Last edited by Arashijar
Friday, May 1, 2020 | History

2 edition of Molecular and cellular mechanisms of sulfur mustard-induced lesions of human skin found in the catalog.

Molecular and cellular mechanisms of sulfur mustard-induced lesions of human skin

  • 206 Want to read
  • 40 Currently reading

Published by NKB Offset BV in Bleiswijk .
Written in English

    Subjects:
  • Mustard gas -- Toxicology.,
  • Dermatotoxicology.

  • Edition Notes

    Statementdoor Maria Anna Elisabeth Mol.
    Classifications
    LC ClassificationsRA1247.M8 M65 1992
    The Physical Object
    Pagination147 p. :
    Number of Pages147
    ID Numbers
    Open LibraryOL1454354M
    LC Control Number93108230

    Mustard Gas is a pale yellow, oily, highly toxic, volatile, liquid alkylating compound with a sweet to garlic-like odor that evaporates to a poisonous gas. Mustard gas is a vesicant that was first used in chemical warfare in World War I, but is now only used in small amounts in research studies involving alkylating agents.   Read "Modulation of sulfur mustard induced cell death in human epidermal keratinocytes using IL‐10 and TNF‐α, Journal of Biochemical and Molecular Toxicology (Formerly Journal of Biochemical Toxicology)" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.   Sulfur mustard (SM) is a blister-forming agent that has been used as a chemical weapon. Sulfur mustard can cause damage in various organs, especially the skin, respiratory system, and eyes. Generally, the multiple complications of mustard gas result from its alkalizing potency; it reacts with cellular components like DNA, RNA, proteins, and lipid membranes. Cited by: Objective. Sulfur mustard (SM) is a highly reactive alkylating agent which produces ocular, respiratory, and skin damages. Eyes are the most sensitive organ to SM due to high intrinsic metabolic and rapid turnover rate of corneal epithelium and aqueous-mucous interfaces of the cornea and conjunctiva. Here we investigate underlying molecular mechanism of SM Cited by: 5.

      The formation of human skin involves a cascade of biochemical signals, which are not well understood. However, they are very important since their failure may cause diseases, such as Atopic.


Share this book
You might also like
Action monitoring for effectiveness

Action monitoring for effectiveness

Miscellaneous poetical novels or tales ... of wit and gallantry in both sexes.

Miscellaneous poetical novels or tales ... of wit and gallantry in both sexes.

Arabian destiny

Arabian destiny

Social sciences in the Soviet Baltic Republics.

Social sciences in the Soviet Baltic Republics.

New methods of resolving old disputes in bankruptcy

New methods of resolving old disputes in bankruptcy

Agricultural and rural development in Indonesia

Agricultural and rural development in Indonesia

Book Report Book for Primary Grades

Book Report Book for Primary Grades

On the presence of arsenic in the body and its secretion by the kidney

On the presence of arsenic in the body and its secretion by the kidney

A personal approach to teaching

A personal approach to teaching

Meditations on hope

Meditations on hope

Molecular and cellular mechanisms of sulfur mustard-induced lesions of human skin by Maria Anna Elisabeth Mol Download PDF EPUB FB2

Sulfur mustard (SM) is a strong alkylating agent, which produces subepidermal blisters, erythema and inflammation after skin contact. Despite the well-described SM-induced gross and histopathological changes, the exact underlying molecular mechanisms of these events are still a matter of research.

Sulfur mustard (SM) is a strong alkylating agent, which produces subepidermal blisters, erythema and inflammation after skin contact. Despite the well-described SM-induced gross and histopathological changes, the exact underlying molecular mechanisms of these events are still a matter of by: Objective: Sulfur mustard (SM) is a potent alkylating agent that can induce severe cutaneous injury.

