Mukesh Verma - Academia.edu (original) (raw)

Papers by Mukesh Verma

Journal of Allergy and Clinical Immunology, 2018

Journal of Allergy and Clinical Immunology, 2019

Journal of Allergy and Clinical Immunology, 2020

The Journal of allergy and clinical immunology, Jan 10, 2017

IL-33 plays an important role in the development of experimental asthma. We sought to study the r... more IL-33 plays an important role in the development of experimental asthma. We sought to study the role of the IL-33 receptor suppressor of tumorigenicity 2 (ST2) in the persistence of asthma in a mouse model. We studied allergen-induced experimental asthma in ST2 knockout (KO) and wild-type control mice. We measured airway hyperresponsiveness by using flexiVent; inflammatory indices by using ELISA, histology, and real-time PCR; and type 2 innate lymphoid cells (ILC2s) in lung single-cell preparations by using flow cytometry. Airway hyperresponsiveness was increased in allergen-treated ST2 KO mice and comparable with that in allergen-treated wild-type control mice. Peribronchial and perivascular inflammation and mucus production were largely similar in both groups. Persistence of experimental asthma in ST2 KO mice was associated with an increase in levels of thymic stromal lymphopoietin (TSLP), IL-9, and IL-13, but not IL-5, in bronchoalveolar lavage fluid. Expectedly, ST2 deletion cau...

The Journal of allergy and clinical immunology, Jan 19, 2017

ILC2s represent an important type 2 immune cell. Glucocorticoid regulation of human ILC2s is larg... more ILC2s represent an important type 2 immune cell. Glucocorticoid regulation of human ILC2s is largely unknown. To assess steroid resistance of human blood and airway ILC2s from asthmatic patients and examine its mechanism of induction. We studied human blood and lung ILC2s from asthmatic and control subjects by flow cytometry and ELISA. Dexamethasone (Dex) inhibited (P=0.04) CRTH2 and type 2 cytokine expression by blood ILC2s stimulated with IL25 and IL33. However, it failed to do so when ILC2s were stimulated with IL7 and TSLP, two ligands of IL7Rα. Unlike blood ILC2s, BAL ILC2s from asthmatic patients were resistant to Dex. BAL from the asthmatic patients had elevated TSLP but not IL7. The BAL TSLP level correlated (r=0.74) with steroid resistance of ILC2s. TSLP was synergistically induced in epithelial cells by IL13 and human rhinovirus. Mechanistically, Dex upregulated ILC2 expression of IL7Rα , which augmented and sustained STAT5 signaling by TSLP. TSLP induced MEK, c-Fos, ID3, ...

The Journal of allergy and clinical immunology, Jan 2, 2017

Despite the progress in diagnosis and management of asthma, many patients have poorly controlled ... more Despite the progress in diagnosis and management of asthma, many patients have poorly controlled or refractory asthma. The mechanism of this refractory asthma is not well understood. Explore the relationship between neutrophils and other biomarkers of refractory asthma. Sixty subjects with refractory asthma (RA), 30 with non-refractory asthma (NRA) and 20 healthy subjects were enrolled. We performed a comprehensive characterization of these study subjects, which included laboratory and pulmonary function studies, chest CT, and bronchoscopy with bronchoalveolar lavage. We analyzed BAL and serum for a total of 244 biomolecules by multiplex assay and correlated them with the clinical and other laboratory parameters. RA was significantly different from NRA with regard to pulmonary function indices, bronchial basement membrane thickness, and BAL neutrophils and lymphocytes but not eosinophils. BAL neutrophils negatively and positively correlated with the forced vital capacity and age, re...

