. Results: Our M-CS ASF protein vaccine elicited antigen-specific T- and B-cell responses, both of which are recognized as central correlates of protection against ASFV. Conclusions: These promising preliminary immunological findings suggest that this nanoparticle vaccine has the potential to confer protection against ASFV challenge, a hypothesis that will be examined in future studies.

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. Male mice received an antibiotic cocktail consisting of ampicillin, vancomycin, neomycin, and metronidazole in drinking water for 21 days . 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 hybridisation (FISH) to determine bacterial presence and load. Additionally, 16S rRNA sequencing of stool was used to confirm gut decontamination and subsequent FMT engraftment. 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. 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.

Background Turkey arthritis reovirus (TARV) causes arthritic lameness in market-age turkeys. Since 2011, highly pathogenic TARV strains have caused significant economic losses in the turkey industry due to increased culling, reduced market weights, and decreased carcass quality, necessitating more effective control measures. Autogenous vaccine prevention strategies have been inefficacious partly due to a limited understanding of age-related susceptibility of turkeys to TARV. This study investigated age-related host and gut microbiota responses to TARV infection in commercial turkeys derived from vaccinated breeder hens. Poults with known maternally derived antibody titers were orally challenged with TARV O’Neil strain at 1-, 3-, and 7- weeks of age (WOA) and monitored for cloacal virus shedding, gastrocnemius tendon viral tropism, tendon inflammation, weight gain, and changes in gut microbiota. Results A transient TARV-induced weight gain suppression was evident in poults infected at 1- and 3- WOA during the first 3 weeks post-infection. Age-dependent variations in cloacal viral shedding, virus isolation from tendons, and tendon inflammation severity were also observed. There was significant dissimilarity in ileal and cecal bacterial communities between mock and infected groups, but the effect of age of infection was unclear. Conclusions Age dependent host response was observed to TARV based on cloacal virus shedding, weight gain suppression and viral tendon tropism. Our study also indicates that maternally derived antibodies appeared insufficient to prevent virus translocation to the tendons and subsequent pathological changes. This study lays the groundwork for future investigations of better vaccines/vaccination strategies and alternative preventive measures. Importance Turkey arthritis reovirus (TARV) causes lameness due to arthritis and tenosynovitis, commonly in market-age turkeys, resulting in significant economic losses. As a control strategy, the turkey industry used autogenous vaccines, prepared from field TARV isolates in breeder hens, to protect the poults in the early stage of life through maternally derived antibodies (MDAs). This study establishes the level of protection provided by MDAs in young poults with age-based responses to TARV O’Neil reovirus strain. Additionally, this study reveals the dynamics of gut dysbiosis in infected poults at different timepoints, paving the way to ground-breaking investigations into gut microbiome modulation interventions that could potentially improve vaccine efficacy and reduce virus transmission and disease severity.

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.

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.