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4,386 results for “Dysfunction”
DataSet of "No renal dysfunction or salt and water retention in acute mountain sickness at 4,559 m among young resting males after passive ascent"
<p><strong>Abstract</strong></p> <p><strong>Purpose</strong>: This study examined the role and function of the kidney at high altitude in relation to fluid balance and the development of acute mountain sickness (AMS), avoiding confounders that have contributed to conflicting results in previous studies.</p> <p><strong>Methods</strong>: We examined 18 healthy male volunteers (18 - 40 years) not acclimatized to high altitude while on a controlled diet and resting recumbently for 24 h at Lausanne (altitude: 560 m) followed by a period of 44 hours after reaching the Regina Margherita hut (4,559 m) by helicopter.</p> <p><strong>Results</strong>: AMS scores peaked after 20 h at 4,559 m. AMS was defined as functional Lake Louise score <span class="math-tex">\({\ge}\)</span> 2.There were no significant differences between 10 subjects with and 8 subjects without AMS for urinary flow, fluid balance and weight change. Sodium excretion rate was lower in those with AMS after 24 h at altitude. Microalbuminuria increased at altitude but not differently between the groups. Creatinine clearance was not affected by altitude or AMS, while sinistrin and PAH clearances decreased slightly, more markedly in those without AMS. Plasma concentrations of epinephrine, norepinephrine, atrial natriuretic factor and vasopressin increased while renin activity, angiotensin and aldosterone decreased at altitude. Hormones levels did not differ between those with and without AMS.</p> <p><strong>Conclusions</strong>: 1) Renal function is not affected by hypoxia at 4,559 m in resting subjects except for minor microalbuminuria, 2) high altitude diuresis does not occur and 3) AMS is not associated with salt and water retention or renal dysfunction.</p>
Raw data for: "Postsynaptic autism spectrum disorder genes and synaptic dysfunction"
<p>Schematic illustration representing postsynaptic proteins associated to ASD. These proteins are involved in different synaptic functions, either directly (ion channels and glutamate receptors), or indirectly, including transmembrane heterophilic (NLGNs) and homophilic (NrCAM) cell-adhesion molecules, and scaffolding proteins (PSD-95, Shank, Homer), that link transmembrane and membrane-associated protein complexes with the underlying actin cytoskeleton. Additional cellular functions may influence synaptic activity in ASD, such as alternative splicing (PTEN, RBFOX1, nSR100/SRRM4), RNA editing (FMR1, FXR1), transcription (FOXP1, FOXP2, TBR1, TSHZ3), translation (FMR1), degradation (UBE3A), and mitochondrial activity (AGC1).</p>
BIDS wildtype data selection from "Dysfunctional Autism Risk Genes Cause Circuit-Specific Connectivity Deficits With Distinct Developmental Trajectories"
<p>Data package selecting wildtype animals from the “Dysfunctional Autism Risk Genes Cause Circuit-Specific Connectivity Deficits With Distinct Developmental Trajectories” article, formatted corresponding to the Brain Imaging Data Structure. The relevant publication can be found via DOI <a href="https://doi.org/10.1093/cercor/bhy046">10.1093/cercor/bhy046</a> .</p>
Dataset related to: Sirt3 deficiency promotes endothelial dysfunction and aggravates renal injury
<p>The .xlsx file contains raw data related to the article "<i><strong>Sirt3</strong></i><strong> deficiency promotes endothelial dysfunction and aggravates renal injury</strong>. <i>PLOS One</i>. 2023 Oct 10;18(10):e0291909<i>", </i>available at the following <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0291909">link</a>.