Limiting distribution of dense orbits in a moduli space of rank mm discrete subgroups in (m+1)(m+1)-space

Consider the moduli space $X_{m,m+1}$ rank-$m$ discrete subgroups of covolume equal to one in $\mathbb R^{m+1}$. There is a natural action of $\text{SL}(m+1,\mathbb R)$ on $X_{m,m+1}$, and it turns out that for every lattice subgroup $\Gamma \leq\text{SL}(m+1,\mathbb R)$, each orbit $x_0.\Gamma$ is dense in $X_{m,m+1}$. In this paper we compute the limiting distribution of these orbits with respect to a filtration of growing norm balls, where the norm is given by the sum of squares. The main motivation for this result comes from the work of Sargent and Shapira where they studied random walks in $X_{2,3}$. Another motivation for our work is to extend the scope of applications of the duality principle in homogeneous dynamics. The moduli space $X_{m,m+1}$ identifies as $H\backslash \text{SL}(m+1,\mathbb R)$, and the duality principle recasts the above problem into the problem of establishing certain volume growth properties of growing skewed balls in $H$ and proving ergodic theorems of the left action of $H$ on $\text{SL}(m+1,\mathbb R)/\Gamma$ along the skewed balls. Specifically, we use the duality principle as developed in the work of Gorodnik and Weiss. Our ergodic theorems are proven by applying theorems of Shah building on the linearization technique. Previously, the duality principle wasn't applied in the setting where $H$ has infinitely many non-compact connected components. Our general result is in the setting where $H$ is a certain subgroup of a minimal parabolic group of $\text{SL}(m+1,\mathbb R)$ such that in the Levi-component there's a lattice.Comment: All comments are welcome. arXiv admin note: text overlap with arXiv:2305.0413

Paraoxonase Activity and Expression Is Modulated by Therapeutics in Experimental Rat Nonalcoholic Fatty Liver Disease

Objective. The objective of the present study is to investigate the effect of rosiglitazone, metformin, ezetimibe, and valsartan (alone or in combinations) on paraoxonase (PON) activity and PON-mRNA expression in nonalcoholic fatty liver disease (NAFLD). Methods. 54 Male Sprague–Dawley rats were divided to 9 groups: chow diet group (15 weeks); methionine-choline-deficient diet (MCDD) group (15 weeks); MCDD-treated groups for the last 6 weeks with either metformin (M), rosiglitazone (R), metformin plus rosiglitazone (M+R), ezetimibe (E), valsartan (V), or a combination of R+M+V or of R+M+V+E for a total period of 15 weeks. Results. PON activities in serum and liver were decreased in MCDD rats. PON activity in serum increased significantly in all treatment groups. PON activity in liver was also increased significantly, except only in groups R, E, V, R+M+V, and R+M+V+E. Liver PON3 mRNA expression increased significantly in groups R+M, E, V, R+M+V, and R+M+V+E whereas liver PON2 mRNA expression increased significantly in MCDD, R+M, E, V, R+M+V, and R+M+V+E. Conclusions. PON activities in serum and liver were decreased in NAFLD. Treatment with insulin sensitizers, ezetimibe, and valsartan increased PON activity and reduced oxidative stress both in serum and liver

Paraoxonase Activity and Expression Is Modulated by Therapeutics in Experimental Rat Nonalcoholic Fatty Liver Disease

Objective. The objective of the present study is to investigate the effect of rosiglitazone, metformin, ezetimibe, and valsartan (alone or in combinations) on paraoxonase (PON) activity and PON-mRNA expression in nonalcoholic fatty liver disease (NAFLD). Methods. 54 Male Sprague-Dawley rats were divided to 9 groups: chow diet group (15 weeks); methionine-choline-deficient diet (MCDD) group (15 weeks); MCDD-treated groups for the last 6 weeks with either metformin (M), rosiglitazone (R), metformin plus rosiglitazone (M+R), ezetimibe (E), valsartan (V), or a combination of R+M+V or of R+M+V+E for a total period of 15 weeks. Results. PON activities in serum and liver were decreased in MCDD rats. PON activity in serum increased significantly in all treatment groups. PON activity in liver was also increased significantly, except only in groups R, E, V, R+M+V, and R+M+V+E. Liver PON3 mRNA expression increased significantly in groups R+M, E, V, R+M+V, and R+M+V+E whereas liver PON2 mRNA expression increased significantly in MCDD, R+M, E, V, R+M+V, and R+M+V+E. Conclusions. PON activities in serum and liver were decreased in NAFLD. Treatment with insulin sensitizers, ezetimibe, and valsartan increased PON activity and reduced oxidative stress both in serum and liver

Can Campylobacter coli induce Guillain-Barré syndrome?

Campylobacter jejuni enteritis is the most frequently identified infection preceding the Guillain-Barr\ue9 syndrome (GBS) and neural damage is thought to be induced through molecular mimicry between C. jejuni lipo-oligosaccharide (LOS) and human gangliosides. It has been questioned whether or not other Campylobacter species, including C. curvus, C. upsaliensis and C. coli, could be similarly involved. This is relevant because it would imply that bacterial factors considered important in the aetiology of GBS crossed species barriers. Two prior reports have appeared where C. coli was putatively associated with a case of GBS.Peer reviewed: YesNRC publication: Ye