A panel of cultivate specific marker based on polymorphisms at microsatellite markers for Iranian cultivated Almonds (Prunus dulcis).

Molecular markers developed for Prunus also offer a powerful tool to study the evolution of the genome, and for understanding of genome structure and determinants of genetic diversity. Two hundred eighty almond genotypes/cultivars from different origins distributed throughout Iran besides some foreign cultivars and their hybrids with Iranian ones were collected. Microsatellite analysis was carried out using 9 pair flanking SSR sequences previously cloned and sequenced specifically in almond. The total number of detected alleles was 152 (9 to 20 alleles per locus with an average of 16.87). The mean PIC value of the polymorphic loci wasrelatively high (0.81) and the mean value for He was 0.83, so that we were able to distinguish 98% of the genotypes using 5 loci. Incluster analysis, the genotypes were divided into 2 major groups, foreign cultivars and Iranian almond genotypes. Principal coordinate analysis based on Shared Allele method indicated proper distribution of the studied markers through the genome. Some specific markers were recorded among the germ plasm which can be used efficiently in rapid and precise identification of the related genotypes and also in breeding programs through MAS. Genotypes were coded using our suggested coding method for genotype molecular identification

A panel of cultivate specific marker based on polymorphisms at microsatellite markers for Iranian cultivated almonds (Prunus dulcis).

Abstract Molecular markers developed for Prunus also offer a powerful tool to study the evolution of the genome, and for understanding of genome structure and determinants of genetic diversity. Two hundred eighty almond genotypes/cultivars from different origins distributed throughout Iran besides some foreign cultivars and their hybrids with Iranian ones were collected. Microsatellite analysis was carried out using 9 pair flanking SSR sequences previously cloned and sequenced specifically in almond. The total number of detected alleles was 152 (9 to 20 alleles per locus with an average of 16.87). The mean PIC value of the polymorphic loci was relatively high (0.81) and the mean value for H e was 0.83, so that we were able to distinguish 98% of the genotypes using 5 loci. In cluster analysis, the genotypes were divided into 2 major groups, foreign cultivars and Iranian almond genotypes. Principal coordinate analysis based on Shared Allele method indicated proper distribution of the studied markers through the genome. Some specific markers were recorded among the germplasm which can be used efficiently in rapid and precise identification of the related genotypes and also in breeding programs through MAS. Genotypes were coded using our suggested coding method for genotype molecular identification

The effects of long-term saturated fat enriched diets on the brain lipidome

The brain is highly enriched in lipids, where they influence neurotransmission, synaptic plasticity and inflammation. Non-pathological modulation of the brain lipidome has not been previously reported and few studies have investigated the interplay between plasma lipid homeostasis relative to cerebral lipids. This study explored whether changes in plasma lipids induced by chronic consumption of a well-tolerated diet enriched in saturated fatty acids (SFA) was associated with parallel changes in cerebral lipid homeostasis. Male C57Bl/6 mice were fed regular chow or the SFA diet for six months. Plasma, hippocampus (HPF) and cerebral cortex (CTX) lipids were analysed by LC-ESI-MS/MS. A total of 348 lipid species were determined, comprising 25 lipid classes. The general abundance of HPF and CTX lipids was comparable in SFA fed mice versus controls, despite substantial differences in plasma lipid-class abundance. However, significant differences in 50 specific lipid species were identified as a consequence of SFA treatment, restricted to phosphatidylcholine (PC), phosphatidylethanolamine (PE), alkyl-PC, alkenyl-PC, alkyl-PE, alkenyl-PE, cholesterol ester (CE), diacylglycerol (DG), phosphatidylinositol (PI) and phosphatidylserine (PS) classes. Partial least squares regression of the HPF/CTX lipidome versus plasma lipidome revealed the plasma lipidome could account for a substantial proportion of variation. The findings demonstrate that cerebral abundance of specific lipid species is strongly associated with plasma lipid homeostasis

The restorative role of annexin A1 at the blood–brain barrier

Annexin A1 is a potent anti-inflammatory molecule that has been extensively studied in the peripheral immune system, but has not as yet been exploited as a therapeutic target/agent. In the last decade, we have undertaken the study of this molecule in the central nervous system (CNS), focusing particularly on the primary interface between the peripheral body and CNS: the blood–brain barrier. In this review, we provide an overview of the role of this molecule in the brain, with a particular emphasis on its functions in the endothelium of the blood–brain barrier, and the protective actions the molecule may exert in neuroinflammatory, neurovascular and metabolic disease. We focus on the possible new therapeutic avenues opened up by an increased understanding of the role of annexin A1 in the CNS vasculature, and its potential for repairing blood–brain barrier damage in disease and aging

Understanding the role of the perivascular space in cerebral small vessel disease

