WordNet

a minute life form (especially a disease-causing bacterium); the term is not in technical use (同)bug, germ
extremely small in scale or scope or capability

PrepTutorEJDIC

微生物,(特に)細菌

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 原発性骨髄線維症における病態 pathogenetic mechanisms in primary myelofibrosis
2. 軟部および骨肉腫の病原因子 pathogenetic factors in soft tissue and bone sarcomas
3. 非結核性抗酸菌感染症の病因 pathogenesis of nontuberculous mycobacterial infections
4. 橋本病（慢性自己免疫性甲状腺炎）の病因 pathogenesis of hashimotos thyroiditis chronic autoimmune thyroiditis
5. The epidemiology and pathogenesis of pulmonary arterial hypertension (Group 1)

English Journal

Rheumatoid arthritis is caused by a Proteus urinary tract infection.

Ebringer A, Rashid T.Author information Analytical Sciences Group, King's College, London, UK.AbstractGenetic, molecular and biological studies indicate that rheumatoid arthritis (RA), a severe arthritic disorder affecting approximately 1% of the population in developed countries, is caused by an upper urinary tract infection by the microbe, Proteus mirabilis. Elevated levels of specific antibodies against Proteus bacteria have been reported from 16 different countries. The pathogenetic mechanism involves six stages triggered by cross-reactive autoantibodies evoked by Proteus infection. The causative amino acid sequences of Proteus namely, ESRRAL and IRRET, contain arginine doublets which can be acted upon by peptidyl arginine deiminase thereby explaining the early appearance of anti-citrullinated protein antibodies in patients with RA. Consequently, RA patients should be treated early with anti-Proteus antibiotics as well as biological agents to avoid irreversible joint damages.
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica.APMIS.2013 Aug 29. doi: 10.1111/apm.12154. [Epub ahead of print]
Genetic, molecular and biological studies indicate that rheumatoid arthritis (RA), a severe arthritic disorder affecting approximately 1% of the population in developed countries, is caused by an upper urinary tract infection by the microbe, Proteus mirabilis. Elevated levels of specific antibodies
PMID 23992372

Two faces of microbiota in inflammatory and autoimmune diseases: triggers and drugs.

Kverka M, Tlaskalova-Hogenova H.Author information Department of Immunology and Gnotobiology, Institute of Microbiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic. kverka@biomed.cas.czAbstractThe prevalence of chronic autoimmune and inflammatory diseases, such as inflammatory bowel disease, allergies, or rheumatic diseases, is steadily increasing in developed countries. This increase is probably accelerated by environmental factors, such as decrease in infectious burden or changes in food processing. These lifestyle changes then strongly influence the strongest stimulus for the immune system - commensal microbiota. Despite the differences in the affected organ, the immune-mediated diseases have one or more factors in common - microbe either as a trigger or as a protector, mucosal barrier dysfunction, and dysregulation of the immune system. The core questions, which microbes are involved and how these diseases can be cured or even prevented still remain unsolved. Powered by the recent progress in technology, by new insights into the function of immune system, by advances in microbiome research, and extended use of gnotobiological techniques, these mechanisms are now being unravelled and new therapeutic possibilities are emerging. To secure their niche, the microbes devised many ingenious ways, how to dampen the inflammation. Nonpathogenic microorganisms or microbial components isolated from probiotic, commensal or even pathogenic microbes could be, therefore, used to interfere with the pathogenetic mechanisms of immune-mediated diseases.
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica.APMIS.2013 May;121(5):403-21. doi: 10.1111/apm.12007. Epub 2012 Oct 24.
The prevalence of chronic autoimmune and inflammatory diseases, such as inflammatory bowel disease, allergies, or rheumatic diseases, is steadily increasing in developed countries. This increase is probably accelerated by environmental factors, such as decrease in infectious burden or changes in foo
PMID 23094605

A unique herpesviral transcriptional program in KSHV-infected lymphatic endothelial cells leads to mTORC1 activation and rapamycin sensitivity.

Chang HH, Ganem D.Author information Novartis Institutes for BioMedical Research, Emeryville, CA 94608, USA.AbstractImmunosuppression therapy following organ transplantation is a significant factor in the development and progression of Kaposi's sarcoma-associated herpesvirus (KSHV)-induced posttransplant Kaposi's sarcoma (KS). Switching from cyclosporine to the mTOR inhibitor rapamycin is reported to promote KS regression without allograft rejection. Examining the underlying molecular basis for this clinical observation, we find that KSHV infection selectively upregulates mTOR signaling in primary human lymphatic endothelial cells (LECs), but not blood endothelial cells (BECs), and sensitizes LECs to rapamycin-induced apoptosis. Viral transcriptome analysis revealed that while infected BECs display conventional latency, KSHV-infected LECs support a radically different program involving widespread deregulation of both latent and lytic genes. ORF45, a lytic gene selectively expressed in infected LECs, is required for mTOR activation and critical for rapamycin sensitivity. These studies reveal the existence of a unique herpesviral gene expression program corresponding to neither canonical latency nor lytic replication, with important pathogenetic and therapeutic consequences.
Cell host & microbe.Cell Host Microbe.2013 Apr 17;13(4):429-40. doi: 10.1016/j.chom.2013.03.009.
Immunosuppression therapy following organ transplantation is a significant factor in the development and progression of Kaposi's sarcoma-associated herpesvirus (KSHV)-induced posttransplant Kaposi's sarcoma (KS). Switching from cyclosporine to the mTOR inhibitor rapamycin is reported to promote KS r
PMID 23601105

Japanese Journal

發光菌培養基中ニオケル神經親和性物質ノ分離ニツイテ

瀧野増市,川村市郎
日本内分泌学会雑誌 26(11), 329-333, 1951
… After three years of our systematic investigations on the effective component of the products of the non-pathogenetic microbes (e. …
NAID 130001919794