EFFECT OF NOISE STRESS-INDUCED NEUROBEHAVIORAL CHANGES ON WISTAR ALBINO RATS

Objective: The study aims to investigate the effect of acute noise stress on cognitive functions in male Wistar albino rats. Methods: Adult albino rats were randomly divided into two groups. Each group contains six animals. Rats exposed to acute noise stress (100 dB/4 h) were compared with control animal and assessed for cognition using T-maze, hole-board test, open-field test, marble burying test, and social interaction behavior. Results: The rats exposed to acute noise stress showed the significance (p<0.05) of behavioral alterations such as impaired learning and memory, memory retention, increased fear and anxiety, obsessive–compulsive behavior, social avoidance, and decreased social interaction. Conclusion: The results report that acute noise stress affects the cognition, and it became chronic may confer the increased risk of neurodegenerative disorders

IMPACT OF CHRONIC NOISE ON HIPPOCAMPAL MORPHOLOGY AND ITS FUNCTIONS IN WISTAR ALBINO RATS

Objective: The study aims to investigate the effect of chronic noise stress on hippocampal morphology and its functions in male Wistar albino rats. Methods: Adult albino rats were randomly divided into two groups. Each group contained six animals. Rats exposed to chronic noise stress (100 dB/4 h–30 days) were compared with control animal and assessed for behavior using hole-board test, marble burying test, and morphology of hippocampus by histology. Results: The rats exposed to chronic noise stress showed significance (P < 0.05) of behavioral alterations such as increased fear and anxiety, obsessive-compulsive behavior, enlarged lateral ventricle, and reduced hippocampal volume. Conclusion: The results reported that chronic noise stress affects neurobehavioral due to reduced hippocampal volume

Pharmacological and physiological roles of adipokines and myokines in metabolic-related dementia

Dementia is a detrimental neuropathologic condition with considerable physical, mental, social, and financial impact on patients and society. Patients with metabolic syndrome (MetS), a group of diseases that occur in tandem and increase the risk of neurologic diseases, have a higher risk of dementia. The ratio between muscle and adipose tissue is crucial in MetS, as these contain many hormones, including myokines and adipokines, which are involved in crosstalk and local paracrine/autocrine interactions. Evidence suggests that abnormal adipokine and myokine synthesis and release may be implicated in various MetS, such as atherosclerosis, diabetic mellitus (DM), and dyslipidemia, but their precise role is unclear. Here we review the literature on adipokine and myokine involvement in MetS-induced dementia via glucose and insulin homeostasis regulation, neuroinflammation, vascular dysfunction, emotional changes, and cognitive function

Neuroprotective role of Glycyrrhiza glabra on chronic noise induced changes in Hippocampal morphology and its functions in wistar albino rats

Background: Noise has become inexorable stress due to the increase in urbanization, automobile usage, and lifestyle modification.Aim: The study aims to investigate the effect of chronic noise stress on hippocampal morphology and the neuroprotective effect of Glycyrrhiza glabra (GG) on stress-induced male Wistar albino rats.  Methods: Adult albino rats were randomly divided into four groups. Each group contained six animals. Rats exposed to chronic noise stress (100 dB/4 h – 30Days),  Noise + GG (150 mg/kg Bw/Oral), and GG alone were compared with control animal and assessed for behaviour using the hole-board test, marble burying test, the morphology of hippocampus by histology, DNA fragmentation and assessed the Phytochemical constitutes in GG. Results: The rats exposed to chronic noise stress showed significance (p<0.05) of behavioral alterations such as increased fear and anxiety, obsessive-compulsive behaviour, enlarged lateral ventricle, and reduced hippocampal volume. Conclusion: The results reported that chronic noise stress affects the neurobehavioral due to reduced hippocampal volume

