scholarly journals Enzootic bovine leucosis in cows on farms in Almaty and Turkestan regions of Kazakhstan

2020 ◽  
Vol 176 ◽  
pp. 02003
Author(s):  
Assem Ibazhanova ◽  
Ajdar Namet ◽  
Banu Nurgazy ◽  
Zhuldyzaj Kenzhebekova ◽  
Gabdolla Shmanov
Keyword(s):  
Skeletal Muscles ◽  
Leukemic Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Agar Gel ◽  
Disease Mechanisms ◽  
New Knowledge ◽  
Bovine Leukosis ◽  
Haematological Study ◽  
The Brain ◽  
Enzootic Bovine Leucosis

The objective of this study was to evaluate pathomorphological and histopathological characteristics of internal organ tissues and skeletal muscles of Black-Motley cows with bovine laeukemia necropsied between 2013 and 2017. Pathomorphological and histopathological assessment of enzootic bovine leukosis was performed. The viral presence was proved by haematological study, enzyme-linked immunosorbent assay and agar-gel immunodiffusion. There was the pathomorphological manifestation of an immunosuppressive condition in the cattle, as well as leukemic cell accumulations in the brain, kidneys, duodenum, spleen, lymph nodes, cardiac and skeletal muscles. Our study is considered to bear significance concerning the description of microstructural changes involving lymph node trabeculae and myocardial fibres from leukemic cows. This investigation, therefore, provides new knowledge on histopathological features of enzootic bovine leucosis, which potentially may bring new insights into the disease mechanisms.

Berberine Alleviates Amyloid-beta Pathogenesis Via Activating LKB1/AMPK Signaling in the Brain of APP/PS1 Transgenic Mice

2019 ◽  
Vol 19 (5) ◽  
pp. 342-348 ◽  
Author(s):  
Zhi-You Cai ◽  
Chuan-Ling Wang ◽  
Tao-Tao Lu ◽  
Wen-Ming Yang
Keyword(s):  
Transgenic Mice ◽  
Western Blotting ◽  
Amyloid Β ◽  
Adenosine Monophosphate ◽  
Camp Response Element Binding ◽  
Enzyme Linked Immunosorbent Assay ◽  
Synaptic Density ◽  
Ampk Signaling ◽  
The Brain ◽  
Post Synaptic Density

Background:Liver kinase B1 (LKB1)/5’-adenosine monophosphate-activated protein kinase (AMPK) signaling, a metabolic checkpoint, plays a neuro-protective role in the pathogenesis of Alzheimer’s disease (AD). Amyloid-β (Aβ) acts as a classical biomarker of AD. The aim of the present study was to explore whether berberine (BBR) activates LKB1/AMPK signaling and ameliorates Aβ pathology.Methods:The Aβ levels were detected using enzyme-linked immunosorbent assay and immunohistochemistry. The following biomarkers were measured by Western blotting: phosphorylated (p-) LKB1 (Ser334 and Thr189), p-AMPK (AMPKα and AMPKβ1), synaptophysin, post-synaptic density protein 95 and p-cAMP-response element binding protein (p-CREB). The glial fibrillary acidic protein (GFAP) was determined using Western blotting and immunohistochemistry.Results:BBR inhibited Aβ expression in the brain of APP/PS1 mice. There was a strong up-regulation of both p-LKB1 (Ser334 and Thr189) and p-AMPK (AMPKα and AMPKβ1) in the brains of APP/PS1 transgenic mice after BBR-treatment (P<0.01). BBR promoted the expression of synaptophysin, post-synaptic density protein 95 and p-CREB(Ser133) in the AD brain, compared with the model mice.Conclusion:BBR alleviates Aβ pathogenesis and rescues synapse damage via activating LKB1/AMPK signaling in the brain of APP/PS1 transgenic mice.

The Effects of D-aspartate on Neurosteroids, Neurosteroid Receptors, and Inflammatory Mediators in Experimental Autoimmune Encephalomyelitis

2019 ◽  
Vol 19 (3) ◽  
pp. 316-325
Author(s):  
Mahdi Goudarzvand ◽  
Yaser Panahi ◽  
Reza Yazdani ◽  
Hosein Miladi ◽  
Saeed Tahmasebi ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Inflammatory Mediators ◽  
Mouse Serum ◽  
Enzyme Linked Immunosorbent Assay ◽  
Oral Gavage ◽  
Autoimmune Encephalomyelitis ◽  
Beneficial Effects ◽  
17Β Estradiol ◽  
The Brain ◽  
Experimental Autoimmune

