Association analysis of HSP90AA1 polymorphism with thermotolerance in tropically adapted Indian crossbred cattle.

Raising cattle is a lucrative business that operates globally but is confronted by many obstacles, such as thermal stress, which results in substantial monetary losses. A vital role of heat shock proteins (HSPs) is to protect cells from cellular damage. HSP90 is a highly prevalent, extremely adaptable gene linked to physiological resilience in thermal stress. This study aimed to find genetic polymorphisms of the HSP90AA1 gene in Karan Fries cattle and explore their relationship to thermal tolerance and production traits. One SNP (g.3292 A > C) was found in the Intron 8 and three SNPs loci (g.4776 A > G, g.5218T > C and g.5224 A > C) were found in the exon 11 of 100 multiparous Karan Fries cattle. The association study demonstrated that the SNP1-g.3292 A > C was significantly (P < 0.01) linked to the variables respiratory rate (RR), heat tolerance coefficient (HTC) and total milk yield (TMY (kg)) attributes. There was no significant correlation identified between any of the other SNP sites (SNP2-g.4776 A > G; SNP3-g.5218T > C; SNP4-g.5224 A > C) with the heat tolerance and production attributes in Karan Fries cattle. Haploview 4.2 and SHEsis software programs were used to analyse pair linkage disequilibrium and construct haplotypes for HSP90AA1. Association studies indicated that the Hap3 (CATA) was beneficial for heat tolerance breeding in Karan Fries cattle. In conclusion, genetic polymorphisms and haplotypes in the HSP90AA1 were associated with thermal endurance attributes. This relationship can be utilized as a beneficial SNP or Hap marker for genetic heat resistance selection in cow breeding platforms.

Organic waste recycling by vermicomposting amended with rock phosphate impacts the stability and maturity indices of vermicompost.

Recycling organic waste can help the land be nourished, properly disposed of, and protected from the negative impacts of chemical fertilizers. Organic additions like vermicompost can help restore and preserve the quality of the soil, however, producing vermicompost of a high enough standard is difficult. This study was planned to prepare vermicompost by utilizing two different organic wastes viz. household waste and organic residue amended with rock phosphate and further evaluate their stability and maturity indices during vermicomposting for quality of produce. For this study, the organic wastes were collected and vermicompost was prepared by using earthworm (Eisenia fetida) and with or without enriching with rock phosphate. Results showed that pH, bulk density, and biodegradability index were decreased and water holding capacity and cation exchange capacity was increased with the gradual progress of composting starting from 30 to 120 days of sampling/composting (DAS). Initially (upto 30 DAS) water-soluble carbon and water-soluble carbohydrate increased with rock phosphate enrichment. The population of the earthworms and enzymatic activities (CO2 evolution, dehydrogenase, and alkaline phosphatase) were also increased on enriching with rock phosphate and with the progression of the composting period. Rock phosphate addition (enrichment) also reflected the higher content of phosphorus (106% and 120% for household waste and organic residue, respectively) in the final product of vermicompost. The vermicompost prepared from household waste and enriched with rock phosphate showed greater maturity and stability indices. Overall, this can be concluded that the maturity and stability of vermicompost depend on the substrate used and improves on enriching with rock phosphate.Implications: Our study concludes that the quality of vermicompost depends on different substrates, composting period, and enrichment with rock phosphate. The qualities of vermicompost were best found under household waste-based vermicompost enriched with rock phosphate. The efficiency of vermicomposting process using earthworms was found maximum for enriched and without enriched household-based vermicompost. The study also indicated that several stability and maturity indices are influenced by different parameters and hence cannot be determined by a single parameter. The addition of rock phosphate increased the cation exchange capacity, phosphorus content, and alkaline phosphatase. Nitrogen, zinc, manganese, dehydrogenase, and alkaline phosphatase were found higher under household waste-based vermicompost relative to organic residue-based vermicompost. All four substrates promoted earthworm growth and reproduction in vermicompost.

Association of udder type traits with single nucleotide polymorphisms in Sahiwal (Bos indicus) and Karan Fries (Bos taurus × Bos indicus) cattle.

