Identification and genomic characterization of major effect bacterial blight resistance locus (BB-13) in Upland cotton (Gossypium hirsutum L.).

KEY MESSAGE: Identification and genomic characterization of major resistance locus against cotton bacterial blight (CBB) using GWAS and linkage mapping to enable genomics-based development of durable CBB resistance and gene discovery in cotton. Cotton bacterial leaf blight (CBB), caused by Xanthomonas citri subsp. malvacearum (Xcm), has periodically been a damaging disease in the USA. Identification and deployment of genetic resistance in cotton cultivars is the most economical and efficient means of reducing crop losses due to CBB. In the current study, genome-wide association study (GWAS) of CBB resistance using an elite diversity panel of 380 accessions, genotyped with the cotton single nucleotide polymorphism (SNP) 63 K array, and phenotyped with race-18 of CBB, localized the CBB resistance to a 2.01-Mb region in the long arm of chromosome D02. Molecular genetic mapping using an F6 recombinant inbred line (RIL) population showed the CBB resistance in cultivar Arkot 8102 was controlled by a single locus (BB-13). The BB-13 locus was mapped within the 0.95-cM interval near the telomeric region in the long arm of chromosome D02. Flanking SNP markers, i04890Gh and i04907Gh of the BB-13 locus, identified from the combined linkage analysis and GWAS, targeted it to a 371-Kb genomic region. Candidate gene analysis identified thirty putative gene sequences in the targeted genomic region. Nine of these putative genes and two NBS-LRR genes adjacent to the targeted region were putatively involved in plant disease resistance and are possible candidate genes for BB-13 locus. Genetic mapping and genomic targeting of the BB13 locus in the current study will help in cloning the CBB-resistant gene and establishing the molecular genetic architecture of the BB-13 locus towards developing durable resistance to CBB in cotton.

High-density linkage map construction and QTL analyses for fiber quality, yield and morphological traits using CottonSNP63K array in upland cotton (Gossypium hirsutum L.).

BACKGROUND: Improving fiber quality and yield are the primary research objectives in cotton breeding for enhancing the economic viability and sustainability of Upland cotton production. Identifying the quantitative trait loci (QTL) for fiber quality and yield traits using the high-density SNP-based genetic maps allows for bridging genomics with cotton breeding through marker assisted and genomic selection. In this study, a recombinant inbred line (RIL) population, derived from cross between two parental accessions, which represent broad allele diversity in Upland cotton, was used to construct high-density SNP-based linkage maps and to map the QTLs controlling important cotton traits. RESULTS: Molecular genetic mapping using RIL population produced a genetic map of 3129 SNPs, mapped at a density of 1.41 cM. Genetic maps of the individual chromosomes showed good collinearity with the sequence based physical map. A total of 106 QTLs were identified which included 59 QTLs for six fiber quality traits, 38 QTLs for four yield traits and 9 QTLs for two morphological traits. Sub-genome wide, 57 QTLs were mapped in A sub-genome and 49 were mapped in D sub-genome. More than 75% of the QTLs with favorable alleles were contributed by the parental accession NC05AZ06. Forty-six mapped QTLs each explained more than 10% of the phenotypic variation. Further, we identified 21 QTL clusters where 12 QTL clusters were mapped in the A sub-genome and 9 were mapped in the D sub-genome. Candidate gene analyses of the 11 stable QTL harboring genomic regions identified 19 putative genes which had functional role in cotton fiber development. CONCLUSION: We constructed a high-density genetic map of SNPs in Upland cotton. Collinearity between genetic and physical maps indicated no major structural changes in the genetic mapping populations. Most traits showed high broad-sense heritability. One hundred and six QTLs were identified for the fiber quality, yield and morphological traits. Majority of the QTLs with favorable alleles were contributed by improved parental accession. More than 70% of the mapped QTLs shared the similar map position with previously reported QTLs which suggest the genetic relatedness of Upland cotton germplasm. Identification of QTL clusters could explain the correlation among some fiber quality traits in cotton. Stable and major QTLs and QTL clusters of traits identified in the current study could be the targets for map-based cloning and marker assisted selection (MAS) in cotton breeding. The genomic region on D12 containing the major stable QTLs for micronaire, fiber strength and lint percentage could be potential targets for MAS and gene cloning of fiber quality traits in cotton.

