Noncommutative locally anti-de Sitter black holes

We give a review of our joint work on strict deformation of BHTZ 2+1 black holes \cite{BRS02,BDHRS03}. However some results presented here are not published elsewhere, and an effort is made for enlightening the instrinsical aspect of the constructions. This shows in particular that the three dimensional case treated here could be generalized to an anti-de Sitter space of arbitrary dimension provided one disposes of a universal deformation formula for the actions of a parabolic subgroup of its isometry group. Comment: 10 pages, based on a talk given by P.B., to appear in the proceedings of the workshop `Noncommutative Geometry and Physics 2004' (Feb. 2004, Keio University, Japan) (World Scientific

International Workshop on Low-Frequency Propagation and Noise, Woods Hole, Massachusetts, 14-19 October, 1974 /

v.1 (1977

The efficacy of dental floss in addition to a toothbrush on plaque and parameters of gingival inflammation: a systematic review

Objectives: The aim of this study was to assess systematically the adjunctive effect of both flossing and toothbrushing versus toothbrushing alone on plaque and gingivitis. Materials: The MEDLINE and Cochrane Central register of Controlled Trials (CENTRAL) databases were searched through December 2007 to identify appropriate studies. The variables of plaque and gingivitis were selected as outcomes. Results: Independent screening of titles and abstracts of 1166 MEDLINE-Pubmed and 187 Cochrane papers resulted in 11 publications that met the eligibility criteria. Mean values and SD were collected by data extraction. Descriptive comparisons are presented for brushing alone or brushing and flossing. A greater part of the studies did not show a benefit for floss on plaque and clinical parameters of gingivitis. A meta-analysis was performed for the plaque index and gingival index. Conclusions: The dental professional should determine, on an individual patient basis, whether high-quality flossing is an achievable goal. In light of the results of this comprehensive literature search and critical analysis, it is concluded that a routine instruction to use floss is not supported by scientific evidence

Jagged1-mediated myeloid Notch1 signaling activates HSF1/Snail and controls NLRP3 inflammasome activation in liver inflammatory injury.

Notch signaling plays important roles in the regulation of immune cell functioning during the inflammatory response. Activation of the innate immune signaling receptor NLRP3 promotes inflammation in injured tissue. However, it remains unknown whether Jagged1 (JAG1)-mediated myeloid Notch1 signaling regulates NLRP3 function in acute liver injury. Here, we report that myeloid Notch1 signaling regulates the NLRP3-driven inflammatory response in ischemia/reperfusion (IR)-induced liver injury. In a mouse model of liver IR injury, Notch1-proficient (Notch1FL/FL) mice receiving recombinant JAG1 showed a reduction in IR-induced liver injury and increased Notch intracellular domain (NICD) and heat shock transcription factor 1 (HSF1) expression, whereas myeloid-specific Notch1 knockout (Notch1M-KO) aggravated hepatocellular damage even with concomitant JAG1 treatment. Compared to JAG1-treated Notch1FL/FL controls, Notch1M-KO mice showed diminished HSF1 and Snail activity but augmented NLRP3/caspase-1 activity in ischemic liver. The disruption of HSF1 reduced Snail activation and enhanced NLRP3 activation, while the adoptive transfer of HSF1-expressing macrophages to Notch1M-KO mice augmented Snail activation and mitigated IR-triggered liver inflammation. Moreover, the knockdown of Snail in JAG1-treated Notch1FL/FL livers worsened hepatocellular functioning, reduced TRX1 expression and increased TXNIP/NLRP3 expression. Ablation of myeloid Notch1 or Snail increased ASK1 activation and hepatocellular apoptosis, whereas the activation of Snail increased TRX1 expression and reduced TXNIP, NLRP3/caspase-1, and ROS production. Our findings demonstrated that JAG1-mediated myeloid Notch1 signaling promotes HSF1 and Snail activation, which in turn inhibits NLRP3 function and hepatocellular apoptosis leading to the alleviation of IR-induced liver injury. Hence, the Notch1/HSF1/Snail signaling axis represents a novel regulator of and a potential therapeutic target for liver inflammatory injury