Though much is known regarding the gross pathology of SM injury, the molecular and cellular basis for this pathology is not well by: Objective: Sulfur mustard (SM) is a potent alkylating agent that can induce severe cu. taneous injury. Though much is known regarding the gross pathology of SM injury, the.

molecular and cellular basis for this pathology is not well understood. Effective medical treatment and preventive measures for chemical warfare agent sulfur mustard (HD)-caused incapacitating skin toxicity are lacking, owing to limited knowledge of its mechanism of action.

The proliferating basal epidermal cells are primary major sites of attack during HD-caused skin by: Sulfur mustard induced mast cell degranulation in mouse skin is inhibited by a novel anti-inflammatory and anticholinergic bifunctional prodrug Author links open overlay panel Laurie B.

Joseph a Gabriella M. Composto a Roberto M. Perez a Hong-Duck Kim b Robert P. Casillas c Ned D. Heindel d Sherri C. Young d Carl J. Lacey d Jaya Saxena d Christophe D. Guillon d Cited by: 6. Sulfur mustard (SM) is a potent alkylating agent that can induce severe cutaneous injury.

Though much is known regarding the gross pathology of SM injury, the molecular and cellular. Skin is the fi rst organ exposed to sulfur mustard (SM). The mechanism of SM-induced cutaneous injury has not been fully clarifi ed so far, which.

The chemical warfare agent sulfur mustard (SM) severely affects the regeneration capacity of skin. The underlying molecular and cellular mechanisms, however, are far from clear. Review Mechanism and treatment of sulfur mustard-induced cutaneous injury Gu Tianyi, * [email protected] Medical Unit, Armed Forces, WuxiJiangshu Province, China Medical Unit, Armed Forces Wuxi Jiangshu Province, China * Tel: Abstract Skin is the first organ exposed to sulfur mustard (SM).

The mechanism of SM-induced cutaneous injury Cited by: 5. Molecular and cellular mechanisms of sulfur mustard-induced ().

Pagina-navigatie: Main; Save publication. Save as MODS; Export to Mendeley; Save as EndNote; Export to RefWorks; Title: Molecular and cellular mechanisms of sulfur mustard-induced lesions of human skin: Author: Mol, M.A.E. Degree grantor: TU Delft, Delft University of Cited by: 2.

Effective medical treatment and preventive measures for chemical warfare agent sulfur mustard (HD)-caused incapacitating skin toxicity are lacking, because of limited knowledge of its mechanism of action. The proliferating basal epidermal cells are primary major sites of attack during HD-caused skin injury.

Therefore, employing mouse JB6 and human HaCaT Cited by: Sulfur mustard (2,2-dichlorodiethyl sulfide, HD) is a chemical warfare agent that is a threat to both troops and civilians. The focus of HD research has been on intracellular adduct formation leading to apoptosis and/or necrosis in cutaneous by: Molecular and cellular mechanisms of sulfur mustard-induced lesions of human skinCited by: 2.

Modulation of sulfur mustard induced cell death in human Molecular and cellular mechanisms of sulfur mustard-induced lesions of human skin book keratinocytes using IL and TNF-alpha. Molecular basis for mustard-induced vesication. Fundam Appl Toxicol. ;5(6 pt 2):S– Molecular mechanism of the cytotoxic action of difunctional alkylating agents and of resistance to this : Albert L.

Ruff and James F. Dillman. Uri Wormser, Berta Brodsky, Elena Proscura, Julie F. Foley, Tinette Jones and Abraham Nyska, Involvement of tumor necrosis factor-α in sulfur mustard-induced skin lesion; effect of topical iodine, Archives of Toxicology, /s, 79, 11, (), ().Cited by: Introduction.

Sulfur mustard [bis (2-chloroethyl) sulfide, SM], a vesicant, poses a potential threat of being used as a chemical warfare and terrorist weapon (Saladi et al.,Sharma et al.,Smith et al.,Smith and Skelton, ).It is a bi-functional alkylating agent which causes severe skin injuries with delayed vesication, and has been used in World War I and II Cited by: Download PDF: Sorry, we are unable to provide the full text but you may find it at the following location(s): (external link); http://oai Author: M.A.E.