Toxic effects of imidacloprid combined with arsenic: Oxidative stress in rat liver.

Imidacloprid (IMI), a newer neonicotinoid insecticide, induces oxidative insult to hepatocytes due to the formation of reactive metabolites during hepatic metabolism. The present study aimed to determine the potentiating effect of arsenic (As) on IMI-induced hepatic damage in Wistar rats. Rats, randomly divided into eight groups with six in each, were subjected to daily oral administration for 28 days. Group I served as control; group II received IMI at the dose rate of 16.9 mg/kg body weight; groups III, IV, and V received As at the dose rate of 50, 100, and 150 ppb, respectively, in drinking water; groups VI, VII, and VIII received both IMI (16.9 mg/kg) and As in drinking water at the rate of 50, 100, and 150 ppb, respectively. Repeated oral administration of IMI or As resulted in significant ( p < 0.05) elevation of plasma phosphatases, transferases, hepatic malondialdehyde, and advanced oxidation protein product levels, but significantly ( p < 0.05) decreased levels of total proteins, thiols, and activities of antioxidant enzymes that indicate oxidation-induced hepatotoxicity. These findings were further corroborated by histological alterations in hepatic tissue of IMI or As-administered rats. The coadministration of both IMI and As in rats produced more severe alterations in these parameters in hepatic tissue. Reduced antioxidant indices and increased hepatic damage biomarkers with pronounced histopathological alterations in hepatic tissue after combined exposure to toxicants indicate potentiating toxic effect of As on IMI-induced hepatotoxicity.

Contrast Intravasation During Hysterosalpingography.

Hysterosalpingography is an imaging method to evaluate the endometrial and uterine morphology and fallopian tube patency. Contrast intravasation implies backflow of injected contrast into the adjoining vessels mostly the veins and may be related to factors altering endometrial vascularity and permeability. Radiologists and gynaecologists should be well acquainted with the technique of hysterosalpingography, its interpretation, and intravasation of contrast agents for safer procedure and to minimize the associated complications.

Dipyridamole intervention of breast cell carcinogenesis.

Dietary prevention is a cost-efficient strategy to reduce the risk of human cancers. More than 85% breast cancers are sporadic and attributable to long-term exposure to environmental carcinogens through a multistep and multiyear disease process. We used our chronically induced cellular carcinogenesis model as a target to search for preventive agents capable of blocking breast cell carcinogenesis. Dipyridamole (DPM), at a non-cytotoxic physiologically achievable dose of 10 nmol/L, effectively blocked breast cell carcinogenesis induced by cumulative exposures to three unrelated carcinogens 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), benzo[a]pyrene (B[a]P), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The ability of DPM to block H-Ras upregulation, thus blocking ERK pathway activation, reactive oxygen species (ROS) elevation, and DNA damage in each exposure, may account for its mechanisms in intervention of carcinogenesis induced by cumulative exposures to PhIP. Likewise, DPM's ability to block ROS elevation and DNA damage may account for its mechanisms in intervention of carcinogenesis chronically induced by NNK and B[a]P, as well. DPM is approved by the Food and Drug Administration to control platelet aggregation and vasoconstriction in patients. Our study revealed, for the first time, the novel ability of DPM to block breast cell carcinogenesis induced by three unrelated carcinogens. DPM should be seriously considered as a chemopreventive agent in development of strategies for reducing the risk of sporadic breast cancer associated with long-term exposure to environmental carcinogens.

Field efficacy of minidosed pour-on ivermectin and eprinomectin against goat warble fly infestation by Przhevalskiana silenus.

The efficacy of minidose of pour-on ivermectin and eprinomectin formulations against first instar larvae of Przhevalskiana silenus was observed in naturally infested goats in the Jammu region, North India. The study was performed in mid August 2011. A total of 280 goats were randomly divided in to 7 groups of 40 each. Goats of the first three groups were treated with pour-on ivermectin at dosage of 2, 5, and 200 µg/kg body weight, respectively, whereas animals of the fourth to sixth groups were treated with pour-on eprinomectin at 25, 50, and 500 µg/kg body weight, respectively. Group VII animals were kept as untreated control. The results indicated that no warbles were recorded between December 2011 and March 2012 on back of animals treated with pour-on preparations of ivermectin at dosage of 5 and 200 µg/kg body weight, respectively, and eprinomectin at dosage of 50 and 500 µg/kg body weight, respectively. Thus, it is concluded that administration of minidose of pour-on ivermectin (5 µg/kg body weight) and eprinomectin (50 µg/kg body weight) is cost effective and so can be used for warble fly control campaign in Jammu region.

