WorldCat Identities

Petrali, J. P.

Overview
Works: 6 works in 6 publications in 1 language and 6 library holdings
Publication Timeline
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Most widely held works by J. P Petrali
Subcellular localization of antigens by immune and cytochemical techniques in electron microscopy. mitochondria, a site of vaccinia protein( Book )

1 edition published in 1970 in English and held by 1 WorldCat member library worldwide

The intracellular distribution of the following cellular antigens was studied by the immunouranium technique: Fibrinogen in blood platelets, lysozyme in monocytic leukemic blood, and vaccinia antigen in infected HeLa cells. The results of this study suggest the following conclusions. (1) Platelets store fibrinogen. The nature of this association is unclear but implies that the platelet is an alternate source or at least a transporter of fibrinogen in circulating plasma. (2) Monocytes in leukemic blood contain lysozyme within lysosome-like granules in the cytoplasm. This finding implicates the neoplastic monocyte as the source of the elevated levels of urinary and serum lysozyme found in patients with monocytic leukemia. (3) Protein synthesis in mitochondrial fractions of vaccinia-infected HeLa cells was found to be greater than in uninfected cells and increased as infection progressed. Those mitochondria found to be specific for vaccinia protein are probably sites of virus-induced protein synthesis. These findings may help to explain how some DNA mammalian viruses, such as vaccinia, can replicate in the cytoplasm of mammalian cells without the apparent participation of the host cell nucleus. (Author)
Ultrastructural Pathology and Immunohistochemistry of Mustard Gas Lesion( Book )

1 edition published in 1993 in English and held by 1 WorldCat member library worldwide

The ultrastructural pathology of sulfur mustard gas (HD) skin toxicity has been characterized for several in vivo and in vitro model systems. In animal models, the pathology involves the latent lethal targeting of skin basal cells, a disabling of hemidesmosomes and a progressive edema of the lamina lucida, all of which contribute to the formation of characteristic microblisters at the dermal-epidermal junction. However, the effects of HD toxicity on structural proteins of extracellular domains of the dermal-epidermal junction have not been elucidated. We are beginning an immunohistochemical study of these domains in the hairless guinea pig and summarize here the time course effects of HD of three structural proteins: bullous pemphigoid antigen, laminin and Type IV collagen. The results of this combined ultrastructural and immunohistochemical study indicate that proteins of extracellular matrices of the basement membrane are antigenically altered during the development of HD-induced skin pathology and may contribute to the formation of microblisters
Sulfur Mustard-Induced Increase in Intracellular Calcium: A Mechanism of Mustard Toxicity( Book )

1 edition published in 1993 in English and held by 1 WorldCat member library worldwide

The effect of sulfur mustard (SM, bis-(2-chloroethyl) sulfide) on intracellular free Ca2+ concentration (Ca2+)i was studied in vitro using the clonal mouse neuroblastoma-rat glioma hybrid NG108-15 and primary normal human epidermal keratinocyte (NHEK) cell culture models. SM depletes cellular glutathione (GSH) and thus may inhibit GSH-dependent Ca2+-ATPase (Ca2+ pump), leading to a high (Ca2+) and consequent cellular toxicity. Following 0.3 mM SM exposure, GSH levels decreased 20-34% between 1-6 hr in NG108-15 cells. SM increased Ca2+)i, measured using the Ca2+-specific fluorescent probe Fluo-3 AM, in both NG108-15 cells (1030% between 2-6 hr) and NHEK (23-30% between 0.5-3 hr) . Depletion of cellular GSH by buthionine sulfoximine (1 mM), a specific GSH biosynthesis inhibitor, also increased (Ca2+, (88% at 1 hr) in NHEK, suggesting that GSH depletion may lead to increased Ca2+)i. Calcium, localized cytochemically with antimony, accumulated in increased amounts around mitochondria and endoplasmic reticula, in the cytosol, and in particular in the euchromatin regions of the nucleus beginning at 6 hr after 0.3 mM SM exposure of NG108-15 cells. Cell membrane integrity examined with the fluorescent membrane probe calcein AM was unaffected through 6 hr following 1 mM SM exposure; and cell viability (NG108-15 cells) measured by trypan blue exclusion was>80% of control through 9 hr following 0.3 mM SM exposure
DNA Damage-Induced Apoptosis: Inhibition by Calmodulin Antagonist, Fas Receptor Antibody and Caspase Inhibitors( )

1 edition published in 2003 in English and held by 0 WorldCat member libraries worldwide

Sulfur mustard (HD, bis-(2-chloroethyl) sulfide) is a vesicant that causes DNA strand breaks and apoptosis in cultured normal human epidermal keratinocytes (NHEK). HD causes apoptosis via two independent pathways, a Ca2+/calmodulin (CaM)-mediated mitochondrial pathway and Fas receptor (CD95) pathway. We studied the effects of the exogenously added CaM antagonist W7, the CD95 antibody, the caspase-3 inhibitor Ac-DEVD-CHO, and the general caspase inhibitor Z-VAD-fmk on NHEK viability loss (Calcein AM fluorescence assay, LDH release assay) due to HD. All protected against HD. Z-VAD-fmk was the most effective. These results provide a logical approach toward developing an anti-apoptotic vesicant countermeasure
Antivesicant Strategies Based on DNA Repair and Apoptosis( )

1 edition published in 2005 in English and held by 0 WorldCat member libraries worldwide

DNA is a major cellular target of the vesicant chemical warfare agent sulfur mustard (SM, bis-(2-chloroethyl) sulfide). Others and we have proposed a possible role of apoptosis in SM vesication. Our results suggest that in SM-exposed human epidermal keratinicytes (HEK), DNA damage, DNA repair, and apoptosis may be interdependent. In HEK, SM causes cell death accompanied by caspase-3 activation indicating apoptosis. The general caspase inhibitor A-VAD-FMK (benzyl oxycarbonly-Val-Ala (o-methyl-fluromethylketone)) decreases not only SM induced apoptosis, but also protease stimulation consequent degradation of laminin-5 which maintains epidermal-dermal junction integrity. This knowledge may, therefore, be useful in developing successful antivesicant strategies
Comparative Morphology of Sulfur Mustard Effects in the Hairless Guinea Pig and a Human Skin Equivalent( )

1 edition published in 1993 in English and held by 0 WorldCat member libraries worldwide

A commercially available human skin equivalent (HSE) was used as an in vitro organotypic skin model to study temporal morphological effects of sulfur mustard gas (HD). Light and electron microscopic analyses of the HD-human skin equivalent model (HD-HSE) were compared to the HD-hairless guinea pig model (HD-HGP). HSE samples were exposed to 10 micro l HD vapor for 8 min and harvested at selected times up to 24 h. Skin sites of HGP were exposed to the same vapor dose or to 2.0 micro l HD for 30 min and collected at 12 and 24 h. In both models, basal cells of the stratum germinativum were selectively affected. The HD-HSE study revealed that basal cell changes began 3 to 6 h following exposure. These early cellular included an acantholysis of some basal cells with widening of intercellular spaces, disruption of desmosomal attachments, nuclear pyknosis, perinuclear blebbing and repositioning of cytoplasmic tonofilaments to a perinuclear position
 
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