Molecular biology reports, 2015

Nicotine aggravates many chronic inflammatory disorders in females under the protein-malnourished... more Nicotine aggravates many chronic inflammatory disorders in females under the protein-malnourished conditions because women are more susceptible to nicotine-induced diseases due to their low innate immunity. Although curcumin have been found to obliterate the nicotine-induced disorders through its anti-nicotinic activity under the protein-malnourished condition, the exact mechanism of protective action of curcumin is still unclear. Female Wister rats maintained under the normal and protein-restricted diets in two separate groups were injected with the effective dose of nicotine-tartrate (2.5 mg/kg body weight/day, subcutaneously) and supplemented with the effective dose of curcumin (80 mg/kg body weight/day, orally) for 21 days. The morphology of red blood cells (RBCs), molecular docking, lipid profile and activities of antioxidant enzymes in tissues, cytokines profiling (T helper cell type 1; and T helper cell type 2), mRNA and protein expression of cytokines, transcription factors ...

Molecular Biology Reports, 2012

Spatula DD - Peer Reviewed Journal on Complementary Medicine and Drug Discovery, 2014

Archives of Toxicology, 2010

Molecular Biology Reports, 2014

Molecular Biology Reports, 2014

Many studies have suggested that adenosine diphosphate ribosyl transferase (ADPRT), X-ray repair ... more Many studies have suggested that adenosine diphosphate ribosyl transferase (ADPRT), X-ray repair cross-complementing 1 (XRCC1), and xeroderma pigmentosum complementary group D (XPD) are three major DNA base excision repair (BER) genes and that they act interactively in stimulating and executing BER processes. Polymorphisms of these genes may influence the rate of gene transcription, the stability of the messenger RNA, or the quantity and activity of the resulting protein. Thus, the susceptibility or severity of several disorders is influenced by possession of specific alleles of polymorphic genes. So, it is plausible that variations and mutations in these genes affect DNA repair capacity in normal populations, and thus facilitate cancer development in normal or exposed individuals. To promote translation of scientific findings for potential clinical application of DNA repair function, we have searched publications relevant to molecular epidemiology studies of associations between single-nucleotide polymorphisms (SNPs) in the genes, and several frequent human cancer. We have focused on five particular polymorphisms as our starting point: the T-->C polymorphism (Val762Ala) in exon 17 of ADPRT, the novel transition at the promoter region (-77T-->C) of XRCC1, two common nonsynonymous polymorphisms (Arg194Trp and Arg399Gln), and the C-->A silent polymorphism (Arg156Arg) in exon 6 of XPD. We review here the case-control studies examining whether these polymorphisms are correlated with reduced DNA repair efficiency, their influence on the development of different solid tumors, and their possible interactions with other genetic factors and environmental exposures.

Page 1. 41 Molecular markers of cervical squamous cell carcinoma DEEPAK KUMAR1, PH.D., MUKESH VER... more Page 1. 41 Molecular markers of cervical squamous cell carcinoma DEEPAK KUMAR1, PH.D., MUKESH VERMA2, PH.D. Department of Biological and Environmental Sciences, University of the District of Columbia, Washington1 ...

Experimental and Clinical Immunogenetics, Feb 1, 1994

To examine the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on thymic gene expression in... more To examine the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on thymic gene expression in vitro, freshly isolated rat thymocytes were incubated with 10 nM TCDD, and reverse transcriptase polymerase chain reaction experiments were performed using primers specific for prostaglandin G/H synthase (PGHS) and glyceraldehyde 3-phosphate dehydrogenase. TCDD selectively repressed PGHS gene expression, with maximal inhibition occurring within 60 min. Gel retardation assays demonstrated that dioxin transiently induced binding of the ubiquitous transcription factor NF kappa B to its cognate response element at early time points. However, TCDD had little ability to induce transformation of the Ah receptor to the xenobiotic responsive element in thymic cytosol. These results indicate that TCDD exerts changes in thymocyte gene expression prior to inducing toxicity.