Small vessel diseases are a group of disorders that result from pathological alteration of the small blood vessels in the brain, including the small arteries, capillaries and veins. Of the 35-36 million people that are estimated to suffer from dementia worldwide, up to 65% have an SVD component. Furthermore, SVD causes 20-25% of strokes, worsens outcome after stroke and is a leading cause of disability, cognitive impairment and poor mobility. Yet the underlying cause(s) of SVD are not fully understood.Magnetic resonance imaging (MRI) has confirmed enlarged perivascular spaces (PVS) as a hallmark feature of SVD. In healthy tissue, these spaces are proposed to form part of a complex brain fluid drainage system which supports interstitial fluid exchange and may also facilitate clearance of waste products from the brain. The pathophysiological signature of PVS, and what this infers about their function and interaction with cerebral microcirculation, plus subsequent downstream effects on lesion development in the brain has not been established. Here we discuss the potential of enlarged PVS to be a unique biomarker for SVD and related brain disorders with a vascular component. We propose that widening of PVS suggests presence of peri-vascular cell debris and other waste products that forms part of a vicious cycle involving impaired cerebrovascular reactivity (CVR), blood-brain barrier (BBB) dysfunction, perivascular inflammation and ultimately impaired clearance of waste proteins from the interstitial fluid (ISF) space, leading to accumulation of toxins, hypoxia and tissue damage.Here, we outline current knowledge, questions and hypotheses regarding understanding the brain fluid dynamics underpinning dementia and stroke through the common denominator of SVD

Magnetic phase transitions in CoCl

Magnetic intercalation compounds of stage 1, 2, and 3 CoCl2-GIC have been successfully prepared and characterized by x-ray diffraction, Raman scattering, and transmission electron microscopy. The temperature dependence of the magnetic susceptibility of these samples show two superposed peaks. The difference in the magnetic field dependence of these two peaks indicates that at least two magnetic states are present. The higher temperature peak is identified with a Kosterlitz-Thouless type phase transition for finite size systems. Above the upper transition temperature (Tcu), the magnetic system consists of unbound vortices and below Tcu the vortices are bound. For low stage samples (stage ≤ 2), the lower temperature peak is identified with a transition showing crossover from two dimensional to three dimensional behavior. Below the lower transition temperature (Tcl), the system is in a phase showing long range magnetic order in which the spins are coupled ferromagnetically in-plane and antiferromagnetically inter-plane. The spin-flop field from the antiferromagnetic to ferromagnetic state can be determined by measuring the magnetic field dependence of the susceptibility. For the higher stage sample (stage 3), the inter-plane coupling is very small and the system can be treated like a 2D-ferroma- gnet

SCALLING OF TRENCH CAPACITOR CELL FOR NEXT GENERATION DRAMs

When scaling a trench capacitor cell developed for the 4Mbit DRAM further down, both process and device limits are encountered. Device related topics are the subject of this paper. Issues to be discussed are : (1) narrow width effects of pass transistors, (2) short channel effects, (3) effect of storage region on pass transistor, (4) isolation between neighbouring cells

Alginate bead-encapsulated PEDF induces ectopic bone formation in vivo in the absence of co-administered mesenchymal stem cells.

Bone defects can be severely debilitating and reduce quality of life. Osteoregeneration can alleviate some of the complications in bony defects. For therapeutic use in future, a single factor that can cause potent bone regeneration is highly preferred as it will be more cost-effective, any off-target effects will be more easily monitored and potentially managed, and for ease of administration which would lead to better patient compliance and satisfaction. We demonstrate that pigment epithelium-derived factor (PEDF), one such factor that is known to be potent against angiogenesis, promotes osteoblastogenesis in mesenchymal stem cells in vitro, but does not need co-encapsulation of cells in alginate bead scaffolds for osteogeneration in vivo. Osteogenic differentiation by PEDF in vitro was confirmed with immunoblotting and immunocytochemical staining for bone markers (alkaline phosphatase, osteocalcin, osteopontin, collagen I), calcified mineral deposition, and assay for alkaline phosphatase activity. PEDF-mediated bone formation in a muscle pocket in vivo model was confirmed by microcomputed tomography (microCT), histology (haematoxylin and eosin, Alcian blue staining), immunostaining for bone markers and for collagen I-processing proteins (heat shock protein 47 and membrane type I matrix metalloproteinase). PEDF therefore presents itself as a promising biological for osteogeneration

Nicotine Attenuates Disruption of Blood-Brain Barrier Induced by Saturated-Fat Feeding in Wild-Type Mice.

INTRODUCTION: Emerging evidence suggests that integrity of blood-brain barrier (BBB) is pivotal to pathology and pathogenesis of vascular-based neurodegenerative disorders. We have recently reported BBB protective effects of nutraceutical agents with anti-inflammatory properties in an established dietary-induced BBB dysfunction model. Studies also reported that nicotine exhibits anti-oxidative/-inflammatory effects and improve cognitive impairment in Alzheimer's disease. However there has been no studies reporting the effect of nicotine on high-fat-induced BBB dysfunction. METHODS: In the present study, we investigated the effect of nicotine on BBB integrity and neuro-inflammation in an established mouse model of BBB disruption induced by a diet enriched in saturated fatty acids (SFA). RESULTS: Wild-type C57BL/6J mice were fed chow enriched in SFA (23% w/w) with/without nicotine for 10 weeks. Compared to mice maintained on SFA-free and low-fat (LF) chow (4% w/w), capillary permeability indicated by the parenchymal extravasation of plasma derived IgG, was significantly greater in the SFA treatment group. Nicotine provided concomitantly with the SFA diet significantly attenuated IgG extravasation, however it remained significantly greater than LF-controls. Markers of neurovascular inflammation glial fibrillary acidic protein, cyclooxygenase-2, and glucose regulated protein 78 remained exaggerated in SFA+nicotine treated mice compared to LF-controls. Nicotine did however modestly, but not significantly, improve plasma total anti-oxidative status in SFA fed mice. CONCLUSION: Nicotine moderately attenuated BBB disruption induced by chronic ingestion of high-SFA diet, but had no significant effect on neuroinflammation per se