</p><p> </p><p><strong>Abstract</strong></p><p>Sirtuin 3 (SIRT3), the main deacetylase of mitochondria, modulates the acetylation levels of substrates governing metabolism and oxidative stress. In the kidney, we showed that SIRT3 affects the proper functioning of high energy-demanding cells, such as tubular cells and podocytes. Less is known about the role of SIRT3 in regulating endothelial cell function and its impact on the progression of kidney disease. Here, we found that whole body <i>Sirt3</i>-deficient mice exhibited reduced renal capillary density, reflecting endothelial dysfunction, and VEGFA expression compared to wild-type mice. This was paralleled by activation of hypoxia signaling, upregulation of HIF-1α and Angiopietin-2, and oxidative stress increase. These alterations did not result in kidney disease. However, when <i>Sirt3</i>-deficient mice were exposed to the nephrotoxic stimulus Adriamycin (ADR) they developed aggravated endothelial rarefaction, altered VEGFA signaling, and higher oxidative stress compared to wild-type mice receiving ADR. As a result, ADR-treated <i>Sirt3</i>-deficient mice experienced a more severe injury with exacerbated albuminuria, podocyte loss and fibrotic lesions. These data suggest that SIRT3 is a crucial regulator of renal vascular homeostasis and its dysregulation is a predisposing factor for kidney disease. By extension, our findings indicate SIRT3 as a pharmacologic target in progressive renal disease whose treatments are still imperfect.</p>
Cerebral microstructural alterations in Post-COVID-condition are related to cognitive impairment, olfactory dysfunction, and fatigue
<p>After contracting COVID-19, a substantial number of individuals develop a Post-COVID-Condition (PCC), marked by neurologic symptoms such as cognitive deficits, olfactory dysfunction, and fatigue, which can have detrimental socioeconomic consequences. Despite this, biomarkers and pathophysiological understandings of this condition remain limited. Employing magnetic resonance imaging, we conduct a comparative analysis of cerebral microstructure among patients with post-COVID condition, healthy controls, and individuals who contracted COVID-19 without long-term symptoms. This reveals widespread alterations in cerebral microstructure, attributed to a shift in volume from neuronal compartments to free fluid, associated with the severity of the initial infection. Correlating these alterations with cognition, olfaction, and fatigue unveils distinct affected networks, which are in a close anatomical-functional relationship with the respective symptoms. This plausibility of symptom-specific networks not only provides insights into the disease's pathophysiological foundations, which align well with an accelerated aging process but also underscores the significance of microstructure as an imaging biomarker.</p>
Figure 1 in Antioxidant extract of black rice prevents renal dysfunction and renal fibrosis caused by ethanol-induced toxicity
Figure 1. Histopathological changes of kidney sections of 1) NC (Normal Control group) Control section of kidney showing cortical parenchyma to consist of dense rounded structures, the glomeruli (G), surrounded by narrow Bowman's capsular spaces (BCS); 2) PC (Positive Control group) showing glomeruli with mild mesangial proliferation (G), moderate degree of chronic interstitial inflammatory infiltrate and tubular epithelial cells focal degeneration, Cloudy swelling tubular cells with narrow (arrow) or obliterated (yellow arrow); 3) 100 mg/kg bw BREE showing mild interstitial inflammation in the interstitium (arrow); 4) 200 mg/kg bw BREE showing normal appearance of glomerular capillary tuft (G) and Bowman's capsule basement membrane (BCS) and a clear improvement in the general shape of tubes and cells. H&E (Mag. X400).
Figure 2 in Antioxidant extract of black rice prevents renal dysfunction and renal fibrosis caused by ethanol-induced toxicity
Figure 2. Histopathology of nephropathy in 1) NC (Normal Control group) showing minimal amount of collagen around renal tubules, capillary tuft and Bowman's capsules of glomerulus; 2) PC (Positive Control group) showing an increase of the collagen fibers around Bowman's capsule, capillary loops and convoluted tubules of glomerulus and both necrotic and apoptotic changes in the renal tubules; 3) 100 mg/kg bw BREE showing mild to moderate increased collagen fibres; 4) 200 mg/kg bw BREE.Showing a little amount of collagen similar or close to NC. (Masson's Trichrome × 400).
