Review of evidence implicating the plasminogen activator system in blood-brain barrier dysfunction associated with Alzheimer's disease.

Elucidating the pathogenic mechanisms of Alzheimer's disease (AD) to identify therapeutic targets has been the focus of many decades of research. While deposition of extracellular amyloid-beta plaques and intraneuronal neurofibrillary tangles of hyperphosphorylated tau have historically been the two characteristic hallmarks of AD pathology, therapeutic strategies targeting these proteinopathies have not been successful in the clinics. Neuroinflammation has been gaining more attention as a therapeutic target because increasing evidence implicates neuroinflammation as a key factor in the early onset of AD disease progression.

Sex-specific acute and chronic neurotoxicity of acute diisopropylfluorophosphate (DFP)-intoxication in juvenile Sprague-Dawley rats.

Preclinical efforts to improve medical countermeasures against organophosphate (OP) chemical threat agents have largely focused on adult male models. However, age and sex have been shown to influence the neurotoxicity of repeated low-level OP exposure. Therefore, to determine the influence of sex and age on outcomes associated with acute OP intoxication, postnatal day 28 Sprague-Dawley male and female rats were exposed to the OP diisopropylfluorophosphate (DFP; 3.

[Identification of sibling brothers using STR and Y-biallelic markers].

Objective: To explore the methods for identification of sibling brothers with Y-STR locus mutation by detection of genetic markers on autosome and Y-biallelic.

Methods: Goldeneye 20A and 18NC kit were used to genotyped the 35 STRs on autosome from two men. PowerPlex Y kit and Yfiler kit were used to genotyped the 16 STRs on Y chromosome full sibling index was calculated by ITO method.