How is the quality of the available evidence on molar-incisor hypomineralization treatment? An overview of systematic reviews

Clinical Oral Investigations - This overview analyzed the quality of the systematic reviews (SRs) available on treatments for molar-incisor hypomineralization (MIH). Six electronic databases were...     

Relationship between European Mitochondrial Haplogroups and Chronic Renal Allograft Rejection in Patients with Kidney Transplant

Mitochondrial DNA variants may contribute to differences in mitochondrial function, leading to an altered immune system. The aim of this study was to analyze the relationship between mtDNA haplogroups and the development of chronic allograft dysfunction in patients with kidney transplant. A retrospective observational study was carried out on 261 patients who received kidney transplant (114 had stable transplant and 147 patients developed chronic allograft dysfunction). DNA samples were genotyped for 14 mtDNA polymorphisms by using Sequenom''s MassARRAY platform (San Diego, CA, USA). Only European white patients within the N macro-cluster were included. Patients with haplogroups V (odds ratio (OR)=0.32; p=0.037) and J (OR=0.36; p=0.038) showed lower odds for developing CRAD than patients with haplogroup H. After adjusting for the most significant variables, haplogroups V and J tended to statistical significance (p=0.091 and p=0.067 respectively). This is a preliminary study in which mtDNA haplogroups seem to be implicated in susceptibility or protection for developing chronic allograft dysfunction.     

The Cardiovascular Response to Acoustic Stimuli

The purposes of this investigation were to determine whether adults display alterations of cardiac rate under acoustical stimulus conditions and whether such alterations are influenced by signal level. The stimulus consisted of a narrow band of noise centered at 1000 Hz and presented at 20, 40, 60 and 80 dB SPL. The stimulus was found to produce alterations of heart rate significantly different from variation under non-stimulus conditions, indicating that cardiovascular responses occurred. However, the responses themselves were unaffected by differences of sound pressure level.     

Autophagy,mitochondria and 3-nitropropionic acid joined in the same model

Huntington''s disease (HD) is a neurodegenerative disorder caused by a mutation in the gene encoding the huntingtin protein. Although the precise mechanism by which neuronal degeneration occurs is still unclear, several elements are important to its development: (1) altered gene expression and protein synthesis, (2) mitochondrial damage and (3) improper regulation of the autophagy programme. In this issue of British Journal of Pharmacology, Galindo and co-workers provide the first evidence for a role of the mitochondrial permeability transition pore (mPTP) in mitochondrial fragmentation and autophagy activation. In a model of cell death induced by 3-nitropropionic acid (3-NP) in human neural cells, the authors describe clear functions for mPTP and Bax, but not the mitochondrial fusion/fission machinery, mitochondrial fragmentation and autophagy (mitophagy). This commentary summarises the significance of this relationship and suggests several points for future development.