Persistent alveolar type 2 dysfunction and lung structural derangement in post-acute COVID-19
<p>SARS-CoV-2 infection can manifest as a wide range of respiratory and systemic symptoms well after the acute phase of infection in over 50% of patients. Key questions remain on the long-term effect of infection on tissue pathology and on recovered COVID-19 patients. Here we perform multiplexed imaging of post-mortem lung tissue from 12 individuals that died post-acute COVID-19 (PC) and compare them to patients who died during the acute phase of COVID-19, patients who died with idiopathic pulmonary fibrosis (IPF), and otherwise healthy lung. We find evidence of viral presence in the lung up to 359 days after the acute phase of disease, often in patients with negative nasopharyngeal swab test. Our analyses identify accumulation of senescent alveolar type 2 cells, fibrosis with hypervascularization of peribronchial areas and alveolar septa, as the most pronounced pathophysiological features seen in the lung of PC patients. At the cellular level, lung disease of PC patients is distinct from the chronic pulmonary disease of IPF but shares pathological features which may help rationalize interventions for PASC patients. Altogether, this study provides an important ground for the understanding of the long-term effects of SARS-CoV-2 infection at the microanatomical, cellular and molecular level.</p>
Dataset related to: Shiga Toxin 2 Triggers C3a-Dependent Glomerular and Tubular Injury through Mitochondrial Dysfunction in Hemolytic Uremic Syndrome
<p>The files contain all the dataset included in the manuscript, divided by figure in each tab.</p> <p> </p> <p><strong>Abstract</strong></p> <p>Shiga toxin (Stx)-producing <em>Escherichia coli</em> is the predominant offending agent of post-diarrheal hemolytic uremic syndrome (HUS), a rare disorder of microvascular thrombosis and acute kidney injury possibly leading to long-term renal sequelae. We previously showed that C3a has a critical role in the development of glomerular damage in experimental HUS. Based on the evidence that activation of C3a/C3a receptor (C3aR) signaling induces mitochondrial dysregulation and cell injury, here we investigated whether C3a caused podocyte and tubular injury through induction of mitochondrial dysfunction in a mouse model of HUS. Mice coinjected with Stx2/LPS exhibited glomerular podocyte and tubular C3 deposits and C3aR overexpression associated with cell damage, which were limited by C3aR antagonist treatment. C3a promoted renal injury by affecting mitochondrial wellness as demonstrated by data showing that C3aR blockade reduced mitochondrial ultrastructural abnormalities and preserved mitochondrial mass and energy production. In cultured podocytes and tubular cells, C3a caused altered mitochondrial fragmentation and distribution, and reduced anti-oxidant SOD2 activity. Stx2 potentiated the responsiveness of renal cells to the detrimental effects of C3a through increased C3aR protein expression. These results indicate that C3aR may represent a novel target in Stx-associated HUS for the preservation of renal cell integrity through the maintenance of mitochondrial function.</p>
Preventing Persistent Post-Surgical Pain and Dysfunction
ClinicalTrials.gov study NCT03965897. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Curcumin Therapy to Treat Vascular Dysfunction in Children and Young Adults With ADPKD
ClinicalTrials.gov study NCT02494141. IPD Sharing: YES. Countries: 1. Publications: 1.
Multimodal Mobile Intervention Application (App) to Address Sexual Dysfunction in Hematopoietic Stem Cell Transplant Survivors
ClinicalTrials.gov study NCT03967379. IPD Sharing: YES. Countries: 1. Publications: 0.
Spatial coding dysfunction and network instability in the aging medial entorhinal cortex
Open the record for dataset details and reuse information.
Cerebral microstructural alterations in Post-COVID-condition are related to cognitive impairment, olfactory dysfunction, and fatigue
Open the record for dataset details and reuse information.
