Genetic variation in South Indian castes: evidence from Y-chromosome, mitochondrial, and autosomal polymorphisms

Background: Major population movements, social structure, and caste endogamy have influenced the genetic structure of Indian populations. An understanding of these influences is increasingly important as gene mapping and case-control studies are initiated in South Indian populations. Results: We report new data on 155 individuals from four Tamil caste populations of South India and perform comparative analyses with caste populations from the neighboring state of Andhra Pradesh. Genetic differentiation among Tamil castes is low (R = 0.96% for 45 autosomal short tandem repeat (STR) markers), reflecting a largely common origin. Nonetheless, caste- and continent-specific patterns are evident. For 32 lineage-defining Y-chromosome SNPs, Tamil castes show higher affinity to Europeans than to eastern Asians, and genetic distance estimates to the Europeans are ordered by caste rank. For 32 lineage-defining mitochondrial SNPs and hypervariable sequence (HVS) 1, Tamil castes have higher affinity to eastern Asians than to Europeans. For 45 autosomal STRs, upper and middle rank castes show higher affinity to Europeans than do lower rank castes from either Tamil Nadu or Andhra Pradesh. Local between-caste variation (Tamil Nadu R = 0.96%, Andhra Pradesh R = 0.77%) exceeds the estimate of variation between these geographically separated groups (R = 0.12%). Low, but statistically significant, correlations between caste rank distance and genetic distance are demonstrated for Tamil castes using Y-chromosome, mtDNA, and autosomal data. Conclusion: Genetic data from Y-chromosome, mtDNA, and autosomal STRs are in accord with historical accounts of northwest to southeast population movements in India. The influence of ancient and historical population movements and caste social structure can be detected and replicated in South Indian caste populations from two different geographic regions

Molecular genetics of sudden cardiac death in small animals - A review

Sudden cardiac death in small animals is uncommon but often occurs due to cardiac conduction defects or myocardial diseases. Primary cardiac conduction defects are mainly caused by mutations in genes involved in impulse conduction processes (e.g., gapjunction genes and transcription factors) or repolarisation processes (e.g., ion-channel genes), whereas primary cardiomyopathies are mainly caused by defective force generation or force transmission due to gene mutations in either sarcomeric or cytoskeleton proteins. Although over 50 genes have been identified in humans directly or indirectly related to sudden cardiac death, no genetic aetiologies have been identified in small animals. Sudden cardiac deaths have been also reported in German Shepherds and Boxers. A better understanding of molecular genetic aetiologies for sudden cardiac death will be required for future study toward unveiling actiology in sudden cardiac death in small animals. (c) 2005 Elsevier Ltd. All rights reserved

Inherited copper toxicosis in a Bedlington terrier

Inherited copper toxicosis was diagnosed in a Bedlington Terrier using conventional diagnostic methods such as plasma biochemistry, hepatic copper assay, histology and electron microscopy and a recently developed DNA microsatellite marker test. The dog was successfully managed using D-penicillamine and a low copper diet

Survey of veterinary practitioners about their experiences with urinary disorders in dogs and cats

Selected veterinarians were surveyed about their recalled experiences of urinary disorders, especially renal conditions, in current practice. When contacted by phone, 114 veterinarians in four states agreed to participate and 100 of them returned completed questionnaires. The three conditions of most concern nominated by 114 practitioners related to skin, endocrine and gastrointestinal systems (mentioned by 65, 35 and 32%, respectively), followed by urinary, cardiac and respiratory disorders (23, 20, 17%). From the questionnaire, the two body systems most often noted as abnormal in unwell dogs and cats were skin/eyes/ears and alimentary; urinary was third in cats and fifth in dogs. The urinary disorders reported as mast common were bacterial cystitis in dogs and nonobstructed haematuria/dysuria in cats. The frequency of diagnosing renal failure in dogs and cats was mostly "one case per two weeks" (43%), with "one or more per week" (28%) or "one per month" (22%) the main alternatives. Methods used to diagnose or investigate renal disease were generally blood biochemical tests, haematology and urinalysis, but imaging techniques were also popular. Most favoured treatments for chronic renal failure were intravenous fluids, multivitamins, anabolic steroids, and commercial. renal diets. Antimicrobials were often used, but phosphate binders, vitamin D analogues and erythropoietin were rarely employed

Evaluation of haplotypes associated with copper toxicosis in Bedlington Terriers in Australia

Objective-To evaluate the haplotype distribution associated with the copper toxicosis gene and the segregation of the mutated allele in a Bedlington Terrier population in Australia. Animals-131 Bedlington Terriers. Procedure-Samples of DNA and RNA were obtained from each dog. Genetic status of each dog was evaluated by use of the DNA markers C04107; single nucleotide polymorphism (SNP), which was adjacent to exon 2 of Murr1; and a deletion marker for exon 2. A subgroup of the study population was evaluated by use of biochemical and histologic techniques to elucidate the correlation between genotype and phenotype. Results-We identified a recombination between the C04107 marker and Murr1 and a variation in a nucleotide in the splice site of exon 2 in our Bedlington Terrier cohort. Furthermore, we identified a novel haplotype associated with copper toxicosis in this cohort. Conclusions and Clinical Relevance-Our findings indicate that the deletion of exon 2 was not the sole cause of copper toxicosis, although only exon 2 deletion of Murr1 has been responsible for copper toxicosis in Bedlington Terriers. Although we failed to find a novel mutation in our cohort, we identified an affected dog family with an intact exon 2. Furthermore, we found that an SNP in the 5' splicing site of exon 2 may or may not be associated with a novel mutation of the Murr1 gene or other genes. Loss of linkage between the C04107 marker and the Murr1 gene was also identified in a certain family of dogs