Mouse Anti Human DMPK Hybridoma [NBOEN26 6D0]

Multifunctional bio-based epoxy resin (PEMPAE) was synthesized by reacting Diels-Alder adduct of gum rosin and maleic anhydride (MPA) with pentaerythritol to get the esterified product (PEMPA) which was further epoxidized using epichlorohydrin and potassium hydroxide. This paper includes the synthesis of bio-based imidoamine curing agent (IAEDK) by reacting diamino diphenyl ether (DDE) with dimaleopimaryl ketone (DMPK), a dehydrodecarboxylated derivative of MPA. The synthesized products were characterized by Fourier transform infrared Spectroscopy (FTIR), proton and C-13 nuclear magnetic resonance spectroscopy (H-1-NMR and C-13-NMR). Curing dynamics of rosin-based epoxy cured with rosinbased imidoamine crosslinker were evaluated using differential scanning calorimetry (DSC) and were compared with resin cured with synthesized DMPK and commercial DDE curing agents. The mechanical properties and thermal stability of the cured epoxy samples were evaluated using a universal testing machine (UTM) and thennogravimetric analyzer (TGA), respectively. The chemical resistance of the samples was determined in terms of % weight loss when immersed in NaOH, HCl and NaCl solutions. The morphological changes were also evaluated via scanning electron microscopy (SEM). Results revealed that rosin-based epoxy cured with imidoamine curing agent gave preeminent properties over the commercial one. The studies suggested that curing properties were greatly affected by the molecular topology and kind of curing agent used.

Myotonic dystrophy type 1 (DM1) is a multisystemic autosomal dominant disorder characterized by a highly variable phenotype and caused by an unstable CTG repeat expansion in the 3' untranslated region of the dystrophia myotonica protein kinase (DMPK) gene. Longer CTG repeat expansions often correlate with an anticipated age at onset and CTG repeat number may account for 45-60 % of the variance in disease severity. In order to search for candidate genes that could act as modifiers of disease severity, we studied the association between Muscleblind-like protein-1 (MBNL1) gene polymorphisms and the DM1 phenotype. In a group of 301 patients diagnosed with DM1 based on clinical symptoms, diagnosis was confirmed by molecular analysis of the DMPK gene. Patients were divided into four subtypes. The first subtype corresponded to asymptomatic patients or those with a mild phenotype, the second included those with a classic phenotype, the third concerned childhood onset, and the fourth corresponded to the congenital form of DM1. Three SNPs located in the MBNL1 gene promoter, rs323622, rs17283597, and rs17433672, were studied. Case-control analysis revealed that allele frequencies for the latter two were significantly associated with DM1 (p = 0.037 and p = 0.020). Multivariate linear regression analysis using phenotype as the dependent variable demonstrated that the TT genotype of the third SNP, rs323622, was associated with a more severe phenotype (p = 0.0034) and accounted for 1.88 % of the variance in disease severity. We report the association of several genetic variants of the MBNL1 gene with DM1 or with the severity of the disease.