Synergistic induction of cancer cell death and reduction of clonogenic resistance by cisplatin and FK228.

Human urinary bladder cancer is the fifth most common cancer in the United States, and the long-term disease-free survival in patients is still suboptimal with current chemotherapeutic regimens. Development of effective chemotherapeutic regimens is crucial to decrease the morbidity and mortality of this cancer. The goal of this study was to investigate the effectiveness of FK228 in increasing cisplatin's ability to induce bladder cancer cell death and reduce drug resistance. Our study revealed that FK228 combined with cisplatin synergistically induced cell death and reduced clonogenic survival of human urinary bladder cancer cells. The Erk-Nox pathway played an important role in mediating signals highly increased by this combined treatment to induce significantly-elevated levels of reactive oxygen species, leading to substantially-induced caspase activation and synergistically-increased death in cancer cells. Cisplatin was able to enhance the ability of FK228 to significantly reduce glutathione, indicating a novel activity of combined FK228 and cisplatin in reducing drug resistance. The ability of combined FK228 and cisplatin to synergistically induce cell death and reduce clonogenic survival was also applicable to colon cancer cells. Hence, combined use of FK228 with cisplatin should be considered in development of therapeutic strategies to control urinary bladder cancer and other cancer development and recurrence.

Induction of human breast cell carcinogenesis by triclocarban and intervention by curcumin.

More than 85% of breast cancers are sporadic and attributable to long-term exposure to environmental carcinogens and co-carcinogens. To identify co-carcinogens with abilities to induce cellular pre-malignancy, we studied the activity of triclocarban (TCC), an antimicrobial agent commonly used in household and personal care products. Here, we demonstrated, for the first time, that chronic exposure to TCC at physiologically-achievable nanomolar concentrations resulted in progressive carcinogenesis of human breast cells from non-cancerous to pre-malignant. Pre-malignant carcinogenesis was measured by increasingly-acquired cancer-associated properties of reduced dependence on growth factors, anchorage-independent growth and increased cell proliferation, without acquisition of cellular tumorigenicity. Long-term TCC exposure also induced constitutive activation of the Erk-Nox pathway and increases of reactive oxygen species (ROS) in cells. A single TCC exposure induced transient induction of the Erk-Nox pathway, ROS elevation, increased cell proliferation, and DNA damage in not only non-cancerous breast cells but also breast cancer cells. Using these constitutively- and transiently-induced changes as endpoints, we revealed that non-cytotoxic curcumin was effective in intervention of TCC-induced cellular pre-malignancy. Our results lead us to suggest that the co-carcinogenic potential of TCC should be seriously considered in epidemiological studies to reveal the significance of TCC in the development of sporadic breast cancer. Using TCC-induced transient and constitutive endpoints as targets will likely help identify non-cytotoxic preventive agents, such as curcumin, effective in suppressing TCC-induced cellular pre-malignancy.

Impact of Chronic Sodium Fluoride Toxicity on Antioxidant Capacity, Biochemical Parameters, and Histomorphology in Cardiac, Hepatic, and Renal Tissues of Wistar Rats.

The study was designed to determine the fluoride distribution after its oral exposure in drinking water and its associated impact on biochemical, antioxidant markers and histology in the liver, kidney, and heart of male Wistar rats. On 100 ppm exposure, the highest accretion of fluoride occurred in the liver followed by the kidney and heart. Fluoride exposure significantly (p˂0.05) increased the plasma levels of dehydrogenase, aminotransferases, kidney injury molecule-1 (KIM-1), and other plasma renal biomarkers but decreased the levels of total plasma proteins and albumin in a dose-dependent manner. Reduction (p˂0.05) in the activities of antioxidant enzymes viz. acetylcholinesterase, arylesterase, superoxide dismutase, catalase, glutathione peroxidase, and reductase with increased levels of protein and lipid peroxidation was recorded in the liver, kidney, and heart of fluoride-administered rats. Fluoride exposure (100 ppm) induced lipid peroxidation was highest in kidney (4.4 times) followed by liver (2.6 times) and heart (2.5 times) and as compared to their respective control. The percent rise in protein oxidation at 30% was almost equal in the kidney and liver but was 21.5% in the heart as compared to control. The histopathological alterations observed included congestion and hemorrhage along with degeneration and necrosis of parenchymal cells in hepato-renal tissues and myocardium, severity of which varied in a dose-dependent manner. Taken together, fluoride distribution in the liver, heart, and kidney after chronic fluoride intake correlated well with fluoride-induced hepatic and cardio-renal toxicity in a concentration-dependent manner. These results draw attention that chronic fluoride intake pose a significant health risk for human and animal residents of fluoride endemic areas.

