Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “pathogenesis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed2002

CPMK2, an SLT2-homologous mitogen-activated protein (MAP) kinase, is essential for pathogenesis of Claviceps purpurea on rye: evidence for a second conserved pathogenesis-related MAP kinase cascade in phytopathogenic fungi.

Cpmk2, encoding a mitogen-activated protein (MAP) kinase from the ascomycete Claviceps purpurea, is an orthologue of SLT2 from Saccharomyces cerevisiae, the first isolated from a biotrophic, non-appressorium-forming pathogen. Deletion mutants obtained by a gene replacement approach show impaired vegetative properties (no conidiation) and a significantly reduced virulence, although they retain a limited ability to colonize the host tissue. Increased sensitivity to protoplasting enzymes indicates that the cell wall structure of the mutants may be altered. As the phenotypes of these mutants are similar to those observed in strains of the rice pathogen, Magnaporthe grisea, that have been deprived of their MAP kinase gene mps1, the ability of cpmk2 to complement the defects of delta mps1 was investigated. Interestingly, the C. purpurea gene, under the control of its own promoter, was able to complement the M. grisea mutant phenotype: transformants were able to sporulate and form infection hyphae on onion epidermis and were fully pathogenic on barley leaves. This indicates that, despite the differences in infection strategies, which include host and organ specificity, mode of penetration and colonization of host tissue, CPMK2/MPS1 defines a second MAP kinase cascade (after the Fus3p/PMK1 cascade) essential for fungal pathogenicity.

Claviceps↗
PubMed1999

HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) pathogenesis hypothesis. A shift of homologous peptides pairs, central nervous system (CNS)/HTLF-1, HTLV-1/thymus, thymus/CNS, in a thymus-like CNS environment, underlies the pathogenesis of HAM/TSP.

Determinants shared by thymus, brain and HTLV-1 induce lymphocytic neurotropism and demyelinization in HAM/TSP, within the framework thymus-like brain environment. The disease evolves in two phases. The first phase of the disease would be dependent on CD4 T-lymphocytes specific for thymic autoantigens, reactivated by viral antigens homologous to thymus and CNS autoantigens. During this phase, demyelinization could be due initially to a stop in the synthesis of myelin following an altered expression of adhesion proteins at the surface of oligodendrocytes and neurons. The second phase, which covers the inflammatory and chronic character of the disease, would be dependent, on the one hand, on CD8 T-lymphocytes specific for viral peptides, and on the other hand, on CD8 T-lymphocytes specific for peptides arising from the cell-proteases induced progressive proteolysis of protein components from the myelin layers and other protein components of the CNS. Non-specific inflammatory and non-inflammatory cytokines keep the activation going of the different cellular types. The thoracic spinal cord cell-location specificity would be linked to a peptidic coherence between HTLV-1 (significant agent), thymus and thoracic spinal cord antigens, genetically peculiar to HAM/TSP patients.

Brain↗
PubMed2002

[Multiple sclerosis with early onset: pathogenesis, clinical characteristics, possibilities in the treatment of its pathogenesis].

Early onset multiple sclerosis (MS) has some peculiarities in the disease course. 56 patients with definite MS with the onset at the age under 15 years were included in this clinical, immunogenetical and neurophisiological study. The analyses of the relations between different clinical characteristics of MS in children has shown, that patients with onset under 10 years, had rare relapses, but more progressive development of disability in contrast to the patients with MS onset at the age of 11-15 years. Duration of the first remission was associated with the time to sustained disability in children with MS. The number and volume of MRI T2-positive lesions in the white matter of the brain was associated with the age of onset, duration of the disease and with the number of relapses. In several cases the phenomena of clinical-MRI dissociation was observed. Generic HLA-DRB1 genomic typing was performed in all the patients. High frequency of DR2(15) genotype in MS-affected children in comparison with the group of healthy controls was more expressed as compared with MS-affected adults. The comparison of frequencies of DRB1 alleles in transmitted, i.e. appeared in the affected child haplotypes and in non-transmitted haplotypes confirmed results of the case-control study showing the very significant association of MS with DR2 alleles and extremely significant--with its DR15 subtype in children. The data of transmission/disequilibrium test (TDT) analysis provide strong evidence for linkage of DR15 alleles and susceptibility to sporadic MS in patients with disease onset before 15 years. The positive experience of management (beta-interferon-1a) was shown in MS-affected children in three cases.

Adjuvants, Immunologic↗
PubMed2003

HIV lipodystrophy etiology and pathogenesis. Body composition and metabolic alterations: etiology and pathogenesis.

The results of epidemiologic investigations have clearly indicated that the development of lipodystrophy is multifactorial. Factors related to HIV infection, hormonal influences, mitochondrial dysfunction, cytokine activation related to immune reconstitution, and individual genetic predisposition all have been hypothesized as etiologic. Recent studies suggest that immune dysregulation rather than HIV infection per se may be the predominant factor in the development of lipodystrophy.

Antiretroviral Therapy, Highly Active↗