Mol. In agreement with this fact, an interesting study has shown that overexpression of IL following exposure to sulfur mustard can suppress the proinflammatory cytokines (IL-8 and IL-6) in human epidermal keratinocytes and lead to delayed cell death.

These findings are in agreement with our research results showing that TGF-β, like IL, can also have a distinct role in the modulation of skin inflammation Cited by: This book provides a comprehensive review and analysis of the acute toxic effects of sulfur mustard (mustard gas); the injuries that this compound produces in skin, eye, airway, and other tissues; and possibilities for the prevention of these injuries through pharmacological intervention.

The book takes a multidisciplinary approach and is intended for all biomedical researchers. Skin intoxication by bis(β-chloroethyl)sulfide (BCES; sulfur mustard) induces cutaneous lesions similar to thermal burns, characterized by slowness of skin healing.

We have developed an in vitro model of skin equivalent to investigate mechanisms involved in this delay. Direct intoxication of dermal equivalent produced dose- and time-dependent by: To study the mechanisms of SM-induced apoptosis and its prevention in vitro, we have established a convenient fluorometric apoptosis assay using monolayer human epidermal keratinocytes (HEK) adaptable for multiwell plates (.

CiteSeerX - Document Details (Isaac Councill, Lee Giles, Pradeep Teregowda): Objective: Sulfur mustard (SM) is a potent alkylating agent that can induce severe cutaneous injury. Though much is known regarding the gross pathology of SM injury, the molecular and cellular basis for this pathology is not well understood.

General cellular processes such as inflammation, DNA. Although the mechanism responsible for these effects is unknown, it is interesting to notice sulfur mustard-induced AChE activity in neuroblastoma cell cultures, suggesting that cholinergic signaling may play a role in its effects on the CNS (Lanks et al., ).

Thus, while sulfur mustard is typically thought of as a blister agent, clinical. Sulfur mustard is a potent vesicant that induces inflammation, edema and blistering following dermal exposure. To assess molecular mechanisms mediating these responses, we analyzed the effects of the model sulfur mustard vesicant, 2-chloroethyl ethyl sulfide, on EpiDerm-FT™, a commercially available full-thickness human skin by:   Sulfur mustard (SM: 2,2′dichlorodiethyl sulfide) is an alkylating agent (Auerbach, ; Heston, ; Papirmeister et al., ) that has cytotoxic and vesicant properties (Gross et al., ; Papirmeister et al., b) and has been used as a chemical warfare this agent continues to pose a threat as a chemical weapon, tissue models used in skin biology Cited by:   Skin exposure to sulfur mustard (SM) provokes long-term complications in wound healing.

Similar to chronic wounds, SM-induced skin lesions are associated with low levels of oxygen in the wound tissue. Normally, skin cells respond to hypoxia by stabilization of the transcription factor hypoxia-inducible factor 1 alpha (HIF-1α). HIF-1α modulates expression of Cited by: 4.

Sulfur mustard (2,2-dichlorodiethyl sulfide, SM) is one of the vesicant classes of chemical warfare agents that causes blistering in the skin and mucous membranes, where it can have lingering long-term effects for up to ten years (1).

SM was employed extensively by the Iraqi army against not only Iranian soldiers but also civilians between andresulting in overCited by:   Molecular mechanism underlying pathogenesis of lewisite-induced cutaneous blistering and inflammation: Chemical chaperones as potential novel antidotes Time course of lewisite-induced skin lesions and inflammatory response in the SKH-1 hairless mouse model.

Reduced sulfur mustard-induced skin toxicity in cyclooxygenase-2 knockout and Cited by: 2. Development of a reactive topical skin protectant. J Appl Toxicol 19 Suppl 1: S47–S53, Google Scholar; 10 Calvet JH, d'Ortho MP, Jarreau PH, Levame M, Harf A, and Macquin-Mavier I.

