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Cytoplasmic Inclusion

Cytoplasmiic Inclusions are discrete, abnormal structures found within the cytoplasm of cells.
These inclusions may contain proteins, lipids, carbohydrates, or other cellular components, and can be associated with various disease states or cellular dysfunctions.
Understanding the composition and function of cytoplasmic inclusions is an important area of research, as they can provide insight into underlying pathological processes and potential therapeutic targets.

Most cited protocols related to «Cytoplasmic Inclusion»

Gene counts were obtained by aligning reads to the hg38 genome (GRCh38.p5 (NCBI:GCA_000001405.20) using CellRanger software (2.0.0 version) (10× Genomics). To account for unspliced nuclear transcripts, reads mapping to pre-mRNA were counted. After quantification of pre-mRNA using the CellRanger count pipeline on each of the 48 individual libraries, the CellRanger aggr pipeline was employed to aggregate all libraries to equalize the read depth between libraries before data merging (with the default parameter) to generate a gene count matrix. Then, a UMI cutoff of200 was used to select single cells for further analysis. From our pilot sample analysis, we realized that the default cell detection method employed by 10× Genomics (assuming UMI values - a reflection of the RNA content - varies by roughly an order of magnitude among cells) failed to detect a large fraction of the microglia population. Therefore, to determine a more appropriate UMI cutoff value, we plotted a histogram showing cell density as a function of UMI values. Based on this analysis we determined 200 UMIs as the lower cutoff for cell filtering. This resulted in an initial dataset that was then further examined to exclude low quality libraries (see Quality control for cell inclusion).
Publication 2019
Cells Cytoplasmic Inclusion Genes Genome Microglia mRNA Precursor Physiology, Cell Reflex Single-Cell Analysis
Genome-wide gene association analysis was performed using MAGMA v1.0815 (http://ctg.cncr.nl/software/magma). All variants in the GWAS outside of the MHC region (GRCh37: 6:28,477,797–33,448,354) that positionally map within one of the 19,019 protein coding genes were included to estimate the significance value of that gene. Genes were considered significant if the P-value was <0.05 after Bonferroni correction for 19,019 genes. All MAGMA analyses utilized 1KG43 (link) LD information. MAGMA gene-set analysis was performed where variants map to 15,496 gene-sets from the MSigDB v7.0 database52 (link). Gene-sets were considered significant if the P-value was <0.05 after Bonferroni correction for the number of tested gene-sets. Forward selection of significantly associated gene-sets was performed using MAGMA v1.08 conditional analysis53 (link). Initially the most significant gene-set was selected as a covariate and the remaining gene-sets were analyzed. The most significant gene-set from this conditional analysis was added as a covariate in addition to the previous gene-set and a new analysis was run. This process was repeated until no gene-set met the significance threshold (PBonferroni<0.05). MAGMA tissue specificity analysis was performed in FUMA using 30 general tissue type gene expression profiles (from GTEx v8). Tissues were considered significant if the P-value was < 0.05 after Bonferroni correction for 30 tissues.
FUMA cell type specificity analysis16 (link) utilises the MAGMA gene association results to identify cell types enriched in expression of trait associated genes. We focused on brain and immune related cell types with the inclusion of pancreas as a control, therefore selecting the following scRNA-seq datasets: Allen_Human_LGN_level154 (link), Allen_Human_LGN_level254 (link), Allen_Human_MTG_level154 (link), Allen_Human_MTG_level254 (link), DroNc_Human_Hippocampus55 (link), DroNc_Mouse_Hippocampus55 (link), GSE104276_Human_Prefrontal_cortex_all_ages56 (link), GSE67835_Human_Cortex57 (link), GSE81547_Human_Pancreas58 (link), Linnarsson_GSE101601_Human_Temporal_cortex59 (link), MouseCellAtlas_all60 (link), PBMC_10x_68k61 (link), and PsychENCODE_Adult62 . Within-dataset corrected results were reported to indicate which single cells are most likely to be disease relevant. The gene-based and gene-set analyses were also performed without the larger APOE region (19:40000000–50000000).