Childhood leukemia is the most common cancer among children, representing 31% of all cancer cases... more Childhood leukemia is the most common cancer among children, representing 31% of all cancer cases occurring in children younger than the age of 15 years in the USA. There are only few known risk factors of childhood leukemia (sex, age, race, exposure to ionizing radiation, and certain congenital diseases, such as Down syndrome and neurofibromatosis), which account for only 10% of the childhood leukemia cases. Several lines of evidence suggest that childhood leukemia may be more due to environmental rather than genetic factors, although genes may play modifying roles. Human and animal studies showed that the development of childhood leukemia is a two-step process that requires a prenatal initiating event(s) plus a postnatal promoting event(s). Despite a substantial public health effort to reduce cigarette smoking, a large proportion of the US and world population still smoke. Tobacco smoke contains at least 60 known human or animal carcinogens, with the major chemical classes being volatile hydrocarbons, aldehydes, aromatic amines, polycyclic aromatic hydrocarbons, and nitrosamines; among these chemicals, only benzene is an established leukemogen, although other chemicals in the tobacco could interact with one another in a complex way to jointly attain a significant carcinogenic effect on the development of leukemia. Although tobacco smoke is an established risk factor for adult myeloid leukemia, the studies of association between parental smoking and childhood leukemia have produced inconsistent results. The majority of the studies on maternal smoking and childhood leukemia did not find a significant positive association and some even reported an inverse association. In contrast to studies of maternal smoking, studies of paternal smoking and childhood leukemia reported more positive associations but only by less than half of the studies. Future directions to be considered for improving the study of parental smoking and childhood leukemia are: 1) consider all sources of benzene exposure in addition to smoking, including occupational exposure and traffic exhausts; 2) childhood leukemia is a heterogeneous disease and epidemiologic studies of childhood leukemia can be greatly improved by grouping childhood leukemia into more homogeneous groups by molecular techniques (e.g., structural and numerical chromosomal changes); and 3) assess gene-environment interaction. It is hoped that through the continual effort, more will be uncovered regarding the causes of childhood leukemia. In the meantime, more effort should be spent on educating the parents to quit smoking, because parental smoking is known to affect many childhood diseases (e.g., asthma, respiratory tract infection, and otitis media) that are much more prevalent than childhood leukemia.

Http Dx Doi Org 10 1080 00206810902895337, Oct 15, 2009

... Авторы, A. Maheshwari, SK Rajput, M. Verma Department of Geology, University of Rajasthan, Ja... more ... Авторы, A. Maheshwari, SK Rajput, M. Verma Department of Geology, University of Rajasthan, Jaipur M. Coltorti Istituto di Mineralogia, Universita di Ferrara, Ferrara. Журнал, International Geology Review. Издательство, VH Winston & Sons, Inc. ...

Clinical Cancer Research an Official Journal of the American Association For Cancer Research, May 1, 2001

Sensor Letters, 2012

ABSTRACT

Biochemistry International, Aug 1, 1987

Enolase is a vital enzyme of the glycolytic pathway. It exists mainly in two forms, non-neuronal ... more Enolase is a vital enzyme of the glycolytic pathway. It exists mainly in two forms, non-neuronal enolase (NNE) and neuron specific enolase (NSE). Neurospora crassa, a filamentous fungus, was used as the source of pure NNE, and by using DEAE-cellulose and a Sephadex G-150 column chromatography highly purified enzyme (20.4 fold purification with 54.7 percent recovery) was obtained. The development profile of the enzyme shows a peak value after 90 hours of mycelial growth from conidia of N. crassa. In this respect, it differs from neuroblastoma NSE where the peak value of the enzyme activity appears 7 1/2 hours after the splitting of the cells. N. crassa enolase (NNE) is more thermolabile than NG108 NSE and N. crassa enolase is more sensitive to urea, chloride, and fluorophosphate. The Km values for 2-phosphoglycerate and Mg++ were 0.34 mM and 0.47 mM, respectively, for N. crassa enolase, whereas these values were 1.1 mM and 3.1 mM, respectively, in the case of neuroblastoma NSE. N. crassa enolase is a dimer molecule of molecular weight 85,000 daltons. N. crassa enolase is not neutralized by NSE antisera and neutralized by NNE antisera as opposed to neuroblastoma NSE.

