Controlling crystal planes of biomass-derived carbon based Mo2C NPs and the electrochemical performance.

The electrochemical property of Mo2C nanoparticles (NPs) depends on the structure and crystal planes. Herein, Mo2C nanoparticles were prepared and dispersed on carbon nanosheets by the construction of a biomass-derived carbon precursor, and the exposed dual crystal planes were also controlled by optimal conditions. The structure, compositions, and morphology of the carbon-based Mo2C were characterized, and the Mo2C NPs were well dispersed on the carbon nanosheets.

Brain tumor detection and classification in MRI using hybrid ViT and GRU model with explainable AI in Southern Bangladesh.

Brain tumor, a leading cause of uncontrolled cell growth in the central nervous system, presents substantial challenges in medical diagnosis and treatment. Early and accurate detection is essential for effective intervention. This study aims to enhance the detection and classification of brain tumors in Magnetic Resonance Imaging (MRI) scans using an innovative framework combining Vision Transformer (ViT) and Gated Recurrent Unit (GRU) models.

Neuron loss in the brain starts in childhood, increases exponentially with age and is halted by GM-CSF treatment in Alzheimer's disease.

Aging increases the risk of neurodegeneration, cognitive decline, and Alzheimer's disease (AD). Currently no means exist to measure neuronal cell death during life or to prevent it. Here we show that cross-sectional measures of human plasma proteins released from dying/damaged neurons (ubiquitin C-terminal hydrolase-L1/UCH-L1 and neurofilament light/NfL) become exponentially higher from age 2-85; UCH-L1 rises faster in females.

Upgraded and Light-Up Biosensing Platform: Entropy-Driven Catalysis Circuit Manipulates the Configuration Transformation of Novel DNA Silver Nanoclusters on the Graphene Oxide Surface.

To tackle the predicament of the traditional turn-off mechanism, exploring an activated turn-on system remains an intriguing and crucial objective in biosensing fields. Herein, a dark DNA Ag nanocluster (NC) with hairpin-structured DNA containing a six-base cytosine loop (6C loop) as a template is atypically synthesized. Intriguingly, the dark DNA Ag NCs can be lit to display strong red-emission nanoclusters.

Risk Assessment and Sources Apportionment of Toxic Metals in Two Commonly Consumed Fishes from a Subtropical Estuarine Wetland System.

The widespread occurrence of heavy metals in aquatic environments, resulting in their bioaccumulation within aquatic organisms like fish, presents potential hazards to human health. This study investigates the concentrations of five toxic heavy metals (Pb, Hg, Zn, Cu, and Cr) and their potential health implications in two economically important fish species ( and ) from a subtropical estuarine wetland system (Feni estuary, Bangladesh). Muscle and gill samples from 36 individual fish were analyzed using energy dispersive X-ray fluorescence (EDXRF).

Potential Toxic Elements and Their Carcinogenic and Non-Carcinogenic Risk Assessment in Some Commercially Important Fish Species from a Ramsar Site.

Potentially toxic elements (PTEs) such as Hg, As, and Pb have become concentrated in the aquatic ecosystem as a result of increased human activities. However, these substances frequently have synergistic or antagonistic effects on the human body or other animals. As a result, there are concerns world-wide that commercially available food products, especially fish, may be contaminated with hazardous elements.

Increased / expression offsets Alzheimer Aβ-mediated toxicity and cognitive dysfunction.

Previously, we found that amyloid-beta (Aβ) competitively inhibits the kinesin motor protein KIF11 (Kinesin-5/Eg5), leading to defects in the microtubule network and in neurotransmitter and neurotrophin receptor localization and function. These biochemical and cell biological mechanisms for Aβ-induced neuronal dysfunction may underlie learning and memory defects in Alzheimer's disease (AD). Here, we show that KIF11 overexpression rescues Aβ-mediated decreases in dendritic spine density in cultured neurons and in long-term potentiation in hippocampal slices.

The innate immune system stimulating cytokine GM-CSF improves learning/memory and interneuron and astrocyte brain pathology in Dp16 Down syndrome mice and improves learning/memory in wild-type mice.