Glucocorticoids inhibits sulfur mustard-induced airway muscle hyperresponsiveness to substance P. J Appl Physiol –, Link | ISI Google ScholarCited by:   Sulfur mustard (SM), or mustard gas, is a bifunctional alkylating agent (bis[2-chloroethyl] sulfide) (see Fig.

1 for structure). It was first synthesized in the early 19th century by Despretz () and later by Guthrie () and Niemann (), during which time its distinctive mustard and garlic-like odor and blistering action on the skin were by:   This study was conducted to determine whether inhibitors of normal cellular functions can reduce cytotoxicity induced by sulfur mustard (HD).

The compounds examined include inhibitors ofpoly(ADP-ribose) polymerase (PADPRP), inhibitors of mono(ADP-ribose) transferase (MADPRT), inhibitors of lipidperoxidation, and an inhibitor ofprotein by: The BioMAP Diversity PLUS panel of 12 human primary cell/co-culture systems and accompanying database of compounds also profiled in this panel was used to evaluate the phenotypic profiles of these compounds and deconvolute potential mechanisms of skin toxicity for 5–7.

Interestingly, the most active compounds had notable responses in BioMAP Cited by: 5. Abstract. The exact date of the first sulfur mustard synthesis is uncertain [1]. There are several reports on the formation of a chemical compound formed by the reaction of sulfur dichloride and ethylene in the early nineteenth century by the Belgian-French.

The present study was aimed to examine whether apoptosis is involved in the pathogenesis of sulfur mustard (SM)-induced basal cell death. Skin sites of the hairless guinea pig exposed to SM vapor for 8 minutes were harvested at 3, 6, 12, 24, and 48 hours by: was investigated with respect to any effect of sulfur mustard on this response.

The resuits showed a strong, inhibitory effect on the heat shock response in sulfur mustard (0,1 mM) Molecular and cellular mechanisms of sulfur mustard-induced lesions of human skin, Thesis, University of Leiden, 3.

Sulfur mustard (SM, bis-(2-chloroethyl) sulfide) is a well known chemical warfare agent that may cause long-term debilitating injury. Because of the ease of production and storage, it has a strong potential for chemical terrorism; however, the mechanism by which SM causes chronic tissue damage is essentially unknown.

Vol Issue 3, March ISSN: (Print) Cellular and molecular studies on cisplatin-induced apoptotic cell death in rat kidney. Organ Toxicity and Mechanisms. Protective effect of topical iodine containing anti-inflammatory drugs against sulfur mustard-induced skin lesions.

Uri Wormser. From the title, one might expect the book to be about brain mechanisms of drive as they relate to sexual motivation. Essentially, this is a book about the regulation of lordosis, a reflex that is absolutely necessary for insemination, but is only one facet of a sophisticated set of female sexual behaviors and reflexes in by: 1.

cessed by nucleases; (b) HD-exposed human skin grafts in athymic nude mice—a human skin model which provides pertinent morpho-logical, biochemical, and other in vivo data on the development of skin lesions (Papirmeister et al., a,b); and (c) HD-treated human leukocytes—to study relevant biochemical as-pects at the cellular level.

Sulfur mustard (SM) is a vesicant chemical warfare and terrorism agent. Besides skin and eye injury, respiratory damage has been mainly responsible for morbidity and mortality after SM exposure. Previously, it was shown that suppressing the death receptor (DR) response by dominant-negative FADD prior to SM exposure blocked apoptosis andCited by: Sulfur mustard (SM) is a powerful alkylating vesicant that can rapidly penetrate skin, ocular, and lung bronchus mucous membranes and react with numerous nucleophiles in vivo.

Although the lesion mechanisms of SM remain unclear, DNA damage is believed to be the most crucial factor in initiating SM-induced toxicity. Four major DNA adducts were identified for retrospective Cited by: 9. Both lewisite and sulfur mustard-induced inflammatory responses and cell death in the skin keratinocytes were shown to be associated with Cited by: 2.