Journal of Allergy and Clinical Immunology, 2018

Journal of Allergy and Clinical Immunology, 2019

Journal of Allergy and Clinical Immunology, 2020

The Journal of allergy and clinical immunology, Jan 10, 2017

IL-33 plays an important role in the development of experimental asthma. We sought to study the r... more IL-33 plays an important role in the development of experimental asthma. We sought to study the role of the IL-33 receptor suppressor of tumorigenicity 2 (ST2) in the persistence of asthma in a mouse model. We studied allergen-induced experimental asthma in ST2 knockout (KO) and wild-type control mice. We measured airway hyperresponsiveness by using flexiVent; inflammatory indices by using ELISA, histology, and real-time PCR; and type 2 innate lymphoid cells (ILC2s) in lung single-cell preparations by using flow cytometry. Airway hyperresponsiveness was increased in allergen-treated ST2 KO mice and comparable with that in allergen-treated wild-type control mice. Peribronchial and perivascular inflammation and mucus production were largely similar in both groups. Persistence of experimental asthma in ST2 KO mice was associated with an increase in levels of thymic stromal lymphopoietin (TSLP), IL-9, and IL-13, but not IL-5, in bronchoalveolar lavage fluid. Expectedly, ST2 deletion cau...

The Journal of allergy and clinical immunology, Jan 19, 2017

ILC2s represent an important type 2 immune cell. Glucocorticoid regulation of human ILC2s is larg... more ILC2s represent an important type 2 immune cell. Glucocorticoid regulation of human ILC2s is largely unknown. To assess steroid resistance of human blood and airway ILC2s from asthmatic patients and examine its mechanism of induction. We studied human blood and lung ILC2s from asthmatic and control subjects by flow cytometry and ELISA. Dexamethasone (Dex) inhibited (P=0.04) CRTH2 and type 2 cytokine expression by blood ILC2s stimulated with IL25 and IL33. However, it failed to do so when ILC2s were stimulated with IL7 and TSLP, two ligands of IL7Rα. Unlike blood ILC2s, BAL ILC2s from asthmatic patients were resistant to Dex. BAL from the asthmatic patients had elevated TSLP but not IL7. The BAL TSLP level correlated (r=0.74) with steroid resistance of ILC2s. TSLP was synergistically induced in epithelial cells by IL13 and human rhinovirus. Mechanistically, Dex upregulated ILC2 expression of IL7Rα , which augmented and sustained STAT5 signaling by TSLP. TSLP induced MEK, c-Fos, ID3, ...

The Journal of allergy and clinical immunology, Jan 2, 2017

Despite the progress in diagnosis and management of asthma, many patients have poorly controlled ... more Despite the progress in diagnosis and management of asthma, many patients have poorly controlled or refractory asthma. The mechanism of this refractory asthma is not well understood. Explore the relationship between neutrophils and other biomarkers of refractory asthma. Sixty subjects with refractory asthma (RA), 30 with non-refractory asthma (NRA) and 20 healthy subjects were enrolled. We performed a comprehensive characterization of these study subjects, which included laboratory and pulmonary function studies, chest CT, and bronchoscopy with bronchoalveolar lavage. We analyzed BAL and serum for a total of 244 biomolecules by multiplex assay and correlated them with the clinical and other laboratory parameters. RA was significantly different from NRA with regard to pulmonary function indices, bronchial basement membrane thickness, and BAL neutrophils and lymphocytes but not eosinophils. BAL neutrophils negatively and positively correlated with the forced vital capacity and age, re...