Objective: Experimental autoimmune encephalomyelitis (EAE) is a widely used model for multiple sclerosis. The present study has been designed to compare the efficiencies of oral and intraperitoneal (IP) administration of D-aspartate (D-Asp) on the onset and severity of EAE, the production of neurosteroids, and the expression of neurosteroid receptors and inflammatory mediators in the brain of EAE mice. Methods: In this study, EAE was induced in C57BL/6 mice treated with D-Asp orally (D-Asp-Oral) or by IP injection (D-Asp-IP). On the 20th day, brains (cerebrums) and cerebellums of mice were evaluated by histological analyses. The brains of mice were analyzed for: 1) Neurosteroid (Progesterone, Testosterone, 17β-estradiol) concentrations; 2) gene expressions of cytokines and neurosteroid receptors by reverse transcription polymerase chain reaction, and 3) quantitative determination of D-Asp using liquid chromatography-tandem mass spectrometry. Further, some inflammatory cytokines and matrix metalloproteinase-2 (MMP-2) were identified in the mouse serum using enzyme-linked immunosorbent assay kits. Results: Our findings demonstrated that after D-Asp was administered, it was taken up and accumulated within the brain. Further, IP injection of D-Asp had more beneficial effects on EAE severity than oral gavage. The concentration of the testosterone and 17β-estradiol in D-Asp-IP group was significantly higher than that of the control group. There were no significant differences in the gene expression of cytokine and neurosteroid receptors between control, D-Asp-IP, and D-Asp-Oral groups. However, IP treatment with D-Asp significantly reduced C-C motif chemokine ligand 2 and MMP-2 serum levels compared to control mice. Conclusion: IP injection of D-Asp had more beneficial effects on EAE severity, neurosteroid induction and reduction of inflammatory mediators than oral gavage.

scholarly journals Nociceptin Increases Antioxidant Expression in the Kidney, Liver and Brain of Diabetic Rats

Biology ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 621
Author(s):  
Ernest Adeghate ◽  
Crystal M. D’Souza ◽  
Zulqarnain Saeed ◽  
Saeeda Al Jaberi ◽  
Saeed Tariq ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Rats ◽  
Enzyme Linked Immunosorbent Assay ◽  
Kidney Tubules ◽  
Onset Of Diabetes ◽  
Endogenous Antioxidants ◽  
Kidney Liver ◽  
Convoluted Tubules ◽  
The Brain

Nociceptin (NC) consists of 17 amino acids (aa) and takes part in the processing of learning and memory. The role of NC in the induction of endogenous antioxidants in still unclear. We examined the effect of NC on the expression of endogenous antioxidants in kidney, liver, cerebral cortex (CC), and hippocampus after the onset of diabetes mellitus, using enzyme-linked immunosorbent assay and immunohistochemistry. Exogenous NC (aa chain 1–17; 10 µg/kg body weight) was given intraperitoneally to normal and diabetic rats for 5 days. Our results showed that catalase (CAT) is present in the proximal (PCT) and distal (DCT) convoluted tubules of kidney, hepatocytes, and neurons of CC and hippocampus. The expression of CAT was significantly (p < 0.05) reduced in the kidney of normal and diabetic rats after treatment with NC. However, NC markedly (p < 0.001) increased the expression CAT in the liver and neurons of CC of diabetic rats. Superoxide dismutase (SOD) is widely distributed in the PCT and DCT of kidney, hepatocytes, and neurons of CC and hippocampus. NC significantly (p < 0.001) increased the expression of SOD in hepatocytes and neurons of CC and the hippocampus but not in the kidney. Glutathione reductase (GRED) was observed in kidney tubules, hepatocytes and neurons of the brain. NC markedly increased (p < 0.001) the expression of GRED in PCT and DCT cells of the kidney and hepatocytes of liver and neurons of CC. In conclusion, NC is a strong inducer of CAT, SOD, and GRED expression in the kidney, liver and brain of diabetic rats.

scholarly journals Cancer Risks Linked to the Bad Luck Hypothesis and Epigenomic Mutational Signatures

Epigenomes ◽  
2018 ◽  
Vol 2 (3) ◽  
pp. 13
Author(s):  
José Belizário
Keyword(s):  
Stem Cells ◽  
Skeletal Muscles ◽  
Small Population ◽  
Epigenetic Mechanisms ◽  
Cancer Risks ◽  
Mutational Signatures ◽  
Environmental Agents ◽  
Risk Of Malignancy ◽  
The Brain ◽  
Cellular Genome

Exposure to pathogen infection, and occupational and environmental agents, contributes to induction of most types of cancer through different mechanisms. Cancer is defined and characterized by accumulation of mutations and epimutations that lead to changes in the cellular genome and epigenome. According to a recent Bad Luck Hypothesis, random error mutations during DNA replication in a small population of stem cells may be implicated in two-thirds of variation of cancer risk in 25 organs and tissues. What determines stem cell vulnerability and risk of malignancy across the spectrum of organs, such as the brain, bone marrow, skeletal muscles, skin, and liver? Have stem cells pooled in particular tissues or organs evolved some critical ability to deal with DNA damage in the presence of extrinsic environmental factors? This paper describes how the complex replication and repair DNA systems control mutational events. In addition, recent advances on cancer epigenomic signatures and epigenetic mechanisms are discussed, which will guide future investigation of the origin of cancer initiating cells in tissue and organs in a clinical setting.

