Recurrent infarctions due to a dome-shaped pannus above the mitral valve prosthesis

This report describes a unique case of a 56-year-old female who suffered from recurrent stroke after double mechanical valve replacement. During the four years after the surgery, she remained in normal sinus rhythm, received adequate anticoagulation therapy, and no apparent left atrial thrombus was detected. She underwent redo surgery to prevent further stroke after fourth instance of cerebral infarction. Intraoperative findings revealed a ‘dome-shaped’ pannus formation covering the sewing ring of the mitral prosthesis circumferentially, probably leading to clot formation and repeated infarctions. She has been stroke free for three years after pannus resection.     

Neuronal susceptibility to beta‐amyloid toxicity and ischemic injury involves histone deacetylase‐2 regulation of endophilin‐B1

Histone deacetylases (HDACs) catalyze acetyl group removal from histone proteins, leading to altered chromatin structure and gene expression. HDAC2 is highly expressed in adult brain, and HDAC2 levels are elevated in Alzheimer's disease (AD) brain. We previously reported that neuron‐specific splice isoforms of Endophilin‐B1 (Endo‐B1) promote neuronal survival, but are reduced in human AD brain and mouse models of AD and stroke. Here, we demonstrate that HDAC2 suppresses Endo‐B1 expression. HDAC2 knockdown or knockout enhances expression of Endo‐B1. Conversely, HDAC2 overexpression decreases Endo‐B1 expression. We also demonstrate that neurons exposed to beta‐amyloid increase HDAC2 and reduce histone H3 acetylation while HDAC2 knockdown prevents Aβ induced loss of histone H3 acetylation, mitochondrial dysfunction, caspase‐3 activation, and neuronal death. The protective effect of HDAC2 knockdown was abrogated by Endo‐B1 shRNA and in Endo‐B1‐null neurons, suggesting that HDAC2‐induced neurotoxicity is mediated through suppression of Endo‐B1. HDAC2 overexpression also modulates neuronal expression of mitofusin2 (Mfn2) and mitochondrial fission factor (MFF), recapitulating the pattern of change observed in AD. HDAC2 knockout mice demonstrate reduced injury in the middle cerebral artery occlusion with reperfusion (MCAO/R) model of cerebral ischemia demonstrating enhanced neuronal survival, minimized loss of Endo‐B1, and normalized expression of Mfn2. These findings support the hypothesis that HDAC2 represses Endo‐B1, sensitizing neurons to mitochondrial dysfunction and cell death in stroke and AD.     

In vitro wear of indirect composite restoratives

STATEMENT OF PROBLEM: Indirect composite restoratives have been improved in their wear resistance and physical properties. Several new indirect composites claim to be successfully used for full coverage crowns, but there is limited information for wear values of these new indirect composites. PURPOSE: The purpose of this study was to evaluate the wear characteristics of 7 indirect composite restoratives and to compare them with a type III gold alloy by means of an in vitro wear test. MATERIAL AND METHODS: Seven indirect composites (2 photopolymerized and 5 photo/heat-polymerized types) and a type III gold alloy (control) were used. Cylindrical Class I cavities (4-mm diameter and 3-mm depth) were prepared in occlusally flattened extracted human molars. Inlays with respective materials were fabricated on duplicated stone casts according to the manufacturers' instructions. Three types of in vitro wear tests were completed by use of the University of Alabama wear simulator. The wear tests included generalized wear as simulation of the wear during mastication, localized wear as simulation of attrition by occlusal contact, and antagonistic enamel wear, which simulated the wear of enamel created by direct contact with the restorative materials. Seven specimens were tested for each material and wear mode, and the wear depths were measured on profilometric tracings with a 2-dimensional profilometer with 1-microm accuracy. All data were analyzed by 1-way analysis of variance, and multiple comparisons were performed with Fisher's test, for which the significant level was set at.05. RESULTS: The gold alloy control exhibited a very small amount of wear in both generalized wear (0.2 +/- 0.1 microm) and localized wear (13.8 +/- 5.0 microm) as compared with all composite specimens. The antagonistic enamel wear of gold alloy was similar with the value of Sculpture. The material group, which was post polymerized or post heat-treated, included BelleGlass, Sculpture, Estenia, and Cristobal+ and showed small values ranging from 1.6 to 2.2 microm in the generalized wear. For the localized wear, Estenia exhibited the minimum value (12.8 +/- 4.9 microm) that was statistically the same as the value of the gold alloy control. However, Estenia exhibited the greatest antagonistic enamel wear value (66.0 +/- 14.0 microm) of all materials tested in this study. It was statistically significant with other materials (P相似文献   

Bactericidal effects of 2.94 µm and 1.67 µm laser

The bactericidal effects of lasers with wavelengths of 1.67 and 2.94 μm on cariogenic Streptococcus mutans were investigated. Temperature during irradiation was also measured to determine the mechanism underlying the bactericidal effects of the lasers. An aliquot of 2 μl cell suspension of S. mutans JC-2 strain was placed on anhydrous quartz or dentin plate, covering an area of approximately 5.0 mm in diameter to a depth of approximately 0.1 mm. Cell suspension was then irradiated at a power of 0.8 W (3.1 J/cm2) at a rate of 40 pps for 30 sec. After irradiation, the plate was put into a bottle containing PBS and vigorously voltated. Solution was serially diluted and inoculated on MS agar. After incubation anaerobically for 72 hr, colony forming units on the agar were counted. The experimental group, the number of bacteria decreased significantly compared to the control group under all conditions. No significant differences were observed in effect of wavelength or plate on bactericidal activity. In conclusion, laser irradiation at a wavelength of 1.67 μm for 30 sec showed a bactericidal effect on S. mutans, suggesting that this wavelength is more useful than 2.94 μm due to greater tissue penetration.     

Fluoride release from newly developed dental adhesives

This study compared fluoride release from three fluoride-releasing dental adhesives (Trial KBF Bond, One-up Bond F, Reactmer Bond) and one conventional dental adhesive (Clearfil SE Bond) for 70 days in vitro. From each material, five disk-shaped specimens (diameter: 9.0 mm, height: 1.5 mm) were prepared and immersed in 5 ml of 10 mM phosphate buffered solution (pH 7.0). After 1, 3, 7, 14, 21, 28, 35, 42, 49, 56, 63 and 70 days, the samples were transferred into new solutions. The fluoride content was determined with a combined fluoride sensitive electrode attached to an ion analyzer. Data were statistically analyzed with ANOVA, followed by Scheffé's test. Reactmer Bond showed the greatest fluoride release over 70 days (280.2 +/- 10.1 micrograms/cm2) among the materials tested. The values for One-up Bond F and Trial KBF Bond were 83.4 +/- 5.3 micrograms/cm2 and 58.6 +/- 1.5 micrograms/cm2, respectively. The values were significantly different among the four groups (p < 0.0001). Clearfil SE Bond showed almost no fluoride release over 70 days.