Neuroprotective effect of quercetin and Zingiber officinale on sodium arsenate-induced neurotoxicity in rats.

The study was aimed at determining the ameliorative potential of quercetin and Zingiber officinale (ZO) against sodium arsenate-induced neurotoxicity in male Wistar rats. Thirty adult animals were randomly allocated to five groups (n = 6). Group I served as control, groups II and IV were treated with ZO [300 mg/kg, PO (per os)/day], and group V animals were administered quercetin (50 mg/kg, PO/day) for 18 days. Groups III, IV, and V were injected with sodium arsenate (20 mg/kg, intraperitoneally/day) for 4 days starting from day 15. The administration of sodium arsenate resulted in a significant decrease in total antioxidant status, total thiols, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and aryl esterase in brain tissue of the animals compared with the control group. In addition, a significant increase was observed in malondialdehyde, advanced oxidation protein product and plasma nitric oxide levels, indicating oxidative stress-mediated neuronal damage. However, these arsenic-induced alterations were significantly reversed by quercetin or ZO in the treatment groups, indicating their ameliorative potential. These positive effects were further confirmed by histopathological examination of brain tissue revealing the suppression of severe neuronal injury, spongiosis and gliosis in the samples pretreated with quercetin and ZO. Our results suggest that inclusion of ZO and quercetin-rich foods in the diet can help in preventing the neurotoxic effects in areas with elevated levels of arsenic in food chain and ground water.

Protective Effect of Quercetin and Ginger (Zingiber officinale) Extract against Dimethoate Potentiated Fluoride-Induced Nephrotoxicity in Rats.

This study aimed to determine the potential of quercetin and Zingiber officinale (ZO) Roscoe extract to alleviate the renal damage induced by dimethoate (DM) and fluoride (F-) alone and by their combined exposure in rats. A total of 54 adult Wistar rats were randomly allocated to nine groups (n = 6). A sub-lethal dose of DM (1/10th of the median lethal dose) was administered by oral gavage alone and along with F- (4.5 ppm, three-fold the permissible limit) in their drinking water continuously for 28 days. Chromatographical analysis revealed the presence of quercetin, curcumin, and other phytochemicals with strong antioxidant properties in ZO-rhizome extract. Severe changes were observed in the levels of the renal biomarkers and histoarchitecture after co-administration of the toxicants, indicating greater kidney damage. The administration of ZO extract (300 mg/kg) along with either or both toxicants led to a significant restoration of the biochemical markers and renal antioxidant profile and histology.

Intervention of human breast cell carcinogenesis chronically induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine.

More than 85% of breast cancers are sporadic and attributable to long-term exposure to environmental carcinogens, such as those in the diet, through a multistep disease process progressing from non-cancerous to premalignant and malignant stages. The chemical carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is one of the most abundant heterocyclic amines found in high-temperature cooked meats and is recognized as a mammary carcinogen. However, the PhIP's mechanism of action in breast cell carcinogenesis is not clear. Here, we demonstrated, for the first time, that cumulative exposures to PhIP at physiologically achievable, pico to nanomolar concentrations effectively induced progressive carcinogenesis of human breast epithelial MCF10A cells from a non-cancerous stage to premalignant and malignant stages in a dose- and exposure-dependent manner. Progressive carcinogenesis was measured by increasingly- acquired cancer-associated properties of reduced dependence on growth factors, anchorage-independent growth, acinar-conformational disruption, proliferation, migration, invasion, tumorigenicity with metastasis and increased stem-like cell populations. These biological changes were accompanied by biochemical and molecular changes, including upregulated H-Ras gene expression, extracellular signal-regulated kinase (ERK) pathway activation, Nox-1 expression, reactive oxygen species (ROS) elevation, increased HIF-1α, Sp1, tumor necrosis factor-α, matrix metalloproteinase (MMP)-2, MMP-9, aldehyde dehydrogenase activity and reduced E-cadherin. The Ras-ERK-Nox-ROS pathway played an important role in not only initiation but also maintenance of cellular carcinogenesis induced by PhIP. Using biological, biochemical and molecular changes as targeted endpoints, we identified that the green tea catechin components epicatechin-3-gallate and epigallocatechin-3-gallate, at non-cytotoxic doses, were capable of suppressing PhIP-induced cellular carcinogenesis and tumorigenicity.

