Scaling Laws and Effective Dimension in Lattice SU(2) Yang-Mills Theory with a Compactified Extra Dimension

Monte Carlo simulations are performed in a five-dimensional lattice SU(2) Yang-Mills theory with a compactified extra dimension, and scaling laws are studied. Our simulations indicate that as the compactification radius $R$ decreases, the confining phase spreads more and more to the weak coupling regime, and the effective dimension of the theory changes gradually from five to four. Our simulations also indicate that the limit $a_4 to 0$ with $R/a_4$ kept fixed exists both in the confining and deconfining phases if $R/a_4$ is small enough, where $a_4$ is the lattice spacing in the four-dimensional direction. We argue that the color degrees of freedom in QCD are confined only for $R < R_{\rm max}$, where a rough estimate shows that $1/R_{\rm max}$ lies in the TeV range. Comments on deconstructing extra dimensions are given.Comment: 15 pages, TeX, 5 figure

A case of primary thoracic hemangiopericytoma: correlation between Ga-67 scintigraphic and pathological findings

A 27-year-old male was admitted to our hospital with the chief complaint of dyspnea. Radiologically, he was found to have a large tumor shadow in the left hemithorax with pleural effusion. The first thoracotomy was done to resect the tumor on January 14, 1988. The second and third thoracotomies were done because of local recurrence in the left hemithorax. Histological diagnosis was of a hmangio-pericytoma. Before the third operation, Ga-67 scintigraphy was performed. Ga-67 accumulation was noted in parts of the tumor mass. Histological findings of the resected tumor were compared with the degree and location of Ga-67 accumulation. Histologically, Ga-67 accumulation occurred in areas of bleeding and necrosis in the tumor tissue, but not in viable parts of the tumor. Ga-67 accumulation usually occurs in viable tumor cells, but our findings were contrary to this generality

Mitochondrial dysfunction associated with increased oxidative stress and α-synuclein accumulation in PARK2 iPSC-derived neurons and postmortem brain tissue

Abstract Background Parkinson’s disease (PD) is a neurodegenerative disease characterized by selective degeneration of dopaminergic neurons in the substantia nigra (SN). The familial form of PD, PARK2, is caused by mutations in the parkin gene. parkin-knockout mouse models show some abnormalities, but they do not fully recapitulate the pathophysiology of human PARK2. Results Here, we generated induced pluripotent stem cells (iPSCs) from two PARK2 patients. PARK2 iPSC-derived neurons showed increased oxidative stress and enhanced activity of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. iPSC-derived neurons, but not fibroblasts or iPSCs, exhibited abnormal mitochondrial morphology and impaired mitochondrial homeostasis. Although PARK2 patients rarely exhibit Lewy body (LB) formation with an accumulation of α-synuclein, α-synuclein accumulation was observed in the postmortem brain of one of the donor patients. This accumulation was also seen in the iPSC-derived neurons in the same patient. Conclusions Thus, pathogenic changes in the brain of a PARK2 patient were recapitulated using iPSC technology. These novel findings reveal mechanistic insights into the onset of PARK2 and identify novel targets for drug screening and potential modified therapies for PD.</p