Down syndrome (DS) is characterized by chronic neuroinflammation, peripheral inflammation, astrogliosis, imbalanced excitatory/inhibitory neuronal function, and cognitive deficits in both humans and mouse models. Suppression of inflammation has been proposed as a therapeutic approach to treating DS co-morbidities, including intellectual disability (DS/ID). Conversely, we discovered previously that treatment with the innate immune system stimulating cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), which has both pro- and anti-inflammatory activities, improved cognition and reduced brain pathology in a mouse model of Alzheimer's disease (AD), another inflammatory disorder, and improved cognition and reduced biomarkers of brain pathology in a phase II trial of humans with mild-to-moderate AD.

Context Fear Conditioning in Down Syndrome Mouse Models: Effects of Trisomic Gene Content, Age, Sex and Genetic Background.

Down syndrome (DS), trisomy of the long arm of human chromosome 21 (Hsa21), is the most common genetic cause of intellectual disability (ID). Currently, there are no effective pharmacotherapies. The success of clinical trials to improve cognition depends in part on the design of preclinical evaluations in mouse models.

Innate Immune System Activation and Neuroinflammation in Down Syndrome and Neurodegeneration: Therapeutic Targets or Partners?

Innate immune system activation and inflammation are associated with and may contribute to clinical outcomes in people with Down syndrome (DS), neurodegenerative diseases such as Alzheimer's disease (AD), and normal aging. In addition to serving as potential diagnostic biomarkers, innate immune system activation and inflammation may play a contributing or causal role in these conditions, leading to the hypothesis that effective therapies should seek to dampen their effects. However, recent intervention studies with the innate immune system activator granulocyte-macrophage colony-stimulating factor (GM-CSF) in animal models of DS, AD, and normal aging, and in an AD clinical trial suggest that activating the innate immune system and inflammation may instead be therapeutic.

Altered Protein Profiles During Epileptogenesis in the Pilocarpine Mouse Model of Temporal Lobe Epilepsy.

Epilepsy is characterized by recurrent, spontaneous seizures and is a major contributor to the global burden of neurological disease. Although epilepsy can result from a variety of brain insults, in many cases the cause is unknown and, in a significant proportion of cases, seizures cannot be controlled by available treatments. Understanding the molecular alterations that underlie or are triggered by epileptogenesis would help to identify therapeutics to prevent or control progression to epilepsy.

Megacities as drivers of national outbreaks: The 2017 chikungunya outbreak in Dhaka, Bangladesh.

Background: Several large outbreaks of chikungunya have been reported in the Indian Ocean region in the last decade. In 2017, an outbreak occurred in Dhaka, Bangladesh, one of the largest and densest megacities in the world. Population mobility and fluctuations in population density are important drivers of epidemics.

Correlates of healthy life expectancy in low- and lower-middle-income countries.

Background: Healthy life expectancy (HALE) at birth is an important indicator of health status and quality of life of a country's population. However, little is known about the determinants of HALE as yet globally or even country-specific level. Thus, we examined the factors that are associated with HALE at birth in low- and lower-middle-income countries.

The GABAα5-selective Modulator, RO4938581, Rescues Protein Anomalies in the Ts65Dn Mouse Model of Down Syndrome.

Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), is the most common genetic cause of intellectual disability (ID). There are no treatments for the cognitive deficits. The Ts65Dn is a partial trisomy mouse model of DS that shows learning and memory (LM) impairments and other abnormalities relevant to those seen in DS.

Age exacerbates abnormal protein expression in a mouse model of Down syndrome.

The Ts65Dn is a popular mouse model of Down syndrome (DS). It displays DS-relevant features of learning/memory deficits and age-related loss of functional markers in basal forebrain cholinergic neurons. Here we describe protein expression abnormalities in brain regions of 12-month-old male Ts65Dn mice.

Sex differences in protein expression in the mouse brain and their perturbations in a model of Down syndrome.

Background: While many sex differences in structure and function of the mammalian brain have been described, the molecular correlates of these differences are not broadly known. Also unknown is how sex differences at the protein level are perturbed by mutations that lead to intellectual disability (ID). Down syndrome (DS) is the most common genetic cause of ID and is due to trisomy of human chromosome 21 (Hsa21) and the resulting increased expression of Hsa21-encoded genes.

Protein dynamics associated with failed and rescued learning in the Ts65Dn mouse model of Down syndrome.

