Comparative evaluation of pulpal repair after direct pulp capping using stem cell therapy and biodentine: An animal study

The response of the dentin–pulp complex in rat teeth was investigated after direct capping with biodentine with or without bone marrow‐derived stem cells (BMDSCs). Following mechanical exposure, pulps were randomly capped with one of the followings materials: calcium hydroxide, biodentine or 1 × 10⁵ BMDSCs mL^?1 + biodentine. Histological examination was performed by light microscopy after 1, 3 and 5 weeks. Inflammatory reaction, necrotic tissue formation and calcific bridge formation were scored. Analysis showed that compared with the effects of calcium hydroxide or biodentine, BMDSCs + biodentine substantially reduced inflammatory reaction and necrotic tissue while promoting calcified tissue formation. Therefore, the combination of biodentine and BMDSCs could potentially stimulate pulp tissue regeneration after direct pulp capping.     

Methylation of histone H3 lysine 36 enhances DNA repair by nonhomologous end-joining

Given its significant role in the maintenance of genomic stability, histone methylation has been postulated to regulate DNA repair. Histone methylation mediates localization of 53BP1 to a DNA double-strand break (DSB) during homologous recombination repair, but a role in DSB repair by nonhomologous end-joining (NHEJ) has not been defined. By screening for histone methylation after DSB induction by ionizing radiation we found that generation of dimethyl histone H3 lysine 36 (H3K36me2) was the major event. Using a novel human cell system that rapidly generates a single defined DSB in the vast majority of cells, we found that the DNA repair protein Metnase (also SETMAR), which has a SET histone methylase domain, localized to an induced DSB and directly mediated the formation of H3K36me2 near the induced DSB. This dimethylation of H3K36 improved the association of early DNA repair components, including NBS1 and Ku70, with the induced DSB, and enhanced DSB repair. In addition, expression of JHDM1a (an H3K36me2 demethylase) or histone H3 in which K36 was mutated to A36 or R36 to prevent H3K36me2 formation decreased the association of early NHEJ repair components with an induced DSB and decreased DSB repair. Thus, these experiments define a histone methylation event that enhances DNA DSB repair by NHEJ.     

Characterization of a paradoxical post-operative increase in serum cortisol in Cushing disease

Pituitary - In Cushing disease, early post-operative serum cortisol fluctuations have not been adequately characterized, and their association with initial remission and recurrence is unclear. A...     

Pharmacoproteomics of Brain Barrier Transporters and Substrate Design for the Brain Targeted Drug Delivery

Pharmaceutical Research - One of the major reasons why central nervous system (CNS)-drug development has been challenging in the past, is the barriers that prevent substances entering from the...     

Miller Fisher syndrome: unique involvement of ophthalmic division of trigeminal nerve

The clinical, electrophysiological, and radiological features of a patient with a typical Miller Fisher Syndrome are reported. The patient has shown a unique affection of the ophthalmic division of the trigeminal nerve. The significance of serial electrophysiological testing particularly blink reflex study is discussed.     

Toll- like receptor 2 polymorphism and IL-6 profile in relation to disease progression in chronic HBV infection: a case control study in Egyptian patients

Chronic hepatitis B (CHB) has a wide range of outcomes depending on host immune responses mainly Toll-like receptors (TLRs) signaling and released cytokines. Toll-like receptor 2 (TLR2) single nucleotide polymorphisms (SNPs) and interleukin 6 (IL-6) may influence the course of CHB. We aimed to elucidate the relation between TLR-2 polymorphism, IL-6 profile, and CHB progression. We analyzed TLR-2 polymorphism (SNP; rs3804099) in 185 CHB patients and 60 controls using TaqMan allelic discrimination assay. Serum IL-6 levels were assessed by ELISA. IL-6 levels were considerably higher in active CHB and cirrhotic patients compared with inactive carriers and controls (P < 0.001). IL-6 showed positive correlation with ALT and advanced fibrosis in active CHB patients (r = 0.31, P = 0.02). A significant positive correlation was noticed between IL-6 and HBV DNA PCR in all CHB groups. TT genotype of rs3804099/TLR-2 was significantly more prevalent in inactive carriers compared to active hepatitis patients (P = 0.04, OR = 0.39 and 95% CI: 0.16–0.95). Both heterozygous CT and mutant TT genotypes were significantly more frequent among inactive carriers compared to cirrhotic patients (P = 0.01, OR = 0.33, 95% CI: 0.13–0.81 and P = 0.009, OR = 0.32, 95% CI: 0.13–0.77). TT genotype was significantly related to lower IL-6 levels in active hepatitis and cirrhotic groups (P = 0.005 and P = 0.001, respectively) showing that TLR mutations would be associated with milder hepatitis activity and lower possibility for disease progression. There may be a positive association between TLR2 rs3804099 polymorphism and hepatitis B activity. IL-6 is a good indicator of CHB disease progression.

     

HLA antigens in schistosomal hepatic fibrosis patients with haematemesis

20 patients of schistosomal hepatic fibrosis and splenomegaly (SHF) with and without haematemesis were examined. Typing for HLA-A, B and C antigens in these patients were compared with those of a group of 100 Egyptian controls. The study showed the presence of an association between HLA-A1 and B5 antigens in SHF cases. However, there was no significant association between HLA antigens and SHF cases with haematemesis.