Genetic polymorphisms of new 22 autosomal STR loci in the Mongolian ethnic group

The Microreader™ 23SP ID System is a novel STR kit, but there are no Mongolian data related to this kit. In this study, allelic frequencies and forensic parameters were obtained from 505 unrelated healthy Mongolians. These samples were amplified using the kit. The dataset successfully passed quality control after being submitted to STRidER (STRidER dataset reference STR000198). A total of 264 alleles were observed, with corresponding allelic frequencies ranged from 0.001 to 0.378. The combined power of discrimination (CPD) and combined probability of exclusion (CPE) of the 22 autosomal STR loci were 0.999999999999999999999999999217318 and 0.999999999776042, respectively. Furthermore, population differentiation comparisons involving previously reported groups were conducted.

     

Genetic characterization of 19 X-STRs in Sierra Leone population from Freetown

International Journal of Legal Medicine - A total of 550 individuals (265 males and 285 females) from Sierra Leone, a west-African coastal country, were genotyped using the Microreader™ 19X...     

Microbial contamination by a medical carbon dioxide laser

One of the advantages in using the carbon dioxide laser in medicine is the sterilization of the wound at the site of surgical intervention. In microbial studies, using the Sharplan Model 743 Medical Laser, we found substantial contamination of the area directly below the probe by viable bacteria and fungi. The levels of contamination varied from experiment to experiment, but were always substantial. The contamination is likely due to the stream of nitrogen gas emitted during and following laser irradiation in order to cool the lens. Following the implementation of several simple prophylactic procedures, including insertion of a filter on the end of the tube emitting the nitrogen gas, contamination by the gas stream was reduced to insignificant levels.     

Cholesterol homeostasis and the pathophysiology of Alzheimer's disease

The past 4 years have seen a growing interest in cholesterol metabolism and its relationship to Alzheimer's disease. From the first report linking cholesterol and beta-amyloid metabolisms to the recent positive report on the use of atorvastatin (Lipitor, Pfizer Inc.), a cholesterol-lowering drug, in mild-to-moderate Alzheimer's disease, this review examines the scientific progress pertaining to etiopathology of Alzheimer's disease over the past 15 years and the central role of lipids in this field of research. The role of key proteins involved in this metabolic pathway such as apolipoprotein E, lipoprotein lipase, caveolin, hydroxy-methylglutaryl Coenzyme A reductase, low-density lipoprotein receptors, cholesterol 24-hydroxylase, acyl-coenzyme A:cholesterol acyltransferase and beta-amyloid are discussed.     

Pro-inflammatory cytokines modulate glial apolipoprotein E secretion

Alzheimer's disease (AD) is a neurological disorder characterized by plaques and an elevated immune response. Specifically, increased expression of interleukin (IL)-1 and tumour necrosis factor (TNF)-alpha, has been observed in AD cerebrospinal fluid and temporal brain tissue. Both of these immunomodulators were shown to carry genetic variants that increase the risk of developing AD. Studies have also established the apolipoprotein E (apoE) gene to be a risk factor for AD with epsilon4 carriers having been found to show lower levels of brain apoE. In the present study, treatment of primary rat mixed glial cell cultures with IL-1beta induced a significant increase in extracellular apoE protein. In contrast, treatment primary rat astrocyte and mixed glial cell cultures with TNF-alpha significantly reduced extracellular apoE protein levels. These results are consistent with the notion that elevated cytokine expression directly modulates immunosuppression and indirectly apoE-mediated neuronal remodeling.     

A role for lipoprotein lipase during synaptic remodeling in the adult mouse brain

Lipoprotein lipase (LPL) is a member of a lipase family known to hydrolyze triglyceride molecules found in lipoprotein particles. This particular lipase also has a role in the binding of lipoprotein particles to different cell-surface receptors. LPL has been identified in the brain but has no specific function yet. This study aimed at elucidating the role of LPL in the brain in response to injury. Mice were subjected to hippocampal deafferentation using the entorhinal cortex lesion and mRNA and protein expression were assessed over a time-course of degeneration/reinnervation. Hippocampal LPL levels peaked at 2 days post-lesion (DPL) both at the mRNA and protein levels. No change was observed for receptors of the LDL-receptor family or RAP at DPL 2 in the hippocampus but the glia-specific syndecan-4 was found to be significantly upregulated at DPL 2. These results suggest that LPL is involved in the recycling of cholesterol and lipids released from degenerating terminals after a lesion through a syndecan-4-dependent pathway.     

Altered bidirectional plasticity and reduced implicit motor learning in concussed athletes

Persistent motor/cognitive alterations and increased prevalence of Alzheimer's disease are known consequences of recurrent sports concussions, the most prevalent cause of mild traumatic brain injury (TBI) among youth. Animal models of TBI demonstrated that impaired learning was related to persistent synaptic plasticity suppression in the form of long-term potentiation (LTP) and depression (LTD). In humans, single and repeated concussive injuries lead to lifelong and cumulative enhancements of gamma-aminobutyric acid (GABA)-mediated inhibition, which is known to suppress LTP/LTD plasticity. To test the hypothesis that increased GABAergic inhibition after repeated concussions suppresses LTP/LTD and contributes to learning impairments, we used a paired associative stimulation (PAS) protocol to induce LTP/LTD-like effects in primary motor cortex (M1) jointly with an implicit motor learning task (serial reaction time task, SRTT). Our results indicate that repeated concussions induced persistent elevations of GABA(B)-mediated intracortical inhibition in M1, which was associated with suppressed PAS-induced LTP/LTD-like synaptic plasticity. This synaptic plasticity suppression was related to reduced implicit motor learning on the SRTT task relative to normal LTP/LTD-like synaptic plasticity in unconcussed teammates. These findings identify GABA neurotransmission alterations after repeated concussions and suggest that impaired learning after multiple concussions could at least partly be related to compromised GABA-dependent LTP/LTD synaptic plasticity.