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Unveiling the G-quadruplex structure of G/C-rich Hexanucleotide repeats: a common causative factor in C9FTD/ALS and SCA36 diseases.
The mutational expansion of hexanucleotide repeats (HRs) is responsible for different hereditary neurodegenerative disorders in humans. Some of the neurological disorders associated with the expansion of HRs include frontotemporal dementia (C9FTD), amyotrophic lateral sclerosis (ALS) and spinocerebellar ataxia 36 (SCA36). The GGGGCC hexanucleotide repeat (HR) expansion within the ﬁrst intron of the C9ORF72 gene causes frontotemporal dementia (C9FTD) and amyotrophic lateral sclerosis (ALS) while GGGCCT HR expansion within intron 1 of the NOP56 gene on chromosome 20 causes spinocerebellar ataxia 36 (SCA36).
”Making mice Alzheimer’s without manipulating amyloid metabolism; a clue to human late-onset Alzheimer’s disease development”
Alzheimer’s disease (AD) is the leading cause of cognitive impairment and death among elderly people. Underlying pathology is accumulation of neurotoxic amyloid-β protein (“plaques”) and formation of TAU protein-rich neurofibrillary “Tangles” in the brain. Late-onset AD accounts for 95% of human AD while early-onset AD accounts for 5% of human AD. Although previous studies have indicated that early onset AD is caused by mutations in genes involved in amyloid metabolism, such as Amyloid Precursor Protein (APP) and Presenilin 1 genes, the exact cause of late-onset AD has remained unknown.
Saturated fatty acids induce inflammation in blood vessels
Cyclooxygenase-2 (COX-2) catalyzes the biosynthesis of prostanoids that trigger several normal effects during physiological conditions in the human vasculature. However, in pathophysiological conditions the inflammation induced by COX-2 activity may contribute to the development of unstable atherosclerotic plaques or increase the risk of ischemic stroke and heart attack. COX-2 expression is classically induced by cytokines and endotoxins (e.g. lipopolysaccharides), but more recent studies have demonstrated a “sterile” pathway induced by dietary free fatty acids (FFAs) resulting in proinﬂammatory mediator expression in the human vasculature.
Uncoupling FoxO3A Mitochondrial and Nuclear Functions in Cancer Cells Undergoing Metabolic Stress and Chemotherapy
The preservation of normal mitochondrial functions is quintessential to the malignant transformation of a cell. The major genes that play a crucial role in this transformation process include oncogenes and tumor suppressor genes; these genes code for the synthesis of proteins that are involved in tumor cell homeostasis. FoxO3A is a tumor suppressor that can either facilitate or hinder the transformation of non-malignant cells. Its functions are mediated by the activation of a coordinated transcriptional program, which involves genes that regulate the control of cell cycle, cell metabolism, cell death, autophagy, redox balance, and DNA repair.
From fat/adipose to engineered bone organ
There has been an increasing interest in the use of biomimetic and cell-seeded scaffolds in regenerative medicine and bone tissue engineering. Although the use of adipose tissue-derived cells as scaffolding materials exhibits great clinical importance, some of the steps involved in the generation of osteogenic grafts (such as monolayer expansion and the passage of human adipose stromal cells) strongly reduce their differentiation potential. Moreover, factors such as cost, time constraints and the demanding conditions for the clinical implementation of osteogenic engineering limits the successful use of osteogenic grafts.
Targeted Ovarian Cancer Chemotherapy by EGFR-Specific Peptide-Decorated Polymersomal Doxorubicin
Ovarian cancer is the world’s most lethal gynecological cancer. This recurrent disease is recalcitrant to various treatment methods, including the commonly used nanomedicine known as pegylated liposomal doxorubicin hydrochloride (Lipo-Dox). In an attempt to improve the efficacy of Lipo-Dox, researchers have tried to modify liposomes with ligands like folate, antibody, transferrin, and GE11 peptide. GE11 peptide exhibits a high affinity to ovarian cancer cells that overexpress epidermal growth factor receptors (EGFR).
Global and Multi-Focal Changes in Cerebral Blood Flow during Subthalamic Nucleus Stimulation in Parkinson’s disease
There is an increased focus on the electrical stimulation of the subthalamic nucleus (STN) for the treatment of Parkinson’s disease (PD). Although the deep brain stimulation (DBS) of the STN (DBS-STN) effectively controls movement disabilities in patients suffering from PD, the physiological mechanism of this neuro-modulatory therapy is not known. Previous studies have suggested that DBS-STN alters the neurophysiological activity in the basal ganglia via the desynchronization of abnormal oscillations, interference with neural signals, modulation of neurotransmitter and hormonal signaling, and alteration of inhibition and excitation within neural networks.
MECHANISM OF ACTION