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Biomedical subjects

V Kravchenko

Publications and source records attributed to V Kravchenko.

11 recordsLinked to original sources
PubMed2005

Iodine excretion in regions of Ukraine affected by the Chornobyl Accident: experience of the Ukrainian-American cohort study of thyroid cancer and other thyroid diseases.

Urinary iodine concentrations were measured in 11,926 subjects who are participants in the Ukrainian-American Cohort Study of Thyroid Cancer and Other Thyroid Diseases Following the Chornobyl Accident. Measurements were made in two time periods corresponding to the first and second thyroid screening cycles (1998-2000, 2001-2003). These time periods fall before and after initiation of a government program to increase iodine sufficiency. Median urinary iodine concentrations did increase in the later time period compared to the earlier [47.5 microg/L, 95% confidence interval (CI) 46.5-48.9 microg/L versus 41.7 microg/L, 95% CI 40.4-42.5 microg/L], but levels remained in the mild-to-moderate iodine deficiency range as defined by the World Health Organization (WHO), indicating the need for further efforts at iodination. In both time periods, urinary iodine levels were found to vary by place of residence and were lower in rural compared to urban areas. Iodine status needs to be considered when evaluating risk of thyroid cancer and other thyroid diseases.

Adolescent↗
PubMed2004

Bionomics of phlebotomine sandflies in the Galilee focus of cutaneous leishmaniasis in northern Israel.

The bionomics of phlebotomine sandflies (Diptera: Psychodidae) were studied for three years (2001-2003) in the Galilee focus of cutaneous leishmaniasis in northern Israel, where the causative Leishmania tropica (Kinetoplastida: Trypanosomatidae) is transmitted by Phlebotomus (Adlerius) arabicus Theodor and Phlebotomus (Paraphlebotomus) sergenti Parrot, comprising 22% and 8%, respectively, of the local sandfly fauna sampled by light traps. The predominant species overall was Phlebotomus (Larroussius) tobbi Adler & Theodor (51%) with lesser numbers of Phlebotomus (Adlerius) simici Theodor (11%), Phlebotomus (Larroussius) syriacus Adler & Theodor (5%), Phlebotomus (Larroussius) perfiliewi Perfil'ev (3%) and Phlebotomus (Phlebotomus) papatasi Scopoli (0.05%). Sandfly adult populations were prevalent from April to November and peaked between June and August, being more abundant through the summer in irrigated habitats, such as gardens and orchards, than in open grassland. Of the two cutaneous leishmaniasis vectors, P. sergenti preferred boulder mounds located at the outskirts of settlements, whereas P. arabicus was more abundant overall and near houses in particular. Females of all these sandfly species displayed a peak of activity after sunset (20.00-22.00 hours), whereas activity of males persisted longer through the night. Another slight increase in activity was noted before dawn (02.00-04.00 hours). Phlebotomus arabicus appears to be the main vector of L. tropica in the Galilee focus, due to its denser populations, more endophily and preference for peridomestic habitats than shown by P. sergenti in northern Israel.

Animals↗
PubMed2001

Metaxin is required for tumor necrosis factor-induced cell death.

We used retrovirus insertion-mediated random mutagenesis and tumor necrosis factor (TNF) selection to generate TNF-resistant lines from L929 cells. The metaxin gene, which encodes a protein located on the outer membrane of mitochondria, was identified to be the gene disrupted in one of the resistant lines. The requirement of metaxin in TNF-induced cell death of L929 was confirmed by the restoration of TNF sensitivity after ectopic reconstitution of metaxin expression. Analysis of the cell death induced by other stimuli revealed that metaxin deficiency-mediated death resistance was selective to certain stimuli. Studies using deletion mutants of metaxin showed that mitochondrial association of metaxin is required for the function of metaxin. Over-expression of truncated metaxin lacking the mitochondria anchoring sequence mimicked metaxin deficiency in wild-type cells. Interfering with metaxin prevented TNF-induced necrotic cell death in L929 cells and apoptosis in MCF-7 cells. Our work has thus defined a novel component in the death pathway used by TNF and some other death stimuli.