Down syndrome (DS) is caused by an extra copy of human chromosome 21 (Hsa21). Although it is the most common genetic cause of intellectual disability (ID), there are, as yet, no effective pharmacotherapies. The Ts65Dn mouse model of DS is trisomic for orthologs of ∼55% of Hsa21 classical protein coding genes.

Protein profiles associated with context fear conditioning and their modulation by memantine.

Analysis of the molecular basis of learning and memory has revealed details of the roles played by many genes and the proteins they encode. Because most individual studies focus on a small number of proteins, many complexities of the relationships among proteins and their dynamic responses to stimulation are not known. We have used the technique of reverse phase protein arrays (RPPA) to assess the levels of more than 80 proteins/protein modifications in subcellular fractions from hippocampus and cortex of mice trained in Context Fear Conditioning (CFC).

Can an active aging index (AAI) provide insight into reducing elder abuse? A case study in Rajshahi District, Bangladesh.

We use data from respondents aged 60 years and above, collected during April 2009 in the Rajshahi district of Bangladesh, to examine whether high activeness, as captured by an AAI or in sub-domains, can help reduce the risk of elder abuse. The findings suggest that more than half of rural elderly and 14 percent of urban elderly were at some point abused. High activeness in health and security dimensions lowers the risk of being abused while those who are low active in community participation have the lowest risk of being abused in both rural and urban areas.

Protein profiles in Tc1 mice implicate novel pathway perturbations in the Down syndrome brain.

Tc1 mouse model of Down syndrome (DS) is functionally trisomic for ∼120 human chromosome 21 (HSA21) classical protein-coding genes. Tc1 mice display features relevant to the DS phenotype, including abnormalities in learning and memory and synaptic plasticity. To determine the molecular basis for the phenotypic features, the levels of 90 phosphorylation-specific and phosphorylation-independent proteins were measured by Reverse Phase Protein Arrays in hippocampus and cortex, and 64 in cerebellum, of Tc1 mice and littermate controls.

Expression of trisomic proteins in Down syndrome model systems.

Down syndrome (DS) is the most common genetic aberration leading to intellectual disability. DS results from an extra copy of the long arm of human chromosome 21 (HSA21) and the increased expression of trisomic genes due to gene dosage. While expression in DS and DS models has been studied extensively at the RNA level, much less is known about expression of trisomic genes at the protein level.

Pathways to cognitive deficits in Down syndrome.

Major efforts in Down syndrome (DS) research have been directed at the identification and functional characterization of genes encoded by human chromosome 21 (HSA21). In parallel with this, tissue samples and cell lines derived from individuals with DS have been examined for abnormalities in gene expression and cellular morphology, and mouse models of DS have been characterized for abnormalities at the molecular, cellular, electrophysiological, and behavioral level. One goal of such investigations has been the identification of effective targets for pharmacotherapies that can prevent or correct the abnormalities and, by extension to human clinical trials, prevent or lessen aspects of the cognitive deficits seen in people with DS.

Loss of correlations among proteins in brains of the Ts65Dn mouse model of down syndrome.

The Ts65Dn mouse model of Down syndrome (DS) is trisomic for orthologs of 88 of 161 classical protein coding genes present on human chromosome 21 (HSA21). Ts65Dn mice display learning and memory impairments and neuroanatomical, electrophysiological, and cellular abnormalities that are relevant to phenotypic features seen in DS; however, little is known about the molecular perturbations underlying the abnormalities. Here we have used reverse phase protein arrays to profile 64 proteins in the cortex, hippocampus, and cerebellum of Ts65Dn mice and littermate controls.

Preserving protein profiles in tissue samples: differing outcomes with and without heat stabilization.

Post translational modification (PTM) and proteolytic processing of proteins contributes to regulation of their stability, intracellular localization and interactions with other proteins, and to direct enhancement or repression of their activity. Both PTM and proteolysis are dynamic; levels and rates change in response to changes in the cellular environment. Tissue excision, post mortem interval and subsequent methods of tissue processing for protein analysis unavoidably alter the cellular environment and therefore features of protein profiles.

Effects of memantine on soluble Alphabeta(25-35)-induced changes in peptidergic and glial cells in Alzheimer's disease model rat brain regions.

Soluble forms of amyloid-beta (Abeta) have been considered responsible for cognitive dysfunction prior to senile plaque formation in Alzheimer's disease (AD). As its mechanism is not well understood, we examined the effects of repeated i.c.