Udder structure of milking cows is not merely vital to display the visual characteristics, but also important for high milk output and low mastitis risk incidence as well. The present study measured different udder type traits in Sahiwal (Bos indicus) and Karan Fries (Bos taurus × Bos indicus) and investigated their association with single nucleotide polymorphisms in Vitamin D Receptor and Protein Tyrosine Phosphatase, Receptor Type, R genes. GG genotype of SNP rs454303072 was found to have wider rear udder, larger udder circumference, longer distance between fore-rear teats and left-right teats in Karan Fries cattle. Whereas, in Sahiwal cattle, AA genotype of this SNP was found to be associated with the higher and wider rear udder, larger udder circumference and wider udder. AA genotype of SNP rs382671389 was found to be associated with longer fore teat in Karan Fries cattle. The TT and CC genotype of SNP rs435289107 was associated with udder type traits in Karan Fries and Sahiwal cattle respectively. These results suggest that BTA 5 harbors genomic regions associated with udder traits in Bos indicus and Bos indicus x Bos taurus cattle.

Udder and teat morphometry in relation to clinical mastitis in dairy cows.

The present study was undertaken to explore the association of occurrence of clinical mastitis with udder and teat morphometry in cattle. The relationship of nine udder and eight teat morphometric traits with the occurrence of clinical mastitis was analysed using a binomial logistic regression model. A significant association of the udder and teat morphometric traits with the occurrence of mastitis was observed both in Karan Fries and Sahiwal cattle. The rear udder height, rear udder width, udder width and fore udder attachment were found to be the important udder morphometric traits associated with the occurrence of mastitis. In both groups, mastitic animals had broader rear udder width, lower rear udder height and loose fore udder attachment with lengthy and thicker teats. The inclusion of udder and teat morphometric traits in the selection and breeding program of Karan Fries and Sahiwal cattle may help in selection of animals for mastitis resistance.

Genetic polymorphism in HSPB6 gene and their association with heat tolerance traits in Indian Karan Fries (Bos taurus x Bos indicus) cattle.

Heat shock proteins (HSPs) act as a chaperone activity ensuring the folding, unfolding, and refolding of denatured proteins, which help in a protective role during thermal stress in dairy cattle. This study aimed to detect genetic variations of the HSPB6 gene and to determine their association with heat tolerance traits in Karan Fries cattle. Five single nucleotide polymorphisms (SNPs) (SNP 1-5) were reported in the Karan Fries cattle, which included three transitions viz. SNP1-g.161G > A, SNP2-g.436G > A, and SNP4-g.2152A > G and two transversions viz. SNP3-g.1743C > G, SNP5-g.2417A > T. The association analysis revealed that the three SNPs loci i.e., SNP1-g.161G > A, SNP2-g.436G > A, and SNP3-g.1743C > G were significantly (p < 0.01) associated with the respiration rate (RR) and rectal temperature (RT) (°C) traits. Furthermore, in the case of heat tolerance coefficient (HTC) trait was found significantly associated (p < 0.01) with SNPs loci i.e., SNP1-g.161G > A, SNP2-g.436G > A, and SNP3-g.1743C > G. The Hap 4 (GACAT) was found to more adaptable than cattle of other haplotypes as reflected by lower values of RR, RT and HTC. This study provides the first association analyses between the SNPs and haplotypes of HSPB6 gene and heat tolerance traits in Karan Fries cattle, which could be used as effective SNP markers in genetic selection for heat tolerance in cattle breeding program.

WITHDRAWN:Principal component analysis of linear udder type traits and their relationship with milk yield and composition in indigenous Sahiwal cattle.

Ahead of Print article withdrawn by publisher.

Molecular characterization and SNP identification in HSPB6 gene in Karan Fries (Bos taurus x Bos indicus) cattle.

Heat shock proteins (HSPs) act as molecular chaperones which are preferentially transcribed in response to severe perturbations of the cellular homeostasis such as heat stress. The present study was undertaken for molecular characterization and detection of genetic polymorphisms of HSPB6 gene in 100 Karan Fries Cattle. HSPB6 gene was mapped on Bos taurus autosome 18 (BTA 18), comprising three exons and two introns. Four sets of primers for HSPB6 gene were designed using Primer3 software (version 0.4.0). For detecting single nucleotide polymorphisms (SNPs), sequence data was analyzed using BioEdit software (version 7.2). Comparative sequence analysis of HSPB6 gene showed five nucleotide polymorphisms, which included three transitions viz. g.161A > G, g.436G > A and g.2152A > G and two transversions viz. g.1743C > G and g.2417A > T compared to B. taurus (NCBI GenBank: AC_000175.1). HSPB6 gene of Karan Fries cattle exhibited a high percentage of nucleotide identity (47.0-100.0%) with the corresponding mammalian homologue. The present study indicated a high degree of genetic variability in the HSPB6 gene in the Karan Fries cattle populations.