Hepatic Encephalopathy and Melatonin

Hepatic encephalopathy (HE) is a severe metabolic syndrome linked with acute/chronic hepatic disorders. HE is also a pernicious neuropsychiatric complication associated with cognitive decline, coma, and death. Limited therapies are available to treat HE, which is formidable to oversee in the clinic. Thus, determining a novel therapeutic approach is essential. The pathogenesis of HE has not been well established. According to various scientific reports, neuropathological symptoms arise due to excessive accumulation of ammonia, which is transported to the brain via the blood–brain barrier (BBB), triggering oxidative stress and inflammation, and disturbing neuronal-glial functions. The treatment of HE involves eliminating hyperammonemia by enhancing the ammonia scavenging mechanism in systemic blood circulation. Melatonin is the sole endogenous hormone linked with HE. Melatonin as a neurohormone is a potent antioxidant that is primarily synthesized and released by the brain’s pineal gland. Several HE and liver cirrhosis clinical studies have demonstrated impaired synthesis, secretion of melatonin, and circadian patterns. Melatonin can cross the BBB and is involved in various neuroprotective actions on the HE brain. Hence, we aim to elucidate how HE impairs brain functions, and elucidate the precise molecular mechanism of melatonin that reverses the HE effects on the central nervous system

Reactive Oxygen Species and <i>H. pylori</i> Infection: A Comprehensive Review of Their Roles in Gastric Cancer Development

Gastric cancer (GC) is the fifth most common cancer worldwide and makes up a significant component of the global cancer burden. Helicobacter pylori (H. pylori) is the most influential risk factor for GC, with the International Agency for Research on Cancer classifying it as a Class I carcinogen for GC. H. pylori has been shown to persist in stomach acid for decades, causing damage to the stomach’s mucosal lining, altering gastric hormone release patterns, and potentially altering gastric function. Epidemiological studies have shown that eliminating H. pylori reduces metachronous cancer. Evidence shows that various molecular alterations are present in gastric cancer and precancerous lesions associated with an H. pylori infection. However, although H. pylori can cause oxidative stress-induced gastric cancer, with antioxidants potentially being a treatment for GC, the exact mechanism underlying GC etiology is not fully understood. This review provides an overview of recent research exploring the pathophysiology of H. pylori-induced oxidative stress that can cause cancer and the antioxidant supplements that can reduce or even eliminate GC occurrence

LoCoMo-Net : a low -complex deep learning framework for sEMG-based hand movement recognition for prosthetic control

Background: The enhancement in the performance of the myoelectric pattern recognition techniques based on deep learning algorithm possess computationally expensive and exhibit extensive memory behavior. Therefore, in this paper we report a deep learning framework named 'Low-Complex Movement recognition-Net' (LoCoMo-Net) built with convolution neural network (CNN) for recognition of wrist and finger flexion movements; grasping and functional movements; and force pattern from single channel surface electromyography (sEMG) recording. The network consists of a two-stage pipeline: 1) input data compression; 2) data-driven weight sharing. Methods: The proposed framework was validated on two different datasets- our own dataset (DS1) and publicly available NinaPro dataset (DS2) for 16 movements and 50 movements respectively. Further, we have prototyped the proposed LoCoMo-Net on Virtex-7 Xilinx field-programmable gate array (FPGA) platform and validated for 15 movements from DS1 to demonstrate its feasibility for real-time execution. Results: The effectiveness of the proposed LoCoMo-Net was verified by a comparative analysis against the benchmarked models using the same datasets wherein our proposed model outperformed Twin- Support Vector Machine (SVM) and existing CNN based model by an average classification accuracy of 8.5 % and 16.0 % respectively. In addition, hardware complexity analysis is done to reveal the advantages of the two-stage pipeline where approximately 27 %, 49 %, 50 %, 23 %, and 43 % savings achieved in lookup tables (LUT's), registers, memory, power consumption and computational time respectively. Conclusion: The clinical significance of such sEMG based accurate and low-complex movement recognition system can be favorable for the potential improvement in quality of life of an amputated persons

Sulforaphane Inhibits IL-1β-Induced IL-6 by Suppressing ROS Production, AP-1, and STAT3 in Colorectal Cancer HT-29 Cells