Dose-Dependent Oxidative Damage in Erythrocytes and Hepatic Tissue of Wistar Rats Concurrently Exposed with Arsenic and Quinalphos: a Subacute Study.

Concurrent exposure to a multitude of environmental toxicants pose serious health hazard to humans and animals. The present investigation was conceptualized to determine deleterious effects of concomitant subacute arsenic and quinalphos exposure on antioxidant responses of liver and erythrocytes of Wistar rats. Fifty-four Wistar rats were divided into nine groups with six animals in each. Animals were exposed to either quinalphos (1/100th and 1/10th of LD50) through oral gavage daily or arsenic (50 and 100 ppb) in drinking water alone and in combination for 28 days. While treatment with different toxicants alone also significantly reduced hemoglobin concentration, hepatic biomarkers and levels of antioxidant parameters as compared with control values, concomitant exposure significantly (P < 0.05) elevated levels of hepatic transaminases and alkaline phosphatase. Moreover, along with significant depletion in activities of SOD, CAT, TTH, AChE, and enzymes of glutathione complex, a significant enhancement of lipid peroxidation was also recorded in liver and erythrocytes in co-exposed animals in a dose-dependent manner when compared with exposure to individual toxicant. More severe alterations occurred in hepatic histo-architecture of rats receiving combined treatment as compared with those treated with either toxicant. Results indicated that oxidative damage in erythrocytes was more than that of the liver of rats on concomitant exposure of arsenic and quinalphos in a dose-dependent manner. In nutshell, our results revealed that combined treatment of quinalphos with arsenic potentiated toxic effects of either toxicant on antioxidant machinery of liver and erythrocytes and hepatic histomorphology of exposed Wistar rats.

Distribution of Fluoride in Plasma, Brain, and Bones and Associated Oxidative Damage After Induced Chronic Fluorosis in Wistar Rats.

The study was aimed to determine fluoride levels in plasma, brain, and bones of Wistar rats following chronic administration of fluoride at different dose levels and the consequent oxidative damage inflicted in these tissues. Brain histomorphology and bone radiographs were also evaluated to assess the extent of damage in these organs. Eighteen rats were randomly divided into three groups with six animals in each group. Group I served as control and groups II and III received 50 and 100 ppm fluoride in tap water, respectively for 180 days. A dose-dependent rise in the levels of fluoride in plasma, brain, and bones was observed in rats. Significant (P < 0.05) alterations in levels of total thiols, glutathione peroxidase, glutathione reductase, acetylcholinesterase, catalase, superoxide dismutase, lipids, as well as protein peroxidation in blood and brain were observed as compared to control in a dose-dependent manner. Radiological examination of bone revealed thinning of bone cortex with haphazard ossification, reduced bone density, and widening of marrow cavity indicating occurrence of flawed bone remodeling upon chronic fluoride exposure. Improper mineralization in bones of intoxicated rats indirectly reflected reduced bone tensile strength. Moreover, alterations in plasma Ca:P ratio and high levels of fluoride in bone ash indicated that chronic fluoride exposure leads to alterations in the bone matrix further corroborating the radio-graphical findings. Additionally, severe microscopic alterations were recorded in the cerebrum and cerebellum of treated rats which included neuronal necrosis, gliosis, spongiosis, perivascular cuffing, congestion, and hemorrhage which correlated well with oxidative changes induced by fluoride intoxication in the brain tissue of rats.

Insights from Client Experience with Injection Medroxyprogesterone Acetate (MPA) in India: Lessons from the Field.

