Solving N=2 SYM by Reflection Symmetry of Quantum Vacua

The recently rigorously proved nonperturbative relation between u and the prepotential, underlying N=2 SYM with gauge group SU(2), implies both the reflection symmetry $\overline{u(\tau)}=u(-\bar\tau)$ and $u(\tau+1)=-u(\tau)$ which hold exactly. The relation also implies that $\tau$ is the inverse of the uniformizing coordinate u of the moduli space of quantum vacua. In this context, the above quantum symmetries are the key points to determine the structure of the moduli space. It turns out that the functions a(u) and a_D(u), which we derive from first principles, actually coincide with the solution proposed by Seiberg and Witten. We also consider some relevant generalizations.Comment: 12 pg. LaTex, Discussion of the generalization to higher rank groups added. To be published in Phys. Rev.

NOTE ON MANIFEST LORENTZ AND GENERAL COORDINATE INVARIANCE IN DUALITY SYMMETRIC MODELS.

We consider a generalization of a duality symmetric model proposed by Schwarz and Sen. It is based on enlarging the model with a dynamical vector field being a time-like component of a local Lorentz frame. This allows one to preserve the manifest Lorentz invariance of the model in flat space--time. The presence of this field is regarded as a relic of gravitational interaction which respects the general coordinate invariance in curved space--time but breaks the local Lorentz symmetry in tangent space down to its spatial subgroup.Comment: 7 pages, LaTeX file

Clinical and biochemical improvements in a patient with MNGIE following enzyme replacement.

Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a rare autosomal recessive metabolic disorder caused by a deficiency of thymidine phosphorylase (TP, EC2.4.2.4) due to mutations in the nuclear gene TYMP. TP deficiency leads to plasma and tissue accumulations of thymidine and deoxyuridine which generate imbalances within the mitochondrial nucleotide pools, ultimately leading to mitochondrial dysfunction.1 MNGIE is characterized clinically by leukoencephalopathy, external ophthalmoplegia, peripheral polyneuropathy, cachexia, and enteric neuromyopathy manifesting as gastrointestinal dysmotility. The condition is relentlessly progressive, with patients usually dying from a combination of nutritional and neuromuscular failure at an average age of 37 years.2 Allogeneic hematopoietic stem cell transplantation (AHSCT) offers a permanent cure. Clinical and biochemical improvements following AHSCT have been reported but it carries a high mortality risk and is limited by matched donor availability.3 A consensus proposal for standardizing AHSCT recommends treatment of patients without irreversible end-stage disease and with an optimally matched donor; a majority of patients are ineligible and thus there is a critical requirement for an alternative treatment

Poor Outcome in a Mitochondrial Neurogastrointestinal Encephalomyopathy Patient with a Novel TYMP Mutation: The Need for Early Diagnosis.

Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a devastating autosomal recessive disorder due to mutations in TYMP, which cause loss of function of thymidine phosphorylase (TP), nucleoside accumulation in plasma and tissues and mitochondrial dysfunction. The clinical picture includes progressive gastrointestinal dysmotility, cachexia, ptosis and ophthalmoparesis, peripheral neuropathy and diffuse leukoencephalopathy, which usually lead to death in early adulthood. Therapeutic options are currently available in clinical practice (allogeneic hematopoietic stem cell transplantation and carrier erythrocyte entrapped TP therapy) and newer, promising therapies are expected in the near future. However, successful treatment is strictly related to early diagnosis. We report on an incomplete MNGIE phenotype in a young man harboring the novel heterozygote c.199 C>T (Q67X) mutation in exon 2, and the previously reported c.866 A>C (E289A) mutation in exon 7 in TYMP. The correct diagnosis was achieved many years after the onset of symptoms and unfortunately, the patient died soon after diagnosis because of multiorgan failure due to severe malnutrition and cachexia before any therapeutic option could be tried. To date, early diagnosis is essential to ensure that patients have the opportunity to be treated. MNGIE should be suspected in all patients who present with both gastrointestinal and nervous system involvement, even if the classical complete phenotype is lacking

Axial anomalies in gauge theory by exact renormalization group method

The global chiral symmetry of a $SU(2)$ gauge theory is studied in the framework of renormalization group (RG). The theory is defined by the RG flow equations in the infrared cutoff \L and the boundary conditions for the relevant couplings. The physical theory is obtained at \L=0. In our approach the symmetry is implemented by choosing the boundary conditions for the relevant couplings not at the ultraviolet point \L=\L_0\to\infty but at the physical value \L=0. As an illustration, we compute the triangle axial anomalies.Comment: 11 pages + 1 appended EPS figure, LaTeX, UPRF 94-39