Regulators for Rankin-Selberg products of modular forms

We prove a weak version of Beilinson's conjecture for non-critical values of $L$-functions for the Rankin-Selberg product of two modular forms.Comment: 16 pages, submitte

On the anticyclotomic Iwasawa main conjecture for modular forms

We generalize the work of Bertolini and Darmon on the anticyclotomic main conjecture for weight two forms to higher weight modular forms.Comment: The hypothesis (CR+) (3-4) is revise

k-anonymous Microdata Release via Post Randomisation Method

The problem of the release of anonymized microdata is an important topic in the fields of statistical disclosure control (SDC) and privacy preserving data publishing (PPDP), and yet it remains sufficiently unsolved. In these research fields, k-anonymity has been widely studied as an anonymity notion for mainly deterministic anonymization algorithms, and some probabilistic relaxations have been developed. However, they are not sufficient due to their limitations, i.e., being weaker than the original k-anonymity or requiring strong parametric assumptions. First we propose Pk-anonymity, a new probabilistic k-anonymity, and prove that Pk-anonymity is a mathematical extension of k-anonymity rather than a relaxation. Furthermore, Pk-anonymity requires no parametric assumptions. This property has a significant meaning in the viewpoint that it enables us to compare privacy levels of probabilistic microdata release algorithms with deterministic ones. Second, we apply Pk-anonymity to the post randomization method (PRAM), which is an SDC algorithm based on randomization. PRAM is proven to satisfy Pk-anonymity in a controlled way, i.e, one can control PRAM's parameter so that Pk-anonymity is satisfied. On the other hand, PRAM is also known to satisfy ${\varepsilon}$-differential privacy, a recent popular and strong privacy notion. This fact means that our results significantly enhance PRAM since it implies the satisfaction of both important notions: k-anonymity and ${\varepsilon}$-differential privacy.Comment: 22 pages, 4 figure

The hepatic sympathetic nerve plays a critical role in preventing Fas induced liver injury in mice

Background: Although previous studies have shown that the hepatic sympathetic nerve controls various physiological functions in the liver, the role of this nerve in liver injury has yet to be clarified.Aims: The purpose of this study was to elucidate the role of this nerve, based on our newly developed technique for selectively removing the activities of the hepatic sympathetic nerve.Subjects and methods: Male C57BL/6 mice were operated on for hepatic sympathetic denervation. Thereafter, mice were intravenously administered 0.25 or 0.35 mg/g weight of the Fas agonist antibody, Jo-2, after which mortality by fulminant hepatitis was evaluated. Apoptosis in the liver was also examined by both terminal deoxynucleotidyl transferase mediated dUTP nick end labelling and caspase-3 assay.Results: Mortality in sympathectomised mice was significantly higher than that in sham operated mice following administration of Jo-2. This result was also supported by apoptosis data in which sympathectomised livers exhibited a significant elevation in the number of apoptotic hepatocytes and caspase-3 activity after Jo-2 treatment compared with sham operated livers. Moreover, pretreatment with norepinephrine dose dependently inhibited the hepatic sympathectomy induced increase in mortality after Jo-2 injection. Antiapoptotic protein levels of FLICE inhibitory protein, Bcl-xL, and Bcl-2 in the liver were significantly lower in sympathectomised mice at one and two hours following Jo-2 treatment than in sham operated animals. In addition, interleukin 6 supplementation dose dependently suppressed the hepatic sympathectomy induced increase in mortality after Jo-2 treatment.Conclusions: These results suggest that norepinephrine released from the hepatic sympathetic nerve plays a critical role in protecting the liver from Fas mediated fulminant hepatitis, possibly via mechanisms including antiapoptotic proteins and interleukin 6

Electric foot-shock stress drives TNF-alpha production in the liver of IL-6-deficient mice

Objectives: Accumulating evidence has shown that interleukin-6 (IL-6) has pleiotropic effects on a variety of biological functions, including its antiapoptotic potential during liver injury. Our previous work demonstrated that restraint stress-induced elevation of plasma IL-6 negatively regulates plasma tumor necrosis factor-alpha (TNF-alpha). Herein, we further clarified the mechanism underlying the above finding and investigated the effect of IL-6 on liver apoptosis triggered by stress. Methods: Male C57BL/6J and IL-6-deficient C57BL/SV129 mice were exposed to 1 h of electric foot-shock stress. Thereafter, the serum, liver and spleen TNF-alpha levels were measured at several time points. Serum alanine aminotransferase (ALT), liver caspase-3 and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling ( TUNEL) activities were analyzed to evaluate the severity of liver injury and apoptosis. Results: The liver, but not the spleen, of the IL-6-deficient mice exhibited a significant increase in TNF-alpha level after stress in parallel with serum TNF-alpha elevation, whereas no such TNF-alpha responses were found in the wild animals. No significant differences in stress-induced elevation of serum ALT levels, liver caspase-3 activities and the number of TUNEL-positive hepatocytes were found between the wild and IL-6-deficient mice. Conclusions: Taken together, these results indicate that IL-6 may play a critical role in suppressing TNF-alpha production in the liver, thereby decreasing the blood TNF-alpha level. In contrast, IL-6 secretion was shown to have no protective effect on stress-triggered liver injury. Copyright (C) 2004 S. Karger AG, Basel

Social disruption stress exacerbates alpha-galactosylceramide-induced hepatitis in mice

Objective: Psychosocial stress has been suggested as a possible aggravating factor in liver diseases, however, the underlying mechanism has yet to be clarified. Recently, our research revealed that electric foot-shock stress aggravated NK1.1 Ag+ T cell-dependent a-galactosylceramide (alpha-GalCer)-induced hepatitis in mice via a mechanism mediated by endogenous glucocorticoids. In this study, we examined whether or not such aggravation could be applied to a psychosocially stressful situation, e.g. social disruption stress. Methods: Male wildtype C57BL/6 (B6) or B6 hepatitis virus type B surface antigen transgenic (HBs-tg) mice, a hepatitis B virus carrier mouse model, were exposed 3 times in 1 week to social disruption stress in which an 8-month-old aggressive male intruder was placed into their home cage (5 mice per group) for 2 h. Twelve hours after the final exposure to the stress, the wild-type and HBs-tg mice were intravenously injected with alpha-GalCer. Results:The stress-exposed wild-type mice exhibited significantly reduced thymus weight loss compared with the control animals. Moreover, this stress regimen led to a significant increase in serum alanine aminotransferase levels in both the wild-type and the HBs-tg mice, although the increase in the HBs-tg mice was higher than that in the wild-type mice. Conclusion: These findings demonstrated that, similar to electric foot-shock stress, social disruption stress exacerbated alpha-GalCer-induced hepatitis. Copyright (C) 2005 S. Karger AG, Basel