Background: The injectable contraceptives have been recently added to the contraceptive basket of Government of India under the National Family Welfare program with the aim to reduce the unmet need of contraception in the country. The present study has been conducted to analyse the continuation rates and concerns among the acceptors of injection MPA. Materials and Methods: The present study was an ambispective observational study conducted in the out-patient department of family welfare division at a tertiary care hospital in New Delhi over a period of 6 months. The study enrolled 483 acceptors of injection MPA who were interviewed in person or telephonically, and a proforma was filled which included the demographic profile, obstetric history of the women, source of information about injection and its timing, number of doses received, side effects experienced and the compliance status. The data obtained was subjected to statistical analysis. Results: The mean age of the studied population was 28.44 ± 4.73 years and average parity was 2. It was found that injection MPA was initiated in the interval period in 304 women (63.3%), post-abortal in 124 (25.8%), and postnatal in 52 (10.8%). The source of information about the injection for most women was health workers (83.5%). Most women (74.3%) were pleased with the injection and showed their willingness to continue, and 67.7% were continuing with the injection at the time of interview. Menstrual irregularity was the most common side effect observed in 48.5% women. Conclusion: The present study showed a good continuation rate of injection MPA for the Indian population. The coverage for this excellent contraceptive modality can be enhanced further if more efforts to disseminate awareness about this method are made. Menstrual irregularity is the most common side effect causing discontinuation which can be mitigated to a significant extent with an effective pre-administration counseling.

First report of Przhevalskiana silenus derived recombinant hypodermin C based indirect ELISA for serodiagnosis of goat warble fly myiasis.

Goat warble fly infestation (GWFI) is a subcutaneous myiasis caused by larvae of Przhevalskiana silenus, an insect belonging to the order Diptera. The diagnosis of GWFI is challenging in the early larval instars (L1 and L2) as they are occult under the skin and hair coat causing prolonged economic loss in form of meat and hide damage. This necessitates early diagnosis for disease control at herd level and its prophylactic management to prevent economic losses. Hypodermins, a class of serine proteases from Hypoderminae subfamily have been used as serodiagnostic antigens for the past four decades for diagnosis of warble fly myiasis. In this study,the immunodominant antigen Hypodermin C (HyC) from P. silenus has been recombinantly expressed in E. coli and immunogenic characterisation of expressed protein was done. The protein shows hallmark residues in conserved cysteine and catalytic triad typical of serine proteases along with similar profile of immunoreactivity towards Hypoderminae infestation. The present study reports an optimised indirect-ELISA based on recombinant HyC derived from P. silenus for early diagnosis of GWFI. The optimised indirect ELISA provides a sensitive and specific immunodiagnostic for mass surveillance of the GWFI with diagnostic specificity and sensitivity of 96% and 100%, respectively and not showing any cross reactivity against other important parasitic and bacterial diseases of goats. This study presents the first report of indirect ELISA based on recombinant Hypodermin C antigen derived from P. silenus for the serosurveillance of goat warble fly disease.

Neuroprotective potential of hydroethanolic hull extract of Juglans regia L. on isoprenaline induced oxidative damage in brain of Wistar rats.

The study was aimed at assessing isoprenaline (ISO) induced oxidative damage in brain of Wistar rats and its protection by hydroethanolic hull extract of Juglans regia. Administration of ISO significantly increases catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), malondialdehyde (MDA) and advanced oxidation protein product (AOPP) levels and significantly reduced activities of antioxidant status (TAS), total thiols (TTH), acetylcholinesterase (AChE), arylesterase (AE), and glutathione peroxidase (GPx) in rat brain. Histopathologically, neuronal degeneration, spongiosis and gliosis were seen in cerebral cortex after ISO administration. Pretreatment with hull extract restored TAS, TTH, AChE, CAT and SOD values. Additionally, significant reductions were noted in levels of MDA, AOPP, and severity of histomorphological changes in cerebral cortex following hull extract treatment. Altered antioxidant biomarkers along with histopathological changes indicate oxidative injury in rat brain following ISO administration. Repeated administration of J. regia hull extract demonstrating presence of neuroprotective properties against ISO induced oxidative damage in rat brain.

Increasing postpartum IUCD coverage through a QI initiative: a step towards reducing the unmet need of postpartum contraception.

