Journal: Journal of Epilepsy Research

Article Title: Effect of Valproate on Serum BDNF and MMP-9 in Pediatric Epilepsy

doi: 10.14581/jer.25012

Figure Lengend Snippet: Patient disposition and follow-up of the study. BDNF, brain-derived neurotrophic factor; MMP-9, matrix metalloproteinase-9; VSMS, vineland social maturity scale; DST, developmental screening test.

Article Snippet: Serum BDNF levels were estimated using a commercially available human BDNF ELISA kit (GENLISA TM ; KRISHGEN BioSystems, Cerritos, CA, USA) according to the manufacturer’s