Blotting, Northern↗
PubMed2001

Leptospiral lipopolysaccharide activates cells through a TLR2-dependent mechanism.

Leptospira interrogans are zoonotic pathogens that have been linked to a recent increased incidence of morbidity and mortality in highly populated tropical urban centers. They are unique among invasive spirochetes in that they contain outer membrane lipopolysaccharide (LPS) as well as lipoproteins. Here we show that both these leptospiral outer membrane constituents activate macrophages through CD14 and the Toll-like receptor 2 (TLR2). Conversely, it seems that TLR4, a central component for recognition of Gram-negative LPS, is not involved in cellular responses to L. interrogans. We also show that for intact L. interrogans, it is LPS, not lipoprotein, that constitutes the predominant signaling component for macrophages through a TLR2 pathway. These data provide a basis for understanding the innate immune response caused by leptospirosis and demonstrate a new ligand specificity for TLR2.

Animals↗
PubMed1999

The effects of two antiinflammatory pretreatments on bacterial-induced lung injury.

BACKGROUND: Two antiinflammatory therapies that have been effective in preventing acid-induced lung injury were evaluated. Specifically, their effects on a subsequent bacterial-airspace challenge were compared. Bacteria were instilled 24 h after acid-induced lung injury. Pseudomonas aeruginosa PAO-1 was used as the bacteria, because its effects in healthy lungs was documented previously. METHODS: New Zealand white rabbits were anesthetized and three pretreatments were administered: (1) pentoxifylline pretreatment (a 20-mg/kg bolus dose and then 6 mg x kg(-1) x h(-1) given intravenously), (2) 1 ml anti-tumor necrosis factor alpha antiserum given intravenously, or (3) normal saline given intravenously. The pretreatment doses were shown previously to prevent acid-induced lung injury. Then 1.2 ml/kg hydrochloric acid (HCl), pH 1.25, was instilled into the rabbits' right lungs. All the animals underwent mechanical ventilation for 8 h. Twenty-four hours after the acid instillation, the rabbits were anesthetized again and 2 ml/kg (10(9) colony forming units/ml) PAO-1 was instilled into their left lungs. The rabbits' breathing was aided by mechanical ventilation for another 8 h, and then they were killed and exsanguinated. RESULTS: Both pretreatments attenuated the acid-induced lung injury of the noninstilled left lungs. Arterial oxygen tension and the lung edema of pretreated, acid-exposed animals were significantly and almost equally improved (compared with no pretreatments) by either of the pretreatments. However, when the bacteria were instilled into the left lungs 24 h after the acid injury, the pentoxifylline pretreatment but not the anti-tumor necrosis factor alpha pretreatment prevented much of the bacteria-induced lung injury. Pentoxifylline pretreatment significantly improved the measurements of left lung edema and epithelial and endothelial permeability. There was also a trend for improved oxygenation in the pentoxifylline-pretreated and infected animals. In contrast, the anti-tumor necrosis factor alpha pretreatment did not prevent the bacteria-induced lung injury and increased some of the measurements of lung injury. CONCLUSIONS: Two antiinflammatory therapies that prevented acid-induced lung injury to the noninstilled left lungs had significantly different effects on a subsequent bacteria-induced lung injury to the left lungs. The therapies differed in their mechanism of tumor necrosis factor alpha blockade, and this may have affected the bacteria-induced injury to the lungs.

Animals↗
PubMed1995

Molecular cloning of human p38 MAP kinase.