Publication 2021
ApoE protein, human Brain Cells Chromosome Mapping Cytoplasmic Inclusion Gene Expression Gene Products, Protein Genes Genome-Wide Association Study Homo sapiens Mus Pancreas Prefrontal Cortex Proteins Single-Cell RNA-Seq Tissue Microarray Analysis Tissues Tissue Specificity
The brain was removed a median of 5.5 hours (interquartile range = 5.4) after death which occurred a median of 7.7 months (interquartile range = 7.0) following the last clinical evaluation. One cerebral hemisphere, one cerebellar hemisphere, and the brainstem were fixed in 4% paraformaldehyde for at least 72 hours. The brain was cut coronally into 1-cm slabs and all slabs were examined for gross infarcts. A standard protocol was followed for tissue preservation, tissue sectioning, and quantification of pathologic data by examiners blinded to all clinical data.18 (link),19 (link) We used hemotoxylin and eosin to identify microinfarcts (i.e., visible on microscopic but not gross inspection) in 9 regions in one hemisphere, as previously described.20 (link) In analyses, chronic gross and microscopic infarcts were each treated as present or absent.
Based on prior research,1 (link),21 (link)–26 we investigated TDP-43 pathology in 6 brain regions: amygdala (and periamygdalar region when available), hippocampus CA1/subiculum, dentate gyrus, entorhinal cortex, midfrontal cortex, and middle temporal cortex. Immunostaining was done on 6 μm sections using monoclonal antibodies to phosphorylated TDP-43 (pS409/410;1:100)27 (link) which stain the pathologically phosphorylated TDP-43 proteins in the inclusions seen in amyotrophic lateral sclerosis, frontotemporal lobar degeneration, and other neurodegenerative diseases but not the normal nuclear TDP-43. Each region of interest was reviewed for the presence, severity, and location of TDP-43 cytoplasmic inclusions (both neuronal and glial) and was rated on a 6-point scale based on the number of inclusions in a 0.25mm2 area of greatest density within that region (none, sparse [1–2 inclusions], sparse to moderate [3–5 inclusions], moderate [6–12 inclusions], moderate to severe [13–19 inclusions], severe [20 or more inclusions]) (Figure 1).
An anti-paired helical filaments-tau antibody clone AT8 (ThermoScientific, Rockford, IL USA; 1:2000) and computer assisted sampling28 (link) were used to measure density of tau-immunoreactive neurofibrillary tangles in at least 2 sections from 8 limbic and neocortical regions (entorhinal cortex, CA1/subiculum, anterior cingulate cortex, dorsolateral prefrontal cortex, superior frontal cortex, inferior temporal cortex, inferior parietal cortex, primary visual cortex). The raw scores in each section and region were averaged to yield a composite measure of tangle density/mm2, as previously described.26 Beta amyloid-immunoreactive plaques were assessed in the 8 regions examined for tau using a monoclonal antibody (1:50; Beta-Amyloid, Clone 6F/3D, Dako, North America) with diaminobenzidine as the reporter with 2.5% nickel sulphate to enhance contrast. Computer assisted sampling and image analysis were used to quantify the percent of each area occupied by beta-amyloid-immunoreactive pixels. Regional measures were averaged to yield a composite measure of amyloid burden.28 (link)Lewy bodies were identified in the substantia nigra, 2 limbic sites (entorhinal cortex, anterior cingulate cortex), and 3 neocortical sites (midfrontal cortex, superior or middle temporal cortex, inferior parietal cortex) using a monoclonal antibody to alpha-synuclein (Zymed LB 509; 1:50).18 (link) We used a modified version29 (link),30 (link) of the staging criteria of McKeith et al31 (link) to classify Lewy body disease as nigral, limbic, or neocortical. Neocortical disease required Lewy bodies in frontal, temporal, or parietal cortex and was usually accompanied by nigral and limbic Lewy bodies.
