Tauonic B decays in the Minimal Supersymmetric Standard Model

We study new physics effects on B decay processes including a final $\tau$ particle, namely $B \to D \tau \nu$ and $B \to \tau \nu$. An important feature of these processes is that a charged Higgs boson can contribute to the decay amplitude at the tree level in models such as Two Higgs Doublet Model and the Minimal Supersymmetric Standard Model (MSSM). We derive a resummed effective Lagrangian for charged-Higgs mediated interactions in the MSSM with the Minimal Flavor Violation. Including supersymmetric (SUSY) loop corrections for down-type-quark and charged-lepton Yukawa couplings, we calculate the branching ratios of the $B \to D \tau \nu$ and $B \to \tau \nu$ processes. We find that SUSY correction due to gluino-sbottom diagrams can change the Higgs exchange contribution by $\pm50$%, whereas stau-neutralino diagrams can make corrections up to 20%. We also discuss relationship between SUSY corrections in the tauonic decays and flavor changing neutral current processes such as $B_s \to \mu^+\mu^-$ and $b \to s \gamma$.Comment: 29 pages, 22 figure

Antineoplastic Effects of Gamma Linolenic Acid on Hepatocellular Carcinoma Cell Lines

The aim of this study was to investigate the effect and the mechanism of gamma linolenic acid (GLA) treatment on human hepatocellular (HCC) cell lines. The human HCC cell line HuH7 was exposed to GLA. Cell proliferation and reactive oxygen species (ROS) generation including lipid peroxidation and apoptosis were compared. We then used a cDNA microarray analysis to investigate the molecular changes induced by GLA. GLA treatment significantly reduced cell proliferation, generated ROS, and induced apoptosis. After 24 h exposure of Huh7 cells to GLA, we identified several genes encoding the antioxidant proteins to be upregulated: heme oxygenase-1 (HO-1), aldo-keto reductase 1 family C1 (AKR1C1), C4 (AKR1C4), and thioredoxin (Trx). The HO-1 protein levels were overexpressed in Huh7 cells after GLA exposure using a Western blot analysis. Furthermore, chromium mesoporphyrin (CrMP), an inhibitor of HO activity, significantly potentiated GLA cytotoxicity. GLA treatment has induced cell growth inhibition, ROS generation including lipid peroxidation, and HO-1 production for antioxidant protection against oxidative stress caused by GLA in Huh7 cells. GLA treatment should be considered as a therapeutic modality in patients with advanced HCC

Neuropathology does not Correlate with Regional Differences in the Extent of Expansion of CTG Repeats in the Brain with Myotonic Dystrophy Type 1

Myotonic dystrophy (DM1) is known to be an adult-onset muscular dystrophy caused by the expansion of CTG repeats within the 3' untranslated region of the dystrophin myotonin protein kinase (DMPK) gene. The clinical features of DM1 include CNS symptoms, such as cognitive impairment and personality changes, the pathogenesis of which remains to be elucidated. We hypothesized that the distribution of neuropathological changes might be correlated with the extent of the length of the CTG repeats in the DMPK genes in DM1 patients. We studied the neuropathological changes in the brains of subjects with DM1 and investigated the extent of somatic instability in terms of CTG repeat expansion in the different brain regions of the same individuals by Southern blot analysis. The neuropathological changes included état criblé in the cerebral deep white matter and neurofibrillary tangles immunoreactive for phosphorylated tau in the hippocampus and entorhinal cortex, both of which were compatible with the subcortical dementia in DM1 patients. However, the length of the CTG repeats did not correlate with the regional differences in the extent of neuropathological changes. Our data suggested that pathomechanisms of dementia in DM1 might be more multifactorial rather than a toxic gain-of-function due to mutant RNA

Astrocytic gliomas: MRI and pathological grade.

The relationship between MR configuration and pathological grade was studied in 41 histologically verified supratentorial astrocytic gliomas with a 0.5T superconductive MR system. The gliomas included 13 low-grade astrocytomas (LGAs), 14 anaplastic astrocytomas (AAs) and 14 glioblastoma multiformes (GBMs). MRI configurations were classified into nine criteria which were scored and statistically analyzed. The mean values of LGAs, AAs and GBMs were 0.45 +/- 0.31, 1.18 +/- 0.20 and 1.47 +/- 0.22. In each grade, MRI score increased as pathological grades increased (p &#60; 0.01-0.001). LGAs had significantly lower values than AAs in five of the nine criteria (55.6%); heterogeneity, cyst or necrosis, edema or mass effect, border definition, and the degree of contrast enhancement, and lower values than GBMs in eight criteria (88.9%) except for hemorrhage. Three criteria (33.3%), heterogeneity, cyst or necrosis, and flow void sign were significantly higher in GBMs than AAs. The four variables, heterogeneity, cyst or necrosis, edema or mass effect and border definition, proved to be important factors related to the pathological grade in a multiple regression analysis.</p

Brain development in mice lacking L1–L1 homophilic adhesion

A new mouse line has been produced in which the sixth Ig domain of the L1 cell adhesion molecule has been deleted. Despite the rather large deletion, L1 expression is preserved at normal levels. In vitro experiments showed that L1–L1 homophilic binding was lost, along with L1-α5β1 integrin binding. However, L1–neurocan and L1–neuropilin binding were preserved and sema3a responses were intact. Surprisingly, many of the axon guidance defects present in the L1 knockout mice, such as abnormal corticospinal tract and corpus callosum, were not observed. Nonetheless, when backcrossed on the C57BL/6 strain, a severe hydrocephalus was observed and after several generations, became an embryonic lethal. These results imply that L1 binding to L1, TAG-1, or F3, and L1-α5β1 integrin binding are not essential for normal development of a variety of axon pathways, and suggest that L1–L1 homophilic binding is important in the production of X-linked hydrocephalus