Mitogen-activated protein (MAP) kinases are intracellular serine/threonine kinases activated by dual phosphorylation of adjacent threonine (T) and tyrosine (Y). A diverse number of extracellular signals induce activation of MAP kinases. Here we describe the cloning of a cDNA encoding human p38 MAP kinase (p38). The amino acid sequence of human p38 is 99.4% identical to mouse p38 [Han et al. (1994) Science 265, 808-11]. Like murine p38, the dual phosphorylation site of human p38 MAP kinase is characterized by a TGY sequence. Previous studies have described activation of p38 following exposure to products of microbial pathogens, physical-chemical stimuli and cytokines. The highly conserved nature of p38 suggests the importance of its function in regulating cellular responses.

Amino Acid Sequence↗
PubMed1993

Glycosyl-phosphatidylinositol-anchored or integral membrane forms of CD14 mediate identical cellular responses to endotoxin.

Endotoxin stimulates leukocytes to release cytokines that initiate septic shock in humans and animals. CD14, a glycosyl-phosphatidylinositol-anchored membrane glycoprotein, is an endotoxin receptor on leukocytes, and endotoxin binding to CD14 induces cytokine production. Here we show that glycosyl-phosphatidylinositol-anchored or integral membrane CD14 mediates identical cellular responses to endotoxin, including NF-kappa B activation and protein tyrosine phosphorylation. We also show that an anti-CD14 monoclonal antibody that does not block endotoxin binding to CD14 nonetheless inhibits cell activation by endotoxin. These findings suggest that binding of endotoxin to cell-surface CD14 is followed by subsequent interactions of the endotoxin-CD14 complex with additional membrane component(s) that enable transmembrane signaling. This function of CD14 may be prototypic for other members of the glycosyl-phosphatidylinositol-anchored family of proteins that do not play a primary role in signal transduction but rather are the principal ligand-binding units of membrane-bound receptor complexes.

Amino Acid Sequence↗
PubMed1992

Participation of lipopolysaccharide-binding protein in lipopolysaccharide-dependent macrophage activation.

Only recently has the mechanism for lipopolysaccharide (LPS) recognition by macrophages been elucidated. In contrast to many ligand receptor interactions, the interaction of LPS with its receptor, CD14, on myeloid cells is greatly enhanced by prior complexation of LPS with LPS-binding protein (LBP), a recently discovered plasma glycoprotein. LBP is found in normal serum or plasma in the 5 to 10 micrograms/ml range. In plasma, it reacts rapidly but transiently with LPS. LPS-LBP complexes then react with CD14 bearing cells. Blocking CD14 with monoclonal antibodies or removal of LBP from plasma blocks the ability of the cells to react with LPS-LBP complexes and also blocks release of cytokines and other mediators from the cells. In the normal lung, bronchoalveolar lavage fluid contains low levels of LBP. However, during acute lung injury, LBP levels may rise by transudation and enhance activation of alveolar macrophages to release injurious mediators. Description of this pathway for LPS recognition by macrophages and other leukocytes offers the possibility of developing new reagents to block LPS recognition and prevent the development of endotoxemia.

Acute-Phase Proteins↗
PubMedDate not supplied

Reactivity of murine and human recombinant LPS-binding protein (LBP) within LPS and gram negative bacteria.

The serum lipopolysaccharide (LPS) binding protein, LBP, has been shown to greatly enhance cellular responses to low concentrations of LPS. Purified LBP facilitates the transfer of LPS to membrane-bound or soluble CD14; the CD14/LPS complex then triggers a signal in responsive cells. We have cloned and sequenced a cDNA encoding murine LBP, and produced recombinant murine LBP using a baculovirus expression system. Using either a solid-phase or a cytofluorometric assay, recombinant murine and human LBP were found to bind avidly to free LPS, but only weakly to live bacteria from most LPS-containing Gram negative strains. Binding correlated loosely with the length and composition of the polysaccharide O chains. However, recombinant LBP did bind well to all heat-killed bacterial preparations. These findings suggest that LBP could be implicated in the response to killed but not live Gram negative bacteria.

Acute-Phase Proteins↗