Publication 2013
alpha-Synuclein Amygdaloid Body Amyloid beta-Peptides Amyotrophic Lateral Sclerosis Antibodies, Anti-Idiotypic Brain Brain Stem Cerebellum Cerebral Hemispheres Clone Cells Cortex, Cerebral Cytoplasmic Inclusion Dorsolateral Prefrontal Cortex Entorhinal Area Eosin Frontotemporal Lobar Degeneration Gyrus, Anterior Cingulate Gyrus, Dentate Hematoxylin Inclusion Bodies Infarction Lewy Bodies Lewy Body Disease Lobe, Frontal Microscopy Monoclonal Antibodies Neurodegenerative Disorders Neurofibrillary Tangle Neuroglia Neurons nickel sulfate paraform Parietal Cortex, Inferior Parietal Lobe Proteins protein TDP-43, human Seahorses Senile Plaques Serum Amyloid A Protein Stains Striate Cortex Subiculum Substantia Nigra Temporal Lobe Tissue Preservation Tissues Vision

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Publication 2017
Chromosomes Cytoplasmic Inclusion Genes Genome Neoplasms Signal Transduction
For this study, paraffin blocks of 14 brain regions that included the eight original regions, as well as six newly reported regions (basal forebrain, insular cortex, ventral striatum, substantia nigra, midbrain tectum and inferior olive) were sectioned and immunostained for TDP-43 (polyclonal antibody MC2085 that recognizes a peptide sequence in the 25-kDA C-terminal fragment[44 (link)] with a DAKO-Autostainer (DAKA-Cytomaton, Carpinteria, CA) with 3,3’-diaminobenzidine as the chromogen. A region was considered TDP-43 positive if there were any TDP-43 immunoreactive neuronal cytoplasmic inclusions, dystrophic neurites, or neuronal intranuclear inclusions identified at 400× magnification. These lesion types were chosen as all three lesion types have been identified in amyotrophic lateral sclerosis[4 (link),31 (link),38 (link)], frontotemporal lobar degeneration[4 (link),14 (link),22 (link),38 (link)] and Alzheimer’s disease[3 (link),5 (link),8 (link),19 (link),21 (link),23 (link),24 (link),28 (link),41 (link)], and are therefore considered to be abnormal. The definition of TDP-43 positivity used in this study is unchanged from that used to develop the original TDP-43 in Alzheimer’s disease staging scheme [23 (link)].
Publication 2016
Alzheimer's Disease Amyotrophic Lateral Sclerosis Anesthesia, Conduction azo rubin S Basal Forebrain Brain Cytoplasmic Inclusion Frontotemporal Lobar Degeneration Immunoglobulins Insula of Reil Neurites Neurons Nuclear Inclusion Olivary Nucleus Paraffin Peptide Fragments polypeptide C protein TDP-43, human Substantia Nigra Tectum Mesencephali Ventral Striatum

Most recents protocols related to «Cytoplasmic Inclusion»

Tissues were fixed in 4% buffered formaldehyde, stored > 24 h prior to further processing, embedded in paraffin, and cut into 2 µm thick sections. Hematoxylin and eosin (H&E), Picrosirius red (PSR) and wheat germ agglutinin (WGA)/DAPI fluorescence staining were performed as previously described (14 (link)). Microscopy of H&E and PSR stains was performed using a BX43 light microscope (Olympus, Tokyo, Japan) and an Observer.Z1 fluorescence microscope (Zeiss, Wetzler, Germany) for WGA/DAPI stains. Liver fat content was assessed as area percentage of hepatocytes with macro- or microvesicular cytoplasmatic fat inclusions. Hepatic fibrosis was evaluated according to the ISHAK score (21 (link)), and liver sections were scored for steatosis, lobular inflammation, and hepatocyte ballooning according to the NAFLD activity score (NAS) (22 (link)). For immunohistological quantification of skeletal muscle fiber area, sections were deparaffinized, stained with WGA, and sections with WGA staining of the cellular membrane were selected for stereological quantification, which was performed using the AxioVision software (Zeiss, Wetzler, Germany). Kidney sections showing cortex and medulla were evaluated for histopathologic abnormalities with focus on the presence of tubular ischemia and necrosis, glomerular ischemia, microthrombi, arteriosclerosis and glomerulosclerosis. Sections were analyzed by an experienced pathologist blinded for the group of mice investigated.
Publication 2023
Arteriosclerosis Cell-Derived Microparticles Congenital Abnormality Cortex, Cerebral Cytoplasmic Inclusion DAPI Eosin Fibrosis, Liver Fluorescence Formaldehyde Hematoxylin Hepatocyte Inflammation Ischemia Kidney Kidney Glomerulus Light Microscopy Liver Medulla Oblongata Mice, House Microscopy Microscopy, Fluorescence Necrosis Non-alcoholic Fatty Liver Disease Paraffin Embedding Pathologists Plasma Membrane Skeletal Myocytes Steatohepatitis Tissues Wheat Germ Agglutinins
To assess our models we used a 10-fold cross validation strategy which randomized training and test set inclusion across the cell line and compound combinations. Thus, for any given viability curve resulting from treatment of a cell line with a compound, all of the results from the assay were considered as one unit for cross validation purposes. All steps of feature selection were also conducted under this cross validation framework as well. For every fold of our data, we recalculated the correlation coefficient between cell viability and the features available to the model (kinase inhibition state, gene expression, etc) using only the data in the training set. The number of features was varied as specified in the results section. We used the entire data set to build the final model used to make the predictions in S1 Table and the results displayed in Fig 6.