Raw data to "Specialized pro-resolving lipid mediators are differentially altered in peripheral blood of patients with multiple sclerosis and attenuate monocyte and blood-brain barrier dysfunction"
<p>Background: Lack of resolution of inflammation may be considered a critical player for the onset and progression of multiple sclerosis. To demonstrate this we extracted lipids from plasma samples of healthy donors and MS patients and we quantified over 65 lipid mediators (LMs) through LC-MS-MS using signature diagnostic ions via multiple reaction monitoring.</p> <p>Results: Out of the 65 lipid mediators analyzed, only 42 were detected and out of those only 27 were finally revealed to show differences between healthy subjects and MS patients. These 27 LMs belonged to the arachidonic (AA), docosahexaenoic (DHA) or eicosapentaenoic (EPA) acid metabolomes and we could clusterize each form of MS into a specific profile by means of principal component analysis. Altogether, compared to healthy subjects, MS patients showed a strong production of several AA-derived eicosanoids (i.e. PGE2, PGD2 and PGF2a) (Fig.1D) and a little production of two DHA-derived pro-resolving mediators (SPMs), i.e. Protectin D1 (D1) and protectin DX (PDX) (Fig.1A). However, no production of DHA-derived resolvins and maresins (Fig. 1B) as well as EPA-derived resolvins (Fig.1 C) was observed.</p> <p>When stratifying MS patients according to disease form, both relapsing MS patients showed production of only two pro-resolving mediators (SPMs), i.e. Resolvin D1 (RvD1) and Protectin D1 (D1) compared to healthy subjects, whereas remitting MS patients showed a production of only few AA- and DHA-derived metabolic pathway markers and progressive MS patients a strong production of several eicosanoids as well as other metabolic pathway markers.</p> <p>Conclusions: These data suggest that along disease progression, there is a lack of production of anti-inflammatory and pro-resolving lipid mediators associated to a higher production of pro-inflammatory ones.</p>
Data from: Paradoxical aortic stiffening and subsequent cardiac dysfunction in Hutchinson–Gilford progeria syndrome
<p>Hutchinson–Gilford progeria syndrome (HGPS) is an ultra-rare disorder with devastating sequelae resulting in early death, presently thought to stem primarily from cardiovascular events. We analyse novel longitudinal cardiovascular data from a mouse model of HGPS (<i>Lmna<sup>G609G/G609G</sup></i>) using allometric scaling, biomechanical phenotyping, and advanced computational modelling and show that late-stage diastolic dysfunction, with preserved systolic function, emerges with an increase in the pulse wave velocity and an associated loss of aortic function, independent of sex. Specifically, there is a dramatic late-stage loss of smooth muscle function and cells and an excessive accumulation of proteoglycans along the aorta, which result in a loss of biomechanical function (contractility and elastic energy storage) and a marked structural stiffening despite a distinctly low intrinsic material stiffness that is consistent with the lack of functional lamin A. Importantly, the vascular function appears to arise normally from the low-stress environment of development, only to succumb progressively to pressure-related effects of the lamin A mutation and become extreme in the peri-morbid period. Because the dramatic life-threatening aortic phenotype manifests during the last third of life there may be a therapeutic window in maturity that could alleviate concerns with therapies administered during early periods of arterial development.</p>
Deferoxamine Regulates Neuroinflammation and Iron Homeostasis in a Mouse Model of Postoperative Cognitive Dysfunction
<p>The raw data of the manuscript” Deferoxamine Regulates Neuroinflammation and Iron Homeostasis in a Mouse Model of Postoperative Cognitive Dysfunction”</p>
Increased Drp1 acetylation by lipid overload induces cardiomyocyte death and heart dysfunction
