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Rationale PhosPhatidic-Acid-Phosphatase-type-2B (PPAP2B), an integral membrane protein that inactivates lysophosphatidic acid, was implicated in coronary artery disease (CAD) by genome-wide-association-studies (GWAS). However, it is unclear whether GWAS-identified CAD genes including PPAP2B participate in mechanotransduction mechanisms by which vascular endothelia respond to local athero-relevant hemodynamics that contribute to the regional nature of atherosclerosis. Objective To establish the critical role of PPAP2B in endothelial responses to hemodynamics. Methods and Results Reduced PPAP2B was detected in vivo in mouse and swine aortic arch endothelia exposed to chronic disturbed flow, and in mouse carotid artery endothelia subjected to surgically-induced acute disturbed flow. In humans, PPAP2B was reduced in the downstream part of carotid plaques where low shear stress prevails. In culture, reduced PPAP2B was measured in human aortic endothelial cells (HAEC) under athero-susceptible waveform mimicking flow in human carotid sinus. Flow-sensitive microRNA-92a and transcription factor KLF2 were identified as upstream inhibitor and activator of endothelial PPAP2B, respectively. PPAP2B suppression abrogated athero-protection of unidirectional flow; Inhibition of lysophosphatidic acid receptor 1 (LPAR1) restored the flow-dependent, anti-inflammatory phenotype in PPAP2B-deficient cells. PPAP2B inhibition resulted in myosin-light-chain phosphorylation and intercellular gaps, which were abolished by LPAR1/2 inhibition. Expression-quantitative-trait-locus-mapping demonstrated PPAP2B CAD risk allele is not linked to PPAP2B expression in various human tissues but significantly associated with reduced PPAP2B in HAEC. Conclusions Athero-relevant flows dynamically modulate endothelial PPAP2B expression through miR-92a and KLF2. Mechano-sensitive PPAP2B plays a critical role in promoting anti-inflammatory phenotype and maintaining vascular integrity of endothelial monolayer under athero-protective flow.

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The purposes of this study were to test the effectiveness of laser treatment (pulsed CO₂ and pulsed Nd-YAG) on in vitro acid resistance of human enamel. Thirty enamel surfaces were prepared from 10 extracted permanent premolars (3 surfaces per tooth). Two experimental surfaces on each tooth were irradiated with either CO₂ or Nd-YAG lasers. All specimens were demineralized in 10 ml lactate buffer for 24 or 72 h after laser treatment. After 24-hour acid treatment the mean concentration of calcium that dissolved into the lactate buffer in the CO₂ laser group was significantly less than in the control group, while the dissolved calcium concentration in the Nd-YAG laser group did not differ from the control group (p > 0.05). The erosion depth in the CO₂ laser group was significantly shallower than in the Nd-YAG laser group (p < 0.001). After 72-hour acid treatment, the acid resistances of neither group of laser-treated surfaces differed significantly from the controls. By scanning electron microscopy, the acid-eroded laser-treated enamel surfaces had type I and type II etching patterns, fissures, and disordered rough surfaces compared to control enamel, with a regular type II etching pattern. CO₂ laser-treated tooth enamel was more resistant to acid challenge than was Nd-YAG laser-treated enamel, given the same fluence, but neither type of laser increased acid resistance of subsurface enamel.

Our findings suggest that CXCL3 and its receptor CXCR2 are overexpressed in prostate cancer cells, prostate epithelial cells and prostate cancer tissues, which may play multiple roles in prostate cancer progression and metastasis.

The differences in upper and lower face infections and differences in gender were not clinically significant. Surgical or dental interventions can be delayed through the proper use of antibiotics. With correct diagnosis, antibiotic treatment and appropriate timing for surgical or dental interventions, rapid resolution of the infection is expected.

BackgroundTo investigate the association between metabolic syndrome, including its factors, and gallstone disease (GSD) in a Taiwanese population.MethodsWe conducted a cross-sectional study during 2011 ~ 2012. A total of 12050 subjects who completed a questionnaire and underwent physical examination, laboratory tests and abdominal ultrasonography formed the study population.ResultsThe prevalences of metabolic syndrome and gallstone disease were 24.09% and 6.16%. In an age- and sex-adjusted logistic regression model, metabolic syndrome was associated with gallstone disease (OR = 1.61; P < 0.0001). Age, abdominal obesity, and lower high-density lipoprotein cholesterol were associated with gallstone disease after adjusting for other factors. Females had a higher odds ratio than males in waist circumference for GSD, whereas males had a lower odds ratio than females in HDL-C for GSD.ConclusionsThe present study suggests that metabolic syndrome is related to gallstone disease. Waist circumference and high-density lipoprotein cholesterol are all associated with GSD. Men and women may possibly have different priorities and strategies to reduce the burden of GSD.

The 12-month space changes in the maxillary dental arch after premature loss of a primary maxillary first molar consist mainly of distal drift of the primary canine toward the extraction site. Mesial movement of permanent molars or tilting of the primary molars did not occur. An increased arch dimension was found especially in the anterior segment (intercanine width and length). There is no need for the use of space maintainers from the results in this study in cases of premature loss of a primary first molar.