Emission estimates of particulate matter and heavy metals from mobile sources in Delhi (India).

An attempt has been made to make a comprehensive emission inventory of particulate matter (PM) of various size fractions and also of heavy metals (HMs) emitted from mobile sources (both exhaust and non-exhaust) from the road transport of Delhi, India (1991-2006). COPERT-III and 4 models were mainly used toestimate these emissions. Results show that the annual exhaust emission of PM of size upto 2.5 micrometer (PM2.5) has increased from 3Gg to 4.5Gg during 1991-2006 irrespective of'improvement in vehicle-technology and fuel use. PM emission from exhaust and non-exhaust sources in general has increased. Heavy commercial vehicles-need attention to control particulate emission as it emerged as a predominant source of PM emissions. Among non-exhaust emissions of total suspended particulate matter (TSP), road-surface wear (~49%) has the prime contribution. As a result of-introduction of unleaded gasoline Pb has significantly reduced (~8 fold) whereas share of Cu and Zn are still considerable. Among non-exhaust sources, Pb release was the most significant one from tyre-wear whereas from break-wear, Cu release was found to be the most significant followed by Pb and Cr + Zn. Because of public health concerns further policies need to be developed to reduce emissions of PM and HMs from the road transport of megacity Delhi.

Chronic exposure to arsenic causes increased cell survival, DNA damage, and increased expression of mitochondrial transcription factor A (mtTFA) in human prostate epithelial cells.

Arsenic is a known carcinogen, and its exposure is associated with cancers in multiple target organs including the prostate. Whether arsenic causes cancer by increased cell proliferation or cell survival is not clear. Additionally, mitochondria have been shown to play important roles in arsenic-induced DNA damage and carcinogenesis. However, the mechanism of mitochondrial involvement in arsenic-induced cancer is not clear. Therefore, the objectives of this study were to investigate the effect of arsenic on cell proliferation/survival and genotoxicity, and to determine the effect of arsenic on the expression of mitochondrial transcription factor A (mtTFA) in human prostate epithelial cells, RWPE-1. Results of this study revealed that chronic exposure to arsenic causes increased cell survival. Arsenic also induced nuclear DNA damage and mutations in mitochondrial DNA. Expressions of DNA repair genes ERCC6, XPC, OGG1, and reactive oxygen species (ROS) scavenger MnSOD was also altered in arsenic-exposed cells. Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway. In summary, this study suggests that chronic exposure to arsenic causes DNA damage and increased cell survival that may ultimately result in neoplastic transformation of human prostate epithelial cells. Additionally, this study also provides evidence that arsenic controls mitochondrial function by regulating mtTFA expression.

Urban and country level greenhouse gas emissions and carbon footprints: A comparative study of a megacity, Delhi and India.

This paper describes the contribution and comparison of carbon footprints of megacity Delhi with that of India over the period from 1990 to 2000. Two published studies were taken as base to calculate carbon footprint in terms of CO2 equivalents (CO(2)-e) by taking into account CO2, CH4 and N2O emissions mainly from transport, power plants, domestic, industries, agriculture and waste sectors. It is found that carbon footprints have increased more in India (-45%) in comparison to Delhi (-33%) between 1990-2000. However, the average per capita carbon footprints at India level is less than for Delhi. Also, carbon footprint per km area in Delhi is - 40 times to that for India. In India (2000) the contribution to carbon footprint's share primarily comes from power plants, industries and agriculture sector whereas it comes from power plants and transport in case of Delhi. Various control measures taken into account in Delhi during 1990-2000 have resulted in decreasing share of CO2 in the total greenhouse gas (GHG) emissions in comparison to what appears at India level. It indicates that suitable policy measures and norms are required to be implemented at India level to control other GHGs along with CO2 to reduce net carbon footprints at the country level.

Simulated microgravity-induced epigenetic changes in human lymphocytes.