Abstract TP274: Orosomucoid-1 Protein Increases Following Ischemic Stroke in the Brain and Periphery

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Hetal Mistry ◽  
Madeline Levy ◽  
Meaghan Roy-O'Reilly ◽  
Louise McCullough
Keyword(s):  
Sex Differences ◽  
Ischemic Stroke ◽  
Rna Sequencing ◽  
Multiple Testing ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mrna Levels ◽  
Stroke Patients ◽  
Post Stroke ◽  
Protein Levels ◽  
The Brain

Background and Purpose: Orosomucoid-1 (ORM-1) is an abundant protein with important roles in inflammation and immunosuppression. We utilized RNA sequencing to measure mRNA levels in human ischemic stroke patients, with confirmation by serum ORM-1 protein measurements. A mouse model of ischemic stroke was then used to examine post-stroke changes in ORM-1 within the brain itself. Hypothesis: We tested the hypothesis that ORM-1 levels increase following ischemic stroke, with sex differences in protein dynamics over time. Methods: RNA sequencing was performed on whole blood from ischemic stroke patients (n=23) and controls (n=12), with Benjamini-Hochberg correction for multiple testing. Enzyme-linked immunosorbent assay was performed on serum from ischemic stroke patients (n=28) and controls (n=8), with analysis by T-test. For brain analysis, mice (n=14) were subjected to a 90-minute middle cerebral artery occlusion (MCAO) surgery and sacrificed 6 or 24 hours after stroke. Control mice underwent parallel “sham” surgery without occlusion. Western blotting was used to detect ORM-1 protein levels in whole brain, with analysis by two-way ANOVA. Results: RNA sequencing showed a 2.8-fold increase in human ORM-1 at 24 hours post-stroke (q=.0029), an increase also seen in serum ORM-1 protein levels (p=.011). Western blot analysis of mouse brain revealed that glycosylated (p=0.0003) and naive (p=0.0333) forms of ORM-1 were higher in female mice compared to males 6 hours post-stroke. Interestingly, ORM-1 levels were higher in the brains of stroke mice at 6 hours (p=.0483), while at 24 hours ORM-1 levels in stroke mice were lower than their sham counterparts (p=.0212). In both human and mouse data, no sex differences were seen in ORM-1 levels in the brain or periphery at 24 hours post-stroke. Conclusion: In conclusion, ORM-1 is a sexually dimorphic protein involved in the early (<24 hour) response to ischemic stroke. This research serves as an initial step in determining the mechanism of ORM-1 in the ischemic stroke response and its potential as a future therapeutic target for both sexes.

Something Old, Something New, Something Borrowed, Something Blue: Part 3 – An Elephant Never Forgets

2017 ◽  
Vol 26 (3) ◽  
pp. 433-437
Author(s):  
Mark Dougherty
Keyword(s):  
Artificial Intelligence ◽  
Intelligent Systems ◽  
Natural Systems ◽  
European Court ◽  
New Knowledge ◽  
The Right ◽  
Contextual Environment ◽  
The Brain ◽  
Index Services ◽  
Incomplete Picture

AbstractForgetting is an oft-forgotten art. Many artificial intelligence (AI) systems deliver good performance when first implemented; however, as the contextual environment changes, they become out of date and their performance degrades. Learning new knowledge is part of the solution, but forgetting outdated facts and information is a vital part of the process of renewal. However, forgetting proves to be a surprisingly difficult concept to either understand or implement. Much of AI is based on analogies with natural systems, and although all of us have plenty of experiences with having forgotten something, as yet we have only an incomplete picture of how this process occurs in the brain. A recent judgment by the European Court concerns the “right to be forgotten” by web index services such as Google. This has made debate and research into the concept of forgetting very urgent. Given the rapid growth in requests for pages to be forgotten, it is clear that the process will have to be automated and that intelligent systems of forgetting are required in order to meet this challenge.

scholarly journals Myelin Defects in Niemann–Pick Type C Disease: Mechanisms and Possible Therapeutic Perspectives

2021 ◽  
Vol 22 (16) ◽  
pp. 8858
Author(s):  
Antonietta Bernardo ◽  
Chiara De Nuccio ◽  
Sergio Visentin ◽  
Alberto Martire ◽  
Luisa Minghetti ◽  
...  
Keyword(s):  
Wide Spectrum ◽  
Autophagic Flux ◽  
Unesterified Cholesterol ◽  
A2a Adenosine Receptor ◽  
Disease Mechanisms ◽  
Mitochondrial Functions ◽  
Type C ◽  
Niemann Pick ◽  
Cellular Compartments ◽  
The Brain