Colorectal cancer (CRC) stands as a major cause of cancer-related mortality globally, accounting for approximately 881,000 deaths each year. Traditional approaches such as chemotherapy and surgery have been the primary treatment modalities, yet the outcomes for patients with metastatic CRC are often unsatisfactory. Recent research has focused on targeting the pathways involved in oxidative stress, inflammation, and metastasis to enhance the survival of CRC patients. Within this context, sulforaphane (SFN), a notable phytochemical found predominantly in cruciferous vegetables, has been recognized as a potential anticancer agent. However, the specific mechanisms through which SFN may exert its chemopreventive effects in CRC remain unclear. This study explores the impact of SFN on IL-1β-induced IL-6 activation and MAPK and AP-1 signaling in HT-29 cells. Our findings reveal that SFN treatment not only diminishes IL-1β-stimulated IL-6 expression but also reduces oxidative stress by curtailing reactive oxygen species (ROS) production. Furthermore, it hinders the proliferation and invasiveness of HT-29 cells through the modulation of MAPK/AP-1 and STAT3 signaling pathways. These results indicate that SFN mitigates IL-1β-induced IL-6 expression in CRC cells by attenuating ROS production and disrupting MAPK/AP-1 signaling. This suggests that SFN holds significant potential as a chemotherapeutic agent for both treating and preventing CRC

(-)-Epigallocatechin-3-Gallate Prevents IL-1&beta;-Induced uPAR Expression and Invasiveness via the Suppression of NF-&kappa;B and AP-1 in Human Bladder Cancer Cells

(-)-Epigallocatechin-3-O-gallate (EGCG), a primary green tea polyphenol, has powerful iron scavengers, belongs to the family of flavonoids with antioxidant properties, and can be used to prevent cancer. Urokinase-type plasminogen activator receptors (uPARs) are glycosylphosphatidylinositol (GPI)-anchored cell membrane receptors that have crucial roles in cell invasion and metastasis of several cancers including bladder cancer. The mechanism of action of EGCG on uPAR expression has not been reported clearly yet. In this study, we investigated the effect of EGCG on interleukin (IL)-1&beta;-induced cell invasion and uPAR activity in T24 human bladder cancer cells. Interestingly, nuclear factor (NF)-&kappa;B and activator protein (AP)-1 transcription factors were critically required for IL-1&beta;-induced high uPAR expression, and EGCG suppressed the transcriptional activity of both the ERK1/2 and JNK signaling pathways with the AP-1 subunit c-Jun. EGCG blocked the IL-1&beta;-stimulated reactive oxygen species (ROS) production, in turn suppressing NF-&kappa;B signaling and anti-invasion effects by inhibiting uPAR expression. These results suggest that EGCG may exert at least part of its anticancer effect by controlling uPAR expression through the suppression of ERK1/2, JNK, AP-1, and NF-&kappa;B

Identification of IGF-1 Effects on White Adipose Tissue and Hippocampus in Alzheimer’s Disease Mice via Transcriptomic and Cellular Analysis

Alzheimer’s disease (AD) stands as the most prevalent neurodegenerative disorder, characterized by a multitude of pathological manifestations, prominently marked by the aggregation of amyloid beta. Recent investigations have revealed a compelling association between excessive adiposity and glial activation, further correlating with cognitive impairments. Additionally, alterations in levels of insulin-like growth factor 1 (IGF-1) have been reported in individuals with metabolic conditions accompanied by memory dysfunction. Hence, our research endeavors to comprehensively explore the impact of IGF-1 on the hippocampus and adipose tissue in the context of Alzheimer’s disease. To address this, we have conducted an in-depth analysis utilizing APP/PS2 transgenic mice, recognized as a well-established mouse model for Alzheimer’s disease. Upon administering IGF-1 injections to the APP/PS2 mice, we observed notable alterations in their behavioral patterns, prompting us to undertake a comprehensive transcriptomic analysis of both the hippocampal and adipose tissues. Our data unveiled significant modifications in the functional profiles of these tissues. Specifically, in the hippocampus, we identified changes associated with synaptic activity and neuroinflammation. Concurrently, the adipose tissue displayed shifts in processes related to fat browning and cell death signaling. In addition to these findings, our analysis enabled the identification of a collection of long non-coding RNAs and circular RNAs that exhibited significant changes in expression subsequent to the administration of IGF-1 injections. Furthermore, we endeavored to predict the potential roles of these identified RNA molecules within the context of our study. In summary, our study offers valuable transcriptome data for hippocampal and adipose tissues within an Alzheimer’s disease model and posits a significant role for IGF-1 within both the hippocampus and adipose tissue