scholarly journals A rapid diagnosis (SK-013) for periodontitis based on the enzymatic activity of periodontopathic bacteria. The relationship between the enzymatic activity (SK-013) and B.gingivalis, B.forsythus, T.denticola in subgingival microflora.

Author(s):  
Kizuku SEIDA ◽  
Atsushi SAITO ◽  
Satoru YAMADA ◽  
Masatake TSUNODA ◽  
Tetsuichiro SATO ◽  
...  
2021 ◽  
Vol 22 (7) ◽  
pp. 3728
Author(s):  
Masahiro Hatasa ◽  
Sumiko Yoshida ◽  
Hirokazu Takahashi ◽  
Kenichi Tanaka ◽  
Yoshihito Kubotsu ◽  
...  

Periodontal disease is an inflammatory disease caused by pathogenic oral microorganisms that leads to the destruction of alveolar bone and connective tissues around the teeth. Although many studies have shown that periodontal disease is a risk factor for systemic diseases, such as type 2 diabetes and cardiovascular diseases, the relationship between nonalcoholic fatty liver disease (NAFLD) and periodontal disease has not yet been clarified. Thus, the purpose of this review was to reveal the relationship between NAFLD and periodontal disease based on epidemiological studies, basic research, and immunology. Many cross-sectional and prospective epidemiological studies have indicated that periodontal disease is a risk factor for NAFLD. An in vivo animal model revealed that infection with periodontopathic bacteria accelerates the progression of NAFLD accompanied by enhanced steatosis. Moreover, the detection of periodontopathic bacteria in the liver may demonstrate that the bacteria have a direct impact on NAFLD. Furthermore, Porphyromonas gingivalis lipopolysaccharide induces inflammation and accumulation of intracellular lipids in hepatocytes. Th17 may be a key molecule for explaining the relationship between periodontal disease and NAFLD. In this review, we attempted to establish that oral health is essential for systemic health, especially in patients with NAFLD.


2018 ◽  
Vol 115 (7) ◽  
pp. E1465-E1474 ◽  
Author(s):  
Shaoxun Xiang ◽  
Hao Gu ◽  
Lei Jin ◽  
Rick F. Thorne ◽  
Xu Dong Zhang ◽  
...  

The oncoprotein c-Myc plays an important role in regulating glycolysis under normoxia; yet, in cancer cells, HIF1α, which is essential for driving glycolysis under hypoxia, is often up-regulated even in the presence of oxygen. The relationship between these two major regulators of the Warburg effect remains to be fully defined. Here we demonstrate that regulation of a long noncoding RNA (lncRNA), named IDH1-AS1, enables c-Myc to collaborate with HIF1α in activating the Warburg effect under normoxia. c-Myc transcriptionally repressed IDH1-AS1, which, upon expression, promoted homodimerization of IDH1 and thus enhanced its enzymatic activity. This resulted in increased α-KG and decreased ROS production and subsequent HIF1α down-regulation, leading to attenuation of glycolysis. Hence, c-Myc repression of IDH1-AS1 promotes activation of the Warburg effect by HIF1α. As such, IDH1-AS1 overexpression inhibited cell proliferation, whereas silencing of IDH1-AS1 promoted cell proliferation and cancer xenograft growth. Restoring IDH1-AS1 expression may therefore represent a potential metabolic approach for cancer treatment.


1967 ◽  
Vol 13 (10) ◽  
pp. 1333-1342 ◽  
Author(s):  
James T. Staley ◽  
William L. Boyd

Escherichia coli and Pseudomonas aeruginosa were grown at several temperatures ranging from 0° to 37 °C and assayed at each temperature for L-serine dehydratase activity. The relationship between enzymatic activity and growth temperature is quite different for the mesophile and psychrophile. In addition, the stimulatory effect of natural plant lecithin upon serine deamination was different for each organism, suggesting that there is either a difference in permeability or that this substance has a more direct role in enzymic activity. Also included are data confirming the results of other workers.


1964 ◽  
Vol 120 (4) ◽  
pp. 677-690 ◽  
Author(s):  
Sharad D. Deodhar ◽  
Francis E. Cuppage ◽  
E. Gableman

Renin-induced proteinuria in the rat was investigated, with special emphasis on the relationship between the enzymatic activity and the proteinuric effect of renin. The dependence of the proteinuric effect on the enzymatic activity was shown by using (a) renin preparations of widely varying purity and (b) chemically modified "active" and "inactive" renin derivatives. Angiotensin II, the pressor product of the enzymatic action of renin, also produced significant proteinuria. Adrenalectomy abolished the proteinuria induced by renin. Proteinuria, however, occurred as a result of pretreatment with DOCA, or aldosterone, or without treatment, 7 to 8 weeks after adrenalectomy. Electron microscopic studies of the kidney at the time of maximal proteinuria showed focal flattening and fusion of epithelial foot processes, as well as swelling and vesicle formation in endothelial and epithelial cells of the glomeruli. Studies with intravenously injected saccharated iron oxide showed increased permeability of the glomerular capillary basement membrane to these particles. These changes were transient and were not seen 24 hours after renin injection. Adrenalectomy prevented these changes. It is concluded that renin, acting through angiotensin, causes glomerular capillary damage with increased permeability of these structures to protein and resultant proteinuria. The adrenal glands participate in a permissive role in this phenomenon.


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