scholarly journals Retrograde Amnesia – A Question of Disturbed Calcium Levels?

2021 ◽  
Vol 15 ◽  
Author(s):  
Dirk Montag
Keyword(s):  
Retrograde Amnesia ◽  
Traumatic Event ◽  
Neuronal Loss ◽  
Anterograde Amnesia ◽  
Experimental Models ◽  
Model Systems ◽  
Associative Memories ◽  
Specific Effects ◽  
Underlying Mechanisms ◽  
The Many

Retrograde amnesia is the inability to remember events or information. The successful acquisition and memory of information is required before retrograde amnesia may occur. Often, the trigger for retrograde amnesia is a traumatic event. Loss of memories may be caused in two ways: either by loss/erasure of the memory itself or by the inability to access the memory, which is still present. In general, memories and learning are associated with a positive connotation although the extinction of unpleasant experiences and memories of traumatic events may be highly welcome. In contrast to the many experimental models addressing learning deficits caused by anterograde amnesia, the incapability to acquire new information, retrograde amnesia could so far only be investigated sporadically in human patients and in a limited number of model systems. Apart from models and diseases in which neurodegeneration or dementia like Alzheimer’s disease result in loss of memory, retrograde amnesia can be elicited by various drugs of which alcohol is the most prominent one and exemplifies the non-specific effects and the variable duration. External or internal impacts like traumatic brain injury, stroke, or electroconvulsive treatments may similarly result in variable degrees of retrograde amnesia. In this review, I will discuss a new genetic approach to induce retrograde amnesia in a mouse model and raise the hypothesis that retrograde amnesia is caused by altered intracellular calcium homeostasis. Recently, we observed that neuronal loss of neuroplastin resulted in retrograde amnesia specifically for associative memories. Neuroplastin is tightly linked to the expression of the main Ca2+ extruding pumps, the plasma membrane calcium ATPases (PMCAs). Therefore, neuronal loss of neuroplastin may block the retrieval and storage of associative memories by interference with Ca2+ signaling cascades. The possibility to elicit retrograde amnesia in a controlled manner allows to investigate the underlying mechanisms and may provide a deeper understanding of the molecular and circuit processes of memory.

Cardioprotection by ginseng: experimental and clinical evidence and underlying mechanisms

2018 ◽  
Vol 96 (9) ◽  
pp. 859-868 ◽  
Author(s):  
Xiaohong Tracey Gan ◽  
Morris Karmazyn
Keyword(s):  
Animal Studies ◽  
Large Scale ◽  
Clinical Evidence ◽  
Artery Bypass ◽  
Antioxidant Properties ◽  
Experimental Models ◽  
Therapeutic Effects ◽  
Ischemic And Reperfusion Injury ◽  
Underlying Mechanisms ◽  
The Many

Protection of the ischemic and reperfused myocardium represents a major therapeutic challenge. Translating results from animal studies to the clinical setting has been disappointing, yet the need for effective intervention, particularly to limit heart damage following infarction or surgical procedures such as coronary artery bypass grafting, is substantial. Among the many compounds touted as cardioprotective agents is ginseng, a medicinal herb belonging to the genus Panax, which has been used as a medicinal agent for thousands of years, particularly in Asian societies. The biological actions of ginseng are very complex and reflect composition of many bioactive components, although many of the biological and therapeutic effects of ginseng have been attributed to the presence of steroid-like saponins termed ginsenosides. Both ginseng and many ginsenosides have been shown to exert cardioprotective properties in experimental models. There is also clinical evidence that traditional Chinese medications containing ginseng exert cardioprotective properties, although such clinical evidence is less robust primarily owing to the paucity of large-scale clinical trials. Here, we discuss the experimental and clinical evidence for ginseng, ginsenosides, and ginseng-containing formulations as cardioprotective agents against ischemic and reperfusion injury. We further discuss potential mechanisms, particularly as these relate to antioxidant properties.

scholarly journals 421 - Mood disorders and its relationship with cognitive impairment and dementia

2020 ◽  
Vol 32 (S1) ◽  
pp. 137-137
Author(s):  
Sandra Torres ◽  
Andreia Lopes
Keyword(s):  
Cognitive Impairment ◽  
Mood Disorders ◽  
Neuronal Loss ◽  
Neurocognitive Impairment ◽  
Attention And Memory ◽  
Psychiatric Illnesses ◽  
Neurocognitive Functions ◽  
The Many ◽  
The One ◽  
Published Research

