Spin-Glass and Chiral-Glass Transitions in a ±J\pm J Heisenberg Spin-Glass Model in Three Dimensions

The three-dimensional $\pm J$ Heisenberg spin-glass model is investigated by the non-equilibrium relaxation method from the paramagnetic state. Finite-size effects in the non-equilibrium relaxation are analyzed, and the relaxation functions of the spin-glass susceptibility and the chiral-glass susceptibility in the infinite-size system are obtained. The finite-time scaling analysis gives the spin-glass transition at $T_{\rm sg}/J=0.21_{-0.02}^{+0.01}$ and the chiral-glass transition at $T_{\rm cg}/J=0.22_{-0.03}^{+0.01}$. The results suggest that both transitions occur simultaneously. The critical exponent of the spin-glass susceptibility is estimated as $\gamma_{\rm sg}= 1.7 \pm 0.3$, which makes an agreement with the experiments of the insulating and the canonical spin-glass materials.Comment: 4 pages, 2 figure

Molecular, clinical, and muscle studies in myotonic dystrophy type 1 (DM1) associated with novel variant CCG expansions

We assessed clinical, molecular and muscle histopathological features in five unrelated Italian DM1 patients carrying novel variant pathological expansions containing CCG interruptions within the 3'-end of the CTG array at the DMPK locus, detected by bidirectional triplet primed PCR (TP-PCR) and sequencing. Three patients had a negative DM1 testing by routine long-range PCR; the other two patients were identified among 100 unrelated DM1 cases and re-evaluated to estimate the prevalence of variant expansions. The overall prevalence was 4.8 % in our study cohort. There were no major clinical differences between variant and non-variant DM1 patients, except for cognitive involvement. Muscle RNA-FISH, immunofluorescence for MBNL1 and RT-PCR analysis documented the presence of ribonuclear inclusions, their co-localization with MBNL1, and an aberrant splicing pattern involved in DM1 pathogenesis, without any obvious differences between variant and non-variant DM1 patients. Therefore, this study shows that the CCG interruptions at the 3'-end of expanded DMPK alleles do not produce qualitative effects on the RNA-mediated toxic gain-of-function in DM1 muscle tissues. Finally, our results support the conclusion that different patterns of CCG interruptions within the CTG array could modulate the DM1 clinical phenotype, variably affecting the mutational dynamics of the variant repeat

Propargylamines by Three-component Coupling Reaction

Quaternisation of methylimidazole by bromoalkanes afforded imidazolium salts (1) which were converted to Ag-NHC complexes bearing imidazol-2-ylidenes, [(C-n mim) Ag-2](2)[Ag2Br4], 2, using the silver oxide. The catalytic activities of silver-N-heterocyclic carbene (NHC) complexes were investigated in the three component coupling reaction of aldehyde, alkyne and amine to propargylamines

Propargylamines by Three-component Coupling Reaction

Quaternisation of methylimidazole by bromoalkanes afforded imidazolium salts (1) which were converted to Ag-NHC complexes bearing imidazol-2-ylidenes, [(C-n mim) Ag-2](2)[Ag2Br4], 2, using the silver oxide. The catalytic activities of silver-N-heterocyclic carbene (NHC) complexes were investigated in the three component coupling reaction of aldehyde, alkyne and amine to propargylamines

Monocyte Chemoattractant Protein 1, Active Carboxypeptidase B and CAPAP at Hospital Admission Are Predictive Markers for Severe Acute Pancreatitis.

Background: CAPAP, the activation peptide of procarboxypeptidase B, is a predictor of severe acute pancreatitis (AP). Active carboxypeptidase (aCAP) may be a better predictor, as its turnover is slower. Monocyte chemotactic protein-1 (MCP-1) is an early inflammatory marker and increases before complications in severe AP. We conducted a cohort study to evaluate these markers as predictors for severe AP. Method: 140 patients with AP were included, retrospectively grouped as severe or mild by the Atlanta classification. CAPAP, MCP-1 and aCAP were analyzed in admission samples. Receiver operating characteristic curves determined high vs. low levels. Results: The levels of all markers were significantly higher in patients with severe disease. High levels of serum MCP-1 was associated with a high risk of developing severe AP (OR 40.8; 95% CI 8.5-195). High ORs were also seen for urine MCP-1 (OR 7.3; 95% CI 2.2-24.3), serum CAPAP (OR 5.4; 95% CI 1.6-17.7), urine CAPAP (OR 4.8; 95% CI 1.6-14.2), and serum aCAP (OR 3.7; 95% CI 1.2-11.3). Conclusion: Serum MCP-1 at admission was strongly associated with development of severe AP. MCP-1 in urine, CAPAP in serum and urine and aCAP may also be useful for predicting severe AP. Copyright (c) 2008 S. Karger AG, Basel and IAP