Comparative immune responses of pups following modified live virus vaccinations against canine parvovirus.

Background And Aim: Canine parvovirus (CPV) is the most important viral cause of enteritis and mortality in pups. Evaluation and monitoring of pre- and post-vaccine immune responses may help to determine the efficacy of the current vaccination schedule being followed in pups in India. This study aimed to evaluate and monitor the pre- and post-vaccine immune responses of CPV vaccinated pups using hemagglutination inhibition (HI) assay.

Characterization of Haptoglobin Isotype in Milk of Mastitis-Affected Cows.

Haptoglobin is a major acute phase protein in bovines and reportedly increases in serum and milk whey during mastitis, highlighting its potential as a diagnostic biomarker. Since haptoglobin is known to undergo tissue specific glycosylation resulting in different isoforms, this study was undertaken to characterize the isoforms of haptoglobin. Milk whey fraction and serum obtained from animals with or without clinical mastitis in Puducherry, India, were subjected to SDS-PAGE followed by western blot and immuno-detection of haptoglobin protein.

Full-length VP2 gene analysis of canine parvovirus reveals emergence of newer variants in India.

The canine parvovirus (CPV) infection is a highly contagious and serious enteric disease of dogs with high fatality rate. The present study was taken up to characterize the full-length viral polypeptide 2 (VP2) gene of CPV of Indian origin along with the commercially available vaccines. The faecal samples from parvovirus suspected dogs were collected from various states of India for screening by PCR assay and 66.

Molecular characterisation of parvoviruses from domestic cats reveals emergence of newer variants in India.

Objectives The present study was undertaken to characterise the viral polypeptide 2 (VP2) gene of parvovirus from domestic cats in India. Methods The faecal samples from diarrhoeic/healthy domestic cats were collected from different geographical regions of India for screening by PCR assay followed by sequence analysis of the VP2 gene. Results Canine parvovirus (CPV)/feline panleukopenia virus (FPV) infections were found in 12 (11.

Phylogenetic analysis of canine parvovirus partial VP2 gene in India.

A total of 85 samples (58.0 %) were found to be positive for Canine parvovirus (CPV) by PCR assay (Hfor/Hrev primers) out of 158 suspected faecal samples of dogs collected from various states/union territories of India. Nine CPV isolates could be obtained in A-72 cell line.

Development and evaluation of loop-mediated isothermal amplification assay for rapid and sensitive detection of canine parvovirus DNA directly in faecal specimens.

Aims:  To develop a specific and highly sensitive loop-mediated isothermal amplification (LAMP) technique for the rapid detection of canine parvovirus (CPV) DNA directly in suspected faecal samples of dogs by employing a simple method of template preparation.

Methods And Results:  LAMP reaction was developed by designing two sets of outer and inner primers, which target a total of six distinct regions on VP2 gene of CPV. The template DNA was prepared by a simple boiling and chilling method.

Isolation, molecular characterization and phylogenetic analysis of canine parvovirus.

Canine parvovirus type 2 (CPV-2) causes acute haemorrhagic enteritis in dogs. Canine parvovirus is prone to genetic evolution and has undergone several mutations that produced different strains like CPV-2a, CPV-2b, New CPV-2a, New CPV-2b and CPV-2c in the past three decades. Mutations affecting the VP2 gene of CPV have been responsible for evolution of different antigenic variants.

Characterization of TLR4 signaling in water buffalo (Bubalus bubalis).

Lipopolysaccharide (LPS) treatment of Peripheral Blood Mononuclear Cells (PBMC) isolated from the water buffalo resulted in the activation of TLR signaling intermediates as supported by the western blot of pERK. Activation of ERK resulted in phosphorylation of IkappaB-alpha which lead to its degradation which in turn followed by nuclear translocation of NF-kappaB, which is also supported by the western blot analysis. The nuclear translocation of NF-kappaB culminated in the induction of mRNA expression of TNF-alpha.

Lipid peroxidation as a possible secondary mechanism of sterigmatocystin toxicity.

Sterigmatocystin (Stg), a major secondary metabolite of Aspergillus versicolor and A. nidulans, is the precursor of aflatoxin B1. In this study, male albino rats were treated with Stg-contaminated diet for 30 days, resulting in reduced levels of glutathione, ascorbic acid, and alpha-tocopherol.

Acrolein-induced toxicity--defective mitochondrial function as a possible mechanism.

Administration of acrolein (2.5 mg/kg body weight/day) to rats for 45 days depleted the glutathione level in liver, which triggered an imbalance in the antioxidant defense, resulting in lipid peroxidation. Enhanced lipid peroxidation damaged the membranous structure of mitochondria, which was indicated by the loss of lamellae, and increased the oxidation of exogenously added NADH.

Acute pulmonary toxicity of acrolein in rats--underlying mechanism.

Acute exposure of rats to acrolein (1 or 2 ppm) resulted in reduced levels of glutathione, ascorbic acid and alpha-tocopherol. The activities of catalase and glutathione peroxidase were reduced whereas an increase in the activities of superoxide dismutase was observed. This led to enhanced lipid peroxidation, which produced extensive lung damage as indicated by the elevated levels of the biochemical markers--angiotensin converting enzyme, lactate dehydrogenase, protein and lactate in the bronchoalveolar lavage.

Effects of acrolein on rat liver antioxidant defense system.

Effect of acrolein (2.5 mg/kg body wt/day) on the rat liver antioxidant defense system was investigated. Following 45 days of acrolein exposure, the levels of glutathione, ascorbic acid and the activity of catalase were decreased whereas the activities of superoxide dismutase and glutathione peroxidase were increased.

Effect of chronic glutathione deficiency on rat lung mitochondrial function.

The effect of chronic glutathione deficiency on lung mitochondrial energy production using buthionine sulphoximine (BSO) as a depletor has been investigated. Prolonged depletion of mitochondrial glutathione produced an imbalance in the antioxidant defence and resulted in lipid peroxidation, which, in turn, damages the membranous structure, leading to the inactivation of inner membrane enzymes, matrix-bound enzymes and mitochondrial cytochrome content. Altered activities of energy-linked enzymes and electron transport resulted in the decreased rate of ADP-stimulated oxygen uptake, respiratory coupling ratio and ATP synthesis.

Buthionine sulfoximine-induced glutathione depletion. Its effect on antioxidants, lipid peroxidation and calcium homeostasis in the lung.

The administration of buthionine sulfoximine (BSO), an irreversible inhibitor of gamma-glutamylcysteine synthetase, produces glutathione (GSH) depletion in tumors, making them sensitive to drugs and radiation. During the process, it also depletes GSH from normal tissues. Certain tumors require frequent doses of BSO for several days to produce GSH depletion.