Molecular biology reports, 2015

Nicotine aggravates many chronic inflammatory disorders in females under the protein-malnourished... more Nicotine aggravates many chronic inflammatory disorders in females under the protein-malnourished conditions because women are more susceptible to nicotine-induced diseases due to their low innate immunity. Although curcumin have been found to obliterate the nicotine-induced disorders through its anti-nicotinic activity under the protein-malnourished condition, the exact mechanism of protective action of curcumin is still unclear. Female Wister rats maintained under the normal and protein-restricted diets in two separate groups were injected with the effective dose of nicotine-tartrate (2.5 mg/kg body weight/day, subcutaneously) and supplemented with the effective dose of curcumin (80 mg/kg body weight/day, orally) for 21 days. The morphology of red blood cells (RBCs), molecular docking, lipid profile and activities of antioxidant enzymes in tissues, cytokines profiling (T helper cell type 1; and T helper cell type 2), mRNA and protein expression of cytokines, transcription factors ...

Molecular Biology Reports, 2012

Spatula DD - Peer Reviewed Journal on Complementary Medicine and Drug Discovery, 2014

Archives of Toxicology, 2010

Molecular Biology Reports, 2014

Molecular Biology Reports, 2014

Many studies have suggested that adenosine diphosphate ribosyl transferase (ADPRT), X-ray repair ... more Many studies have suggested that adenosine diphosphate ribosyl transferase (ADPRT), X-ray repair cross-complementing 1 (XRCC1), and xeroderma pigmentosum complementary group D (XPD) are three major DNA base excision repair (BER) genes and that they act interactively in stimulating and executing BER processes. Polymorphisms of these genes may influence the rate of gene transcription, the stability of the messenger RNA, or the quantity and activity of the resulting protein. Thus, the susceptibility or severity of several disorders is influenced by possession of specific alleles of polymorphic genes. So, it is plausible that variations and mutations in these genes affect DNA repair capacity in normal populations, and thus facilitate cancer development in normal or exposed individuals. To promote translation of scientific findings for potential clinical application of DNA repair function, we have searched publications relevant to molecular epidemiology studies of associations between single-nucleotide polymorphisms (SNPs) in the genes, and several frequent human cancer. We have focused on five particular polymorphisms as our starting point: the T-->C polymorphism (Val762Ala) in exon 17 of ADPRT, the novel transition at the promoter region (-77T-->C) of XRCC1, two common nonsynonymous polymorphisms (Arg194Trp and Arg399Gln), and the C-->A silent polymorphism (Arg156Arg) in exon 6 of XPD. We review here the case-control studies examining whether these polymorphisms are correlated with reduced DNA repair efficiency, their influence on the development of different solid tumors, and their possible interactions with other genetic factors and environmental exposures.

Page 1. 41 Molecular markers of cervical squamous cell carcinoma DEEPAK KUMAR1, PH.D., MUKESH VER... more Page 1. 41 Molecular markers of cervical squamous cell carcinoma DEEPAK KUMAR1, PH.D., MUKESH VERMA2, PH.D. Department of Biological and Environmental Sciences, University of the District of Columbia, Washington1 ...

Experimental and Clinical Immunogenetics, Feb 1, 1994

To examine the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on thymic gene expression in... more To examine the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on thymic gene expression in vitro, freshly isolated rat thymocytes were incubated with 10 nM TCDD, and reverse transcriptase polymerase chain reaction experiments were performed using primers specific for prostaglandin G/H synthase (PGHS) and glyceraldehyde 3-phosphate dehydrogenase. TCDD selectively repressed PGHS gene expression, with maximal inhibition occurring within 60 min. Gel retardation assays demonstrated that dioxin transiently induced binding of the ubiquitous transcription factor NF kappa B to its cognate response element at early time points. However, TCDD had little ability to induce transformation of the Ah receptor to the xenobiotic responsive element in thymic cytosol. These results indicate that TCDD exerts changes in thymocyte gene expression prior to inducing toxicity.