Niemann–Pick type C (NPC) disease is a wide-spectrum clinical condition classified as a neurovisceral disorder affecting mainly the liver and the brain. It is caused by mutations in one of two genes, NPC1 and NPC2, coding for proteins located in the lysosomes. NPC proteins are deputed to transport cholesterol within lysosomes or between late endosome/lysosome systems and other cellular compartments, such as the endoplasmic reticulum and plasma membrane. The first trait of NPC is the accumulation of unesterified cholesterol and other lipids, like sphingosine and glycosphingolipids, in the late endosomal and lysosomal compartments, which causes the blockade of autophagic flux and the impairment of mitochondrial functions. In the brain, the main consequences of NPC are cerebellar neurodegeneration, neuroinflammation, and myelin defects. This review will focus on myelin defects and the pivotal importance of cholesterol for myelination and will offer an overview of the molecular targets and the pharmacological strategies so far proposed, or an object of clinical trials for NPC. Finally, it will summarize recent data on a new and promising pharmacological perspective involving A2A adenosine receptor stimulation in genetic and pharmacological NPC dysmyelination models.

scholarly journals Diminazene aceturate-concentrations in tissues of dogs co-treated with oxtetracycline long acting

2021 ◽  
pp. 41-46
Keyword(s):  
Skeletal Muscles ◽  
Post Treatment ◽  
The Other ◽  
Canine Babesiosis ◽  
Diminazene Aceturate ◽  
Normal Dose ◽  
Drug Of Choice ◽  
The World ◽  
Long Acting ◽  
The Brain

Diminizene aceturate (DA) is the drug of choice for treating Canine Trypanosomosis and Canine Babesiosis in many countries of the world. However, co-administration of the drug with long acting Oxytetracycline (OXY-LA) has been associated with nervous signs suggestive of its toxicity, in treated dogs, even at the normal dose. To investigate what causes this toxicity, fourteen Nigerian indigenous dogs were randomly selected into two groups that comprised six dogs each and the remaining untreated two dogs were used for preparation of tissue standards. One group was treated with DA (3.5mg/kg) alone while the other was, additionally, treated with OXY-LA, 10 minutes post treatment (PT) with DA. Two dogs from each group were sacrificed at 240, 360 and 480 hours, PT and their livers, brains, kidneys, hearts and skeletal muscles were harvested and assayed for DA. Mean DA-concentrations in brains of the DA-OXY-LA group (19.71± 1.31a; 15.86± 2.96a; 9.11± 3.31a) were higher (P≤ 0.05) than 1.39 ± 0.45b; 1.05± 0.29b; 0.71 ± 0.30b of the DA-alone group at 240, 360 and 480 hours, PT, respectively. Also, mean-DA concentration in kidneys (8.00 ±0.46a) of the DA-OXY-LA group was significantly (P≤ 0.05) higher than 3.76±0.32b of the DA-alone group at 360 hours PT. These results suggest that OXY-LA enhances DA-accumulation in the brain and reduces its kidney-elimination, thus making the normal dose to act as overdose, which causes the nervous signs often manifested by treated dogs.

Introduction

Coming of Age ◽  
2019 ◽  
pp. 1-8
Author(s):  
Cheryl L. Sisk ◽  
Russell D. Romeo
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Basic Research ◽  
Adult Individual ◽  
Reproductive Maturation ◽  
New Knowledge ◽  
Methodological Advance ◽  
The Brain ◽  
Adolescent Brain Development

Chapter 1 provides the context and conceptual framework for the authors’ approach to thinking about the science of puberty and adolescence. The overarching principle is that the transition from childhood to adulthood that occurs during puberty and adolescence involves complex and iterative interactions between the developing brain, hormones, and experience. This chapter first introduces the concepts of puberty and adolescence and discusses how they are separate, yet intricately linked, developmental processes. Examples of how puberty, defined as reproductive maturation, can be dissociated from adolescence, defined as maturation of the cognitive, emotional, and social behaviors associated with adulthood, are discussed. Other examples highlight the recurring interactions between the brain, pubertal hormones, and experience that ultimately result in an adult individual. The chapter then traces the evolution and growth of research on puberty and adolescence during the last half of the 20th century, which started with puberty being studied mainly by endocrinologists and adolescence being studied mainly by psychologists, and progressed to both puberty and adolescence becoming a focus for basic research conducted by psychobiologists and developmental neurobiologists. The advent of magnetic resonance imaging made possible imaging of the human brain in healthy adolescents; this methodological advance led to new knowledge of the scope and timing of adolescent brain development and how it is shaped by pubertal hormones.

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