We used random forest, XGBoost, TabNet and linear regression for all of our modeling efforts. All of our models are implemented using the tidymodels framework in R. We used the ranger random forest engine [43 ], the default XGBoost engine [44 ] and the default ordinary least squares linear regression engine. For all of our initial testing of these models we used the default single set of hyperparameter settings to narrow our search for an acceptable model. This search indicated that the random forest model performed the best, so we attempted to further tune three additional parameters, the number of trees, the number of selected predictors and the minimal node size across the following ranges:
Publication 2023
Biological Assay Cell Lines Cell Survival Cytoplasmic Inclusion Gene Expression Phosphotransferases Psychological Inhibition Trees
Automated patch clamp recording was performed using the Nanion SyncroPatch 768PE platform (Nanion Technologies, Munich, Germany) (17 (link)). Single-hole low resistance (2–3.5 MΩ) recording chips were used for this study. Pulse generation and data collection were performed using PatchControl384 v1.6.6 and DataControl384 v1.6.0 software (Nanion Technologies). Whole-cell currents were acquired at 10 kHz, series resistance was compensated 80%, and leak currents were subtracted using P/4 subtraction. Whole-cell currents were recorded at room temperature using voltage protocols illustrated in Fig. S1. The external solution contained (in mM): 140 NaCl, 4 KCl, 2 CaCl2, 1 MgCl2, 10 HEPES, 5 glucose, with the final pH adjusted to 7.4 with NaOH, and osmolality adjusted to 300 mOsm/kg with sucrose. The composition of the internal solution was (in mM): 110 CsF, 10 CsCl, 10 NaCl, 20 EGTA, 10 HEPES, with the final pH adjusted to 7.2 with CsOH, and osmolality adjusted to 300 mOsm/kg with sucrose. High resistance seals were obtained by addition of 10 μl seal enhancer solution comprised of (in mM): 125 NaCl, 3.75 KCl, 10.25 CaCl2, 3.25 MgCl2, 10 HEPES, final pH adjusted to 7.4 with NaOH, followed immediately by addition of 30 μl of external solution to each well. Prior to recording, cells were washed twice with external solution, and the final concentrations of CaCl2 and MgCl2 were 3 mM and 1.3 mM, respectively. Stringent criteria were used to select cells for inclusion in the final analysis (seal resistance ≥ 200 MΩ, access resistance ≤ 20 MΩ, capacitance ≥ 2 pF, and sodium reversal potential between 45 and 85 mV. All biophysical data were collected from cells whose currents were larger than −200 pA. Voltage control was assessed from conductance-voltage (GV) curves and cells were included in the final analysis if two adjacent points on the GV curve showed no more than a 7-fold increase. Unless otherwise noted, all chemicals were obtained from SigmaAldrich (St. Louis, MO, USA).
A typical experiment recorded from cells expressing WT-NaV1.2 and either five NaV1.2 variants or four NaV1.2 variants plus non-transfected cells seeded into 64-well clusters of a 384-well patch clamp plate. Cells recorded at the same time were electroporated with either WT or variant plasmids in parallel on the same day. To ensure that sufficient numbers of cells were recorded to account for attrition from stringent quality control data filters, we recorded from two 384-well plates simultaneously. Because both plates were run simultaneously, and the plate layout was identical, we combined data from both plates and normalized the data for each variant to the average WT values recorded on the same day. Biophysical properties were listed as not-determined (ND) if less than 5 replicates were obtained for that property for any given variant.