BACKGROUND: Unintended pregnancies have a negative impact on the health and economy of a nation, which can be prevented by effective family planning (FP) services. Postpartum intrauterine device (PPIUCD) is a safe and effective FP method which allows women to obtain long-acting contraception before discharge from the point of delivery. We observed poor coverage of deliveries with PPIUCD at our facility. This was the trigger to initiate a quality improvement (QI) initiative to increase the PPIUCD coverage from current rate of 4.5%-10% in 3-month period. METHOD: A fishbone analysis of the problem was done and the following causes were identified: lack of focused counselling for FP, lack of sensitisation and training of resident doctors and inconsistent supply of intrauterine contraceptive devices (IUCDs). A QI team was constituted with representatives from faculty members, residents, interns, nursing officers and FP counsellors. The point of care quality improvement methodology was used. INTERVENTIONS: Daily counselling of antenatal women was started by the counsellors and interns in antenatal wards. A WhatsApp group of residents was made initially to sensitise them; and later for parking of problems and trouble shooting. The residents were provided hands-on training at skills lab. Uninterrupted supply of IUCDs was ensured by provision of buffer stock of IUCDs with respective store keepers. RESULT: The PPIUCD insertion rates improved from 4.5% to 19.2% at 3 months and have been sustained to a current 30%-35% after 1 ½ years of initiation of the project tiding through the turbulence during the COVID-19 pandemic using QI techniques. CONCLUSION: Sensitisation and training of residents as well as creation of awareness among antenatal women through targeted counselling helped improve PPIUCD coverage at the facility. QI initiatives have the potential to facilitate effective implementation of the FP programmes by strategic utilisation of the resources.

Maximum contaminant level of arsenic in drinking water potentiates quinalphos-induced renal damage on co-administration of both arsenic and quinalphos in Wistar rats.

This study was designed to determine alterations in renal biomarkers, antioxidant profile, and histomorphology of renal tissue following subacute exposure to quinalphos alone or in conjunction with arsenic in rats. A total of 54 adult Wistar rats were randomly divided into nine groups of six rats each and were administered sub-lethal concentrations of quinalphos (1/100th and 1/10th of LD50) orally daily and arsenic (50 and 100 ppb) in drinking water for 28 days. Significantly (p < 0.05) decreased levels of antioxidant biomarkers in renal tissue, viz., total thiols, catalase, superoxide dismutase, glutathione peroxidase, glutathione-s-transferase, and glutathione reductase along with increased (p < 0.05) thiobarbituric acid reacting substance (TBRAS) levels indicated that significant oxidative damage to renal tissue occurred following repeated administrations of quinalphos at either dose levels or arsenic at the concentration of 100 ppb when compared with the control rats. The alterations in the antioxidant parameters were observed to be more pronounced in co-administered groups as compared with either toxicant administered group. Similarly, activity of renal acetylcholinesterase was decreased after repeated exposure to quinalphos or arsenic, but inhibition was higher (up to 48%) in rat renal tissue co-exposed with quinalphos and arsenic at the higher concentration. These findings corroborated with the histopathological alterations in renal tissue of toxicant exposed rats. The altered plasma and tissue antioxidant biomarkers along with histopathological changes in the kidney at higher dose level of either toxicant indicate that renal tissue is significantly impacted by these toxicants, and these effects become more pronounced after their co-administration.

The major threshability genes soft glume (sog) and tenacious glume (Tg), of diploid and polyploid wheat, trace their origin to independent mutations at non-orthologous loci.

Threshability is an important crop domestication trait. The wild wheat progenitors have tough glumes enveloping the floret that make spikes difficult to thresh, whereas cultivated wheats have soft glumes and are free-threshing. In hexaploid wheat, the glume tenacity gene Tg along with the major domestication locus Q control threshability. The Q gene was isolated recently and found to be a member of the AP2 class of transcription factors. However, only a few studies have reported on the tough glume trait. Here, we report comparative mapping of the soft glume (sog) gene of diploid Triticum monococcum L. and tenacious glume (Tg) gene of hexaploid T. aestivum L. using chromosome-specific SSR and RFLP markers. The sog gene was flanked by Xgwm71 and Xbcd120 in a 6.8 cM interval on chromosome 2A(m)S of T. monococcum whereas Tg was targeted to a 8.1 cM interval flanked by Xwmc503 and Xfba88 on chromosome 2DS of T. aestivum. Deletion bin mapping of the flanking markers assigned sog close to the centromere on 2AS, whereas Tg was mapped to the most distal region on 2DS. Both 2AS and 2DS maps were colinear ruling out the role of chromosome rearrangements for their non-syntenic positions. Therefore, sog and Tg are not true orthologues suggesting the possibility of a diverse origin.