Real space flight and modeled microgravity conditions result in changes in the expression of genes that control important cellular functions. However, the mechanisms for microgravity-induced gene expression changes are not clear. The epigenetic changes of DNA methylation and chromatin histones modifications are known to regulate gene expression. The objectives of this study were to investigate whether simulated microgravity alters (a) the DNA methylation and histone acetylation, and (b) the expression of DNMT1, DNMT3a, DNMT3b, and HDAC1 genes that regulate epigenetic events. To achieve these objectives, human T-lymphocyte cells were grown in a rotary cell culture system (RCCS) that simulates microgravity, and in parallel under normal gravitational conditions as control. The microgravity-induced DNA methylation changes were detected by methylation sensitive-random amplified polymorphic DNA (MS-RAPD) analysis of genomic DNA. The gene expression was measured by Quantitative Real-time PCR. The expression of DNMT1, DNMT3a, and DNMT3b was found to be increased at 72 h, and decreased at 7 days in microgravity exposed cells. The MS-RAPD analysis revealed that simulated microgravity exposure results in DNA hypomethylation and mutational changes. Gene expression analysis revealed microgravity exposure time-dependent decreased expression of HDAC1. Decreased expression of HDAC1 should result in increased level of acetylated histone H3, however a decreased level of acetylated H3 was observed in microgravity condition, indicating thereby that other HDACs may be involved in regulation of H3 deacetylation. The findings of this study suggest that epigenetic events could be one of the mechanistic bases for microgravity-induced gene expression changes and associated adverse health effects.

Simulated microgravity decreases DNA repair capacity and induces DNA damage in human lymphocytes.

The effect of simulated microgravity on DNA damage and apoptosis is still controversial. The objective of this study was to test whether simulated microgravity conditions affect the expression of genes for DNA repair and apoptosis. To achieve this objective, human lymphocyte cells were grown in a NASA-developed rotating wall vessel (RWV) bioreactor that simulates microgravity. The same cell line was grown in parallel under normal gravitational conditions in culture flasks. The effect of microgravity on the expression of genes was measured by quantitative real-time PCR while DNA damage was examined by comet assay. The result of this study revealed that exposure to simulated microgravity condition decreases the expression of DNA repair genes. Mismatch repair (MMR) class of DNA repair pathway were more susceptible to microgravity condition-induced gene expression changes than base excision repair (BER) and nucleotide excision repair (NER) class of DNA repair genes. Downregulation of genes involved in cell proliferation (CyclinD1 and PCNA) and apoptosis (Bax) was also observed. Microgravity-induced changes in the expression of some of these genes were further verified at the protein level by Western blot analysis. The findings of this study suggest that microgravity may induce alterations in the expression of these DNA repair genes resulting in accumulation of DNA damage. Reduced expression of cell-cycle genes suggests that microgravity may cause a reduction in cell growth. Downregulation of pro-apoptotic genes further suggests that extended exposure to microgravity may result in a reduction in the cells' ability to undergo apoptosis. Any resistance to apoptosis seen in cells with damaged DNA may eventually lead to malignant transformation of those cells.

Long duration exposure to cadmium leads to increased cell survival, decreased DNA repair capacity, and genomic instability in mouse testicular Leydig cells.

Epidemiological and experimental studies have shown that cadmium is carcinogenic to human and experimental animals, however, the mechanism of cadmium-induced carcinogenesis is not clear. The aberrant expression of cell cycle and DNA repair genes resulting in increased cell proliferation and genomic instability are the characteristic features of cancer cells. The purpose of this study was to determine if exposure to cadmium can perturb cell proliferation/survival and causes genomic instability in TM3 cells, a mouse testicular Leydig cell line. The results of this study revealed that short-duration exposure to lower doses of cadmium significantly increase the growth of TM3 cells, whereas, higher doses are toxic and cause cell death. The long duration exposure to higher doses of cadmium, however, results in increased cell survival and acquisition of apoptotic resistance. Gene expression analysis by real-time PCR revealed increased expression of the anti-apoptotic gene Bcl-2, whereas decreased expression of pro-apoptotic gene Bax. Decreased expression of genes for maintenance of DNA methylation, DNMT1, and DNA repair, OGG1 and MYH, was also observed in cells exposed to cadmium for 24h. The random amplified polymorphic DNA (RAPD) assay revealed genomic instability in cells with chronic exposure to cadmium. The findings of this study indicate that mouse testicular Leydig cells adapt to chronic cadmium exposure by increasing cell survival through increased expression of Bcl-2, and decreased expression of Bax. The increased proliferation of cells with genomic instability may result in malignant transformation, and therefore, could be a viable mechanism for cadmium-induced cancers.