Childhood leukemia is the most common cancer among children, representing 31% of all cancer cases... more Childhood leukemia is the most common cancer among children, representing 31% of all cancer cases occurring in children younger than the age of 15 years in the USA. There are only few known risk factors of childhood leukemia (sex, age, race, exposure to ionizing radiation, and certain congenital diseases, such as Down syndrome and neurofibromatosis), which account for only 10% of the childhood leukemia cases. Several lines of evidence suggest that childhood leukemia may be more due to environmental rather than genetic factors, although genes may play modifying roles. Human and animal studies showed that the development of childhood leukemia is a two-step process that requires a prenatal initiating event(s) plus a postnatal promoting event(s). Despite a substantial public health effort to reduce cigarette smoking, a large proportion of the US and world population still smoke. Tobacco smoke contains at least 60 known human or animal carcinogens, with the major chemical classes being volatile hydrocarbons, aldehydes, aromatic amines, polycyclic aromatic hydrocarbons, and nitrosamines; among these chemicals, only benzene is an established leukemogen, although other chemicals in the tobacco could interact with one another in a complex way to jointly attain a significant carcinogenic effect on the development of leukemia. Although tobacco smoke is an established risk factor for adult myeloid leukemia, the studies of association between parental smoking and childhood leukemia have produced inconsistent results. The majority of the studies on maternal smoking and childhood leukemia did not find a significant positive association and some even reported an inverse association. In contrast to studies of maternal smoking, studies of paternal smoking and childhood leukemia reported more positive associations but only by less than half of the studies. Future directions to be considered for improving the study of parental smoking and childhood leukemia are: 1) consider all sources of benzene exposure in addition to smoking, including occupational exposure and traffic exhausts; 2) childhood leukemia is a heterogeneous disease and epidemiologic studies of childhood leukemia can be greatly improved by grouping childhood leukemia into more homogeneous groups by molecular techniques (e.g., structural and numerical chromosomal changes); and 3) assess gene-environment interaction. It is hoped that through the continual effort, more will be uncovered regarding the causes of childhood leukemia. In the meantime, more effort should be spent on educating the parents to quit smoking, because parental smoking is known to affect many childhood diseases (e.g., asthma, respiratory tract infection, and otitis media) that are much more prevalent than childhood leukemia.

Http Dx Doi Org 10 1080 00206810902895337, Oct 15, 2009

... Авторы, A. Maheshwari, SK Rajput, M. Verma Department of Geology, University of Rajasthan, Ja... more ... Авторы, A. Maheshwari, SK Rajput, M. Verma Department of Geology, University of Rajasthan, Jaipur M. Coltorti Istituto di Mineralogia, Universita di Ferrara, Ferrara. Журнал, International Geology Review. Издательство, VH Winston & Sons, Inc. ...

Clinical Cancer Research an Official Journal of the American Association For Cancer Research, May 1, 2001

Sensor Letters, 2012

ABSTRACT

Biochemistry International, Aug 1, 1987

Enolase is a vital enzyme of the glycolytic pathway. It exists mainly in two forms, non-neuronal ... more Enolase is a vital enzyme of the glycolytic pathway. It exists mainly in two forms, non-neuronal enolase (NNE) and neuron specific enolase (NSE). Neurospora crassa, a filamentous fungus, was used as the source of pure NNE, and by using DEAE-cellulose and a Sephadex G-150 column chromatography highly purified enzyme (20.4 fold purification with 54.7 percent recovery) was obtained. The development profile of the enzyme shows a peak value after 90 hours of mycelial growth from conidia of N. crassa. In this respect, it differs from neuroblastoma NSE where the peak value of the enzyme activity appears 7 1/2 hours after the splitting of the cells. N. crassa enolase (NNE) is more thermolabile than NG108 NSE and N. crassa enolase is more sensitive to urea, chloride, and fluorophosphate. The Km values for 2-phosphoglycerate and Mg++ were 0.34 mM and 0.47 mM, respectively, for N. crassa enolase, whereas these values were 1.1 mM and 3.1 mM, respectively, in the case of neuroblastoma NSE. N. crassa enolase is a dimer molecule of molecular weight 85,000 daltons. N. crassa enolase is not neutralized by NSE antisera and neutralized by NNE antisera as opposed to neuroblastoma NSE.