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Effect of hyperthermia on lymphocyte plasma membrane. 1. Permeability for glyceraldehyde-3-phosphate dehydrogenase substrates.

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The effect of hyperthermia on the permeability of porcine lymphocyte plasma membranes for glyceraldehyde-3-phosphate dehydrogenase (G3PDH) substrates was investigated. The permeability increased in the temperature range of 40-45 degrees C. The temperature dependence for the permeability of G3PDH

Potentiation of thermal inactivation of glyceraldehyde-3-phosphate dehydrogenase by photodynamic treatment. A possible model for the synergistic interaction between photodynamic therapy and hyperthermia.

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Thermal inactivation of glyceraldehyde-3-phosphate dehydrogenase appeared to be caused by a conformational mechanism, without involvement of covalent reactions. On the other hand, photodynamic inactivation of the enzyme (induced by illumination in the presence of Photofrin II) was caused by

A glyceraldehyde-3-phosphate dehydrogenase homolog in Borrelia burgdorferi and Borrelia hermsii.

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A polyreactive monoclonal antibody recognized a 38.5-kDa polypeptide with amino-terminal sequence identity to conserved regions of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in Borrelia burgdorferi, the Lyme disease agent, and Borrelia hermsii, an agent of American relapsing fever. This

Multifunctional glyceraldehyde-3-phosphate dehydrogenase of Streptococcus pyogenes is essential for evasion from neutrophils.

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Streptococcus pyogenes is an important pathogen that causes pharyngitis, sepsis, and rheumatic fever. Cell-associated streptococcal C5a peptidase (ScpA) protects S. pyogenes from phagocytosis and has been suggested to interrupt host defenses by enzymatically cleaving complement C5a, a major factor

Metabolic Profiles in Cell Lines Infected with Classical Swine Fever Virus.

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Viruses require energy and biosynthetic precursors from host cells for replication. An understanding of the metabolic interplay between classical swine fever virus (CSFV) and host cells is important for exploring the complex pathological mechanisms of classical swine fever (CSF). In the current

Proteomic alteration of PK-15 cells after infection by classical swine fever virus.

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Viral infections usually result in alterations in the host cell proteome which determine the fate of the infected cells and the progress of pathogenesis. To uncover cellular protein responses in classical swine fever virus-infected PK-15 cells, a proteomic analysis was conducted using 2D PAGE

Investigation of malignant hyperthermia: analysis of skeletal muscle proteins from normal and halothane sensitive pigs by two dimensional gel electrophoresis.

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Two dimensional gel analysis of skeletal muscles from normal pigs and from pigs which were homozygous for halothane sensitivity showed no obvious differences in the patterns of spots attributed to the major contractile proteins and glycolytic enzymes. In muscle from a sensitive pig which died of

Upregulation of IL-10 gene expression in porcine peripheral blood mononuclear cells by porcine reproductive and respiratory syndrome virus.

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Several lines of evidence suggest that porcine reproductive and respiratory syndrome virus (PRRSV) may have immunomodulatory effects on the host immune system. To determine the effect of PRRSV on cytokine production, a multiplex PCR was established. This allowed a semi-quantitative analysis of

Effect of acute infectious disease on human isometric muscle endurance.

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Capacity for isometric endurance work of different muscle groups was recorded in 32 male patients suffering a variety of acute infectious diseases, predominantly of viral or mycoplasmal aetiology. Recordings were performed after abatement of fever, and 1, and 4 months thereafter. Control

Comparison of the cellular molecular stress responses after treatments used in bladder cancer.

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OBJECTIVE To investigate the molecular stress responses related to the quality of recovery of normal tissue after various treatments for bladder cancer, i.e. hyperthermia, ionizing radiation, mitomycin-C and 5-aminolaevulinic acid photodynamic therapy (ALA-PDT). METHODS The study focused

Lower T Regulatory and Th17 Cell Populations Predicted by RT-PCR-Amplified FOXP3 and ROR γ t Genes Are Not Rare in Patients With Primary Immunodeficiency Diseases

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Deficiencies in T regulatory (Treg) and Th17 cells attenuate peripheral tolerance and the IL-17 family of cytokines, contributing to autoimmune disorders and opportunistic (fungal) infections, respectively. Because of limited blood samples from patients with primary immunodeficiency diseases (PIDs),

Development and validation of a harmonized TaqMan-based triplex real-time RT-PCR protocol for the quantitative detection of normalized gene expression profiles of seven porcine cytokines.

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Dysregulation of cytokine responses plays a major role in the pathogenesis of severe and life-threatening infectious diseases like septicemia or viral hemorrhagic fevers. In pigs, diseases like African and classical swine fever are known to show exaggerated cytokine releases. To study these

Development of real-time PCR for detection of Mycoplasma hominis.

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BACKGROUND Mycoplasma hominis is associated with pelvic inflammatory disease, bacterial vaginosis, post partum fever, sepsis and infections of the central nervous system often leading to serious conditions. Association with development of female infertility has also been suggested, but different

Fluoride exposure attenuates expression of Streptococcus pyogenes virulence factors.

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Fluoridation causes an obvious reduction of dental caries by interference with cariogenic streptococci. However, the effect of fluoride on group A streptococci that causes rheumatic fever and acute poststreptococcal glomerulonephritis is not known. We have used proteomic analysis to create a

Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet.

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Considerable insight has been gained into the etiopathogenesis of poststreptococcal glomerulonephritis since the landmark theoretical construct of Clemens von Pirquet postulated that disease-causing immune complexes were responsible for the nephritis that followed scarlet fever. Over the years,

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