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.     

A comparative study of unilateral dislocated mandibular condyle fractures in the rabbit.

PURPOSE: The purpose of this study was to clarify the influence of patients age and the degree of dislocation on the healing of mandibular condyle fractures. MATERIAL AND METHODS: Sixty-two Japanese white rabbits (30 adolescent and 30 adult ones) were used. They underwent unilateral condylar neck osteotomy. The proximal fragments were positioned differently. In group I animals, the fragments were reduced into the original position, in group II animals the small fragment was dislocated 55-90 degrees to the ramus. In group III animals the proximal fragment was dislocated 135 degrees to the ramus. Gross and microscopic assessment was performed 4, 6, 8, 12 and 24 weeks postoperatively. RESULTS: In adolescent animals, complete healing of the fracture was observed, irrespective of the degree of dislocation. In the adult animals, there was complete healing of the fractures in groups I and II. In group III animals, there was a decrease of ramus height accompanied by some fibro-cartilaginous changes. CONCLUSION: Even in rabbits condylar deformation has been found following heavily dislocated artificial condylar fractures in adult animals. This result will help to decide for or against surgical treatment of condylar fractures in humans.