Publication Preprint 2023
Cells cesium chloride Cytoplasmic Inclusion DNA Chips Egtazic Acid Glucose HEPES Magnesium Chloride Phocidae Plasmids Pulse Rate Sodium Sodium Chloride Sucrose Tooth Attrition
The immunofluorescence procedure was similar to the previously reported immunohistochemistry protocol without the quenching step. Blocking was performed with 5% (vol/vol) NGS and 0.1% (vol/vol) Triton X-100 (Sigma-Aldrich) in PBS solution. Corresponding primary antibodies were incubated together overnight at 4°C in 2% (vol/vol) serum. Details about primary and secondary antibodies used for immunofluorescence can be found in Table 1. Adequate Alexa 488 and/or 647-conjugated secondary antibodies were incubated simultaneously for 1 h at room temperature in 2% (vol/vol) serum. Nuclei were stained with Hoechst 33342 (1:2000, Thermo Fisher Scientific, ref: H3570) in 1× PBS for 10 min. Sections were coverslipped using the Dako Cytomation Fluorescent Mounting Medium (Dako).
Immunofluorescent images were taken with a LSM 980 with Airyscan 2 confocal microscopeand were analysed with ZEN 3.1 software (RRID: SCR_013672; http://www.zeiss.com/microscopy/en_us/products/microscope-software/zen.html#introduction). The total number of p62-positive cytoplasmic inclusions was manually determined in a selected SNpc middle section/animal exhibiting high numbers of nigral neurons, including NM-containing neurons, from two different experimental groups: TYR (n = 8) and TYR+VMAT2 (n = 7), at 2 months post-AAV injections. Equivalent anatomical levels (based on Paxinos and Watson19 ) were analysed across animals. All quantifications were performed by an investigator blinded to the experimental groups.
Publication 2023
Animals Antibodies Cell Nucleus Cytoplasmic Inclusion Fluorescent Antibody Technique HOE 33342 Immunohistochemistry Microscopy Neurons Serum Substantia Nigra Triton X-100
The 65 kDa active Cry4Ba toxins were prepared as described previously [40 (link)]. In brief, 130 kDa Cry4Ba-R203Q and its mutants protoxins were overexpressed as cytoplasmic inclusions in E. coli JM109 upon induction with 0.1 mM IPTG for 4 h. After solubilization in carbonate buffer (50 mM Na2CO3/NaHCO3 (pH 9.2)) for 1 h, the protoxins were activated by digestion with TCPK-treated trypsin (1:20, w/w) for 16 h into 65 kDa active toxins. The 65 kDa trypsin-activated toxins were purified using a size exclusion fast protein liquid chromatography system on a Superdex-200 HR column from Amersham-Pharmacia Biotech (Piscataway, NJ, USA) as described previously [22 (link)] and then concentrated using a Vivaspin concentrator column (10 kDa MWCO). The purified proteins were determined for their concentrations based on Bradford assay and analyzed using sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE).
Publication 2023
Bicarbonate, Sodium Biological Assay Buffers Carbonates Cytoplasmic Inclusion Digestion Escherichia coli Isopropyl Thiogalactoside Molecular Sieve Chromatography Proteins SDS-PAGE Toxins, Biological Trypsin

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More about "Cytoplasmic Inclusion"

Cytoplasmic inclusions, also known as cellular inclusions or intracytoplasmic inclusions, are abnormal structures found within the cytoplasm of cells.
These structures can contain a variety of cellular components, including proteins, lipids, carbohydrates, and other biomolecules.
Understanding the composition and function of cytoplasmic inclusions is an important area of research, as they can provide insight into underlying pathological processes and potential therapeutic targets.
Cytoplasmic inclusions are associated with various disease states and cellular dysfunctions.
For example, the accumulation of misfolded proteins, such as those seen in neurodegenerative disorders, can lead to the formation of cytoplasmic inclusions.
These inclusions may disrupt normal cellular processes and contribute to the pathogenesis of the disease.
In addition to their role in disease, cytoplasmic inclusions can also be indicative of normal cellular processes.
For instance, the formation of lipid droplets, which are specialized organelles involved in lipid storage and metabolism, can be considered a type of cytoplasmic inclusion.
Researchers often utilize a variety of techniques to study cytoplasmic inclusions, including microscopy techniques like the Eclipse 50i fluorescent microscope, as well as molecular biology tools such as the RNA Cleaner & Concentrator-5 columns and the SsoAdvanced SYBR Green Master Mix.
Additionally, stains like Toluidine blue and Oil Red O can be used to visualize and characterize the composition of these inclusions.
The study of cytoplasmic inclusions has implications for various fields, such as cell biology, pathology, and drug development.
By understanding the underlying mechanisms and functions of these structures, researchers may be able to identify new therapeutic targets and develop more effective interventions for a range of diseases and cellular dysfunctions.