<p>Metabolic syndrome is a cluster of abnormalities characterized by obesity and insulin resistance, which compromise energy metabolism, damage mitochondria, cause cardiomyocyte death, and eventually impair heart contraction and relaxation performance. Despite the increasing prevalence of heart complications in obese and diabetic patients, our knowledge on how obese and diabetes mellitus impair heart function is very limited. In this study, we used animal and cell culture models in rodents or monkeys and generated lipid overload models to mimic obesity conditions. We found that excessive lipid supply decreased nicotinamide adenine dinucleotide (oxidized) levels and increased the acetylation of a fission protein Drp1 at a specific lysine residue (K642). Drp1 acetylation at K642 activated Drp1 through phosphorylation, mitochondrial translocation, and oligomerization. The excessively activated Drp1 had higher GTPase activity, bound with VDAC1 on mitochondria, induced mitochondrial fission, and caused cardiomyocyte death. These findings provide new information regarding how lipid overload regulates redox environment, protein acetylation, and the function of mitochondrial fission protein Drp1 in the heart.</p>
Comparative proteomic and metabolomic analyses of plasma reveal the novel biomarker panels for thyroid dysfunction
<p><strong>Abstract</strong><strong>:</strong></p> <p><em>Objectives: </em>Thyroid dysfunction such as hypothyroidism (THO) and hyperthyroidism (THE) are the disease caused by pathological processes in the thyroid. The current diagnosis of thyroid dysfunction is variable because of ages and genders. The aim of this study was to explore the novel candidate biomarker panels for hypothyroidism and hyperthyroidism screening with mass spectrometry and bioinformatics.</p> <p><em>Methods:</em> Plasma samples were collected from 15 THE patients, 9 THO patients, and 15 healthy controls. DIA-based proteomic and untargeted metabolomic analyses were performed to identify the novel biomarker panels for THO and THE. Finally, three candidate biomarkers were verified by ELISA in 34 samples.</p> <p><em>Results:</em> A total of 2738 proteins and 6103 metabolites were identified, and 173 proteins and 2487 metabolites were found to be differentially expressed among THE, THO and control groups. The results of the ensemble feature selection, K-means clustering and the least absolute shrinkage and selection operator (LASSO) regression model showed that four proteins (C4A, C3/C5 convertase, APOL1, and ITIH4) and four metabolites (L-arginine, L-proline, cortisol, and cortisone) identified by plasma proteomics and metabolomics could help distinguish THO and THE patients from healthy controls.</p> <p><em>Conclusions:</em> This study identified and verified two pairs of biomarker panels that can distinguish the THE and THO patients regardless of ages and genders. Consequently, our findings represent a comprehensive analyses of thyroid dysfunction plasma, which is significant for the clinical diagnosis.</p> <p> </p>
Data for PNASnexus article Aldehyde dehydrogenase 3A1 deficiency leads to mitochondrial dysfunction and impacts salivary gland stem cell phenotype
<p>Adult salivary stem/progenitor cells (SSPC) have an intrinsic property to self-renew in order to maintain tissue architecture and homeostasis. Adult salivary glands have been documented to harbor SSPC, which have been shown to play a vital role in the regeneration of the glandular structures post radiation damage. We have previously demonstrated that activation of aldehyde dehydrogenase 3A1 (ALDH3A1) after radiation reduced aldehyde accumulation in SSPC, leading to less apoptosis and improved salivary function. We subsequently found that sustained pharmacological ALDH3A1 activation is critical to enhance regeneration of murine submandibular gland after radiation damage. Further investigation shows that ALDH3A1 function is crucial for SSPC self-renewal and survival even in the absence of radiation stress. Salivary glands from <em>Aldh3a1</em>-null mice have fewer acinar structures than wildtype mice. ALDH3A1 deletion or pharmacological inhibition in SSPC leads to a decrease in mitochondrial DNA copy number, lower expression of mitochondrial specific genes and proteins, structural abnormalities, lower membrane potential, and reduced cellular respiration. Loss or inhibition of ALDH3A1 also elevates ROS levels and accumulation of ALDH3A1 substrate 4-hydroxynonenal (4-HNE, a lipid peroxidation product), leading to decreased survival of murine SSPC that can be rescued by treatment with 4-HNE specific carbonyl scavengers. Our data indicate that ALDH3A1 activity protects mitochondrial function and is important for the regeneration activity of SSPC. This knowledge will help to guide our translational strategy of applying ALDH3A1 activators in the clinic to prevent radiation-related hyposalivation in head and neck cancer patients.</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.