ABSTRACT:Mood disorders are common psychiatric illnesses that represent a major cause of disability worldwide. With life expectancy and the percentage of elderly people rising in many developed and undeveloped countries around the globe, cognitive impairment and dementia are gaining a societal importance. The relation between mood disorders and cognitive function is a twofold. On the one hand, cognitive deficits within mood disorders have been studied extensively, in which there seems to be a persistent neurocognitive impairment, both in acute phases and in interepisodic euthymic phases. Although results have not always been consistent, an overall pattern of specific impairments – in executive function, attention and memory - has become evident. On the other hand, recent research suggests that mood disorders, in general, may be risk factors for the development of mild cognitive impairment and dementia. In this sense, of the many models for the association of mood disorders and dementia, two are favored by several authors. One suggests that mood disorders are a risk factor for earlier clinical manifestation of dementia. The second sees mood disorders as the cause of dementing states, for instance through neuronal loss via dysregulation of the glucocorticoid cascade. In fact, there is suggestion that impairment of neuroplasticity may underlie the pathophysiology of mood disorders as such, and not only of neurocognitive impairment. In some patients, specific neurocognitive functions may be present before the onset of mood disorder and may constitute a trait factor or even an endophenotype. The aim of the present work is to, through a basic narrative review of published research on the main databases, summarize the main evidences of the association of mood disorders and dementia.

scholarly journals Mechanisms of electron-phonon coupling unraveled in momentum and time: The case of soft phonons in TiSe2

2021 ◽  
Vol 7 (20) ◽  
pp. eabf2810
Author(s):  
Martin R. Otto ◽  
Jan-Hendrik Pöhls ◽  
Laurent P. René de Cotret ◽  
Mark J. Stern ◽  
Mark Sutton ◽  
...  
Keyword(s):  
Wave Vector ◽  
Density Wave ◽  
Phonon Coupling ◽  
Many Body ◽  
Soft Zone ◽  
Electron Phonon Coupling ◽  
Underlying Mechanisms ◽  
The Many ◽  
Coupling Phenomena ◽  
Electron Pocket

The complex coupling between charge carriers and phonons is responsible for diverse phenomena in condensed matter. We apply ultrafast electron diffuse scattering to unravel electron-phonon coupling phenomena in 1T-TiSe2 in both momentum and time. We are able to distinguish effects due to the real part of the many-body bare electronic susceptibility, R[χ0(q)], from those due to the electron-phonon coupling vertex, gq, by following the response of semimetallic (normal-phase) 1T-TiSe2 to the selective photo-doping of carriers into the electron pocket at the Fermi level. Quasi-impulsive and wave vector–specific renormalization of soft zone-boundary phonon frequencies (stiffening) is observed, followed by wave vector–independent electron-phonon equilibration. These results unravel the underlying mechanisms driving the phonon softening that is associated with the charge density wave transition at lower temperatures.

scholarly journals Experimental Models to Study COVID-19 Effect in Stem Cells

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 91
Author(s):  
Rishi Man Chugh ◽  
Payel Bhanja ◽  
Andrew Norris ◽  
Subhrajit Saha
Keyword(s):  
Stem Cells ◽  
Ex Vivo ◽  
Drug Efficacy ◽  
Cell Loss ◽  
Experimental Models ◽  
Model Systems ◽  
Virus Infectivity ◽  
Ex Vivo Model ◽  
Global Pandemic ◽  
The Impact

The new strain of coronavirus (severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2)) emerged in 2019 and hence is often referred to as coronavirus disease 2019 (COVID-19). This disease causes hypoxic respiratory failure and acute respiratory distress syndrome (ARDS), and is considered as the cause of a global pandemic. Very limited reports in addition to ex vivo model systems are available to understand the mechanism of action of this virus, which can be used for testing of any drug efficacy against virus infectivity. COVID-19 induces tissue stem cell loss, resulting inhibition of epithelial repair followed by inflammatory fibrotic consequences. Development of clinically relevant models is important to examine the impact of the COVID-19 virus in tissue stem cells among different organs. In this review, we discuss ex vivo experimental models available to study the effect of COVID-19 on tissue stem cells.

scholarly journals The Liver and the Hepatic Immune Response in Trypanosoma cruzi Infection, a Historical and Updated View

Pathogens ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1074
Author(s):  
Natalia Vacani-Martins ◽  
Marcelo Meuser-Batista ◽  
Carina de Lima Pereira dos Santos ◽  
Alejandro Marcel Hasslocher-Moreno ◽  
Andrea Henriques-Pons
Keyword(s):  
Immune Response ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Clinical Signs ◽  
Cell Types ◽  
Experimental Models ◽  
Chronic Patients ◽  
The Usa ◽  
Multiple Cell ◽  
Underlying Mechanisms

Chagas disease was described more than a century ago and, despite great efforts to understand the underlying mechanisms that lead to cardiac and digestive manifestations in chronic patients, much remains to be clarified. The disease is found beyond Latin America, including Japan, the USA, France, Spain, and Australia, and is caused by the protozoan Trypanosoma cruzi. Dr. Carlos Chagas described Chagas disease in 1909 in Brazil, and hepatomegaly was among the clinical signs observed. Currently, hepatomegaly is cited in most papers published which either study acutely infected patients or experimental models, and we know that the parasite can infect multiple cell types in the liver, especially Kupffer cells and dendritic cells. Moreover, liver damage is more pronounced in cases of oral infection, which is mainly found in the Amazon region. However, the importance of liver involvement, including the hepatic immune response, in disease progression does not receive much attention. In this review, we present the very first paper published approaching the liver’s participation in the infection, as well as subsequent papers published in the last century, up to and including our recently published results. We propose that, after infection, activated peripheral T lymphocytes reach the liver and induce a shift to a pro-inflammatory ambient environment. Thus, there is an immunological integration and cooperation between peripheral and hepatic immunity, contributing to disease control.

scholarly journals Hypomorphic mutations in the larval photokinesis A (lphA) gene have stage-specific effects on visual system function in Drosophila melanogaster.

Genetics ◽  
1995 ◽  
Vol 139 (4) ◽  
pp. 1623-1629
Author(s):  
B Gordesky-Gold ◽  
J M Warrick ◽  
A Bixler ◽  
J E Beasley ◽  
L Tompkins
Keyword(s):  
Drosophila Melanogaster ◽  
Visual System ◽  
Specific Aspect ◽  
System Structure ◽  
P Element ◽  
System Function ◽  
Specific Effects ◽  
Isolation And Characterization ◽  
In Trans ◽  
The Many

Abstract Of the many genes that are expressed in the visual system of Drosophila melanogaster adults, some affect larval vision. However, with the exception of one X-linked mutation, no genes that have larval-specific effects on visual system structure or function have previously been reported. We describe the isolation and characterization of two mutant alleles that define the larval photokinesis A (lphA) gene, one allele of which is associated with a P-element insertion at cytogenetic locus 8E1-10. Larvae that express lphA mutations are, like normal animals, negatively photokinetic, but they are less responsive to white light than lphA + controls. Larvae that are heterozygous in trans for a mutant lphA allele and a deficiency that uncovers the lphA locus are blind, which indicates that the mutant allele is hypomorphic. lphA larvae respond normally to odorants and taste stimuli. Moreover, the lphA mutations do not affect adult flies' fast phototaxis or visually driven aspects of male sexual behavior, and electroretinograms recorded from the compound eyes of lphA/deficiency heterozygotes and lphA1/lphA2 females are normal. These observations suggest that the lphA gene affects a larval-specific aspect of visual system function.

scholarly journals Paternal diet programs offspring health through sperm- and seminal plasma-specific pathways in mice

2018 ◽  
Vol 115 (40) ◽  
pp. 10064-10069 ◽  
Author(s):  
Adam J. Watkins ◽  
Irundika Dias ◽  
Heather Tsuro ◽  
Danielle Allen ◽  
Richard D. Emes ◽  
...  
Keyword(s):  
Seminal Plasma ◽  
Semen Quality ◽  
Protein Diet ◽  
Male Mating ◽  
Adult Offspring ◽  
Nonalcoholic Fatty Liver ◽  
Low Protein ◽  
Specific Effects ◽  
Underlying Mechanisms ◽  
Offspring Health

The association between poor paternal diet, perturbed embryonic development, and adult offspring ill health represents a new focus for the Developmental Origins of Health and Disease hypothesis. However, our understanding of the underlying mechanisms remains ill-defined. We have developed a mouse paternal low-protein diet (LPD) model to determine its impact on semen quality, maternal uterine physiology, and adult offspring health. We observed that sperm from LPD-fed male mice displayed global hypomethylation associated with reduced testicular expression of DNA methylation and folate-cycle regulators compared with normal protein diet (NPD) fed males. Furthermore, females mated with LPD males display blunted preimplantation uterine immunological, cell signaling, and vascular remodeling responses compared to controls. These data indicate paternal diet impacts on offspring health through both sperm genomic (epigenetic) and seminal plasma (maternal uterine environment) mechanisms. Extending our model, we defined sperm- and seminal plasma-specific effects on offspring health by combining artificial insemination with vasectomized male mating of dietary-manipulated males. All offspring derived from LPD sperm and/or seminal plasma became heavier with increased adiposity, glucose intolerance, perturbed hepatic gene expression symptomatic of nonalcoholic fatty liver disease, and altered gut bacterial profiles. These data provide insight into programming mechanisms linking poor paternal diet with semen quality and offspring health.

New insights in the interaction of FGF/FGFR and steroid receptor signaling in breast cancer

Endocrinology ◽  
2022 ◽  
Author(s):  
Cecilia Pérez Piñero ◽  
Sebastián Giulianelli ◽  
Caroline A Lamb ◽  
Claudia Lanari
Keyword(s):  
Breast Cancer ◽  
Hormone Receptors ◽  
Endocrine Resistance ◽  
Short Review ◽  
Experimental Models ◽  
Luminal Breast Cancer ◽  
Tumor Subtypes ◽  
Stromal Tissue ◽  
The Many

Abstract Luminal breast cancer (BrCa) has a favorable prognosis compared to other tumor subtypes. However, with time tumors may evolve and lead to disease progression. Thus, there is a great interest in unraveling the mechanisms that drive tumor metastasis and endocrine resistance. In this review we focused in one of the many pathways that have been involved in tumor progression, the FGF/FGFR axis. We emphasized in data obtained from in vivo experimental models since we believe that in luminal BrCa, tumor growth relies in a crosstalk with the stromal tissue. We revisited the studies that illustrate the interaction between hormone receptors and FGFR. We also highlighted the most frequent alterations found in BrCa cell lines and we provide a short review on the trials that use FGFR inhibitors in combination with endocrine therapies. The analysis of this data suggests that there are many players involved in this pathway that might be also targeted to decrease FGF signaling in addition to specific FGFR inhibitors that may be exploited to increase their efficacy.

scholarly journals Induced Human Intestinal Organoids (iHIOs) as Model Systems for Chemotherapy-associated Clostridium difficile (CD) Infections

2017 ◽  
Vol 4 (suppl_1) ◽  
pp. S382-S382
Author(s):  
Senu Apewokin ◽  
Suman Pradhan ◽  
Michael Frerick ◽  
Alison Weiss
Keyword(s):  
Cell Death ◽  
Clostridium Difficile ◽  
Experimental Models ◽  
Cytotoxic Chemotherapy ◽  
Model Systems ◽  
Epithelial Barrier ◽  
Histological Changes ◽  
Human Dose ◽  
Therapeutic Doses ◽  
Pathophysiologic Mechanisms

Abstract Background Patients undergoing cytotoxic chemotherapy are ten times more likely to develop Clostridium difficile infections (CDI) than the general patient population. Efforts to outline pathophysiologic mechanisms underlying this disproportionate incidence have been limited by the lack of disease-representative experimental models. We hypothesized that iHIOs could serve as toxicity models to evaluate chemotherapy-associated CDI Methods Intact iHIOs were exposed to cytotoxic chemotherapy (melphalan) in gut media at therapeutic doses (9 μg/mL; which is the equivalent of 140 mg/m2 human dose). Cellular death was assessed by accumulation of the membrane permeant dye, Sytox-orange added at 5-days post treatment. iHIOs were also exposed to CD toxin A and B (TcdA and TcdB respectively) and epithelial barrier damage assessed by actin mislocalization and loss of E-cadherin. For controls iHIOs were exposed / microinjected with saline/PBS. Morphological and histological changes were then captured using light and confocal microscopy Results Morphologic and histologic assessments demonstrated cell death and epithelial barrier damage Conclusion iHIOs demonstrate cell death on exposure to CD toxins and melphalan chemotherapy. These properties could be harnessed in establishing toxicity models for evaluation of chemotherapy-associated CDI Disclosures S. Apewokin, T2 biosystems: Investigator, Research support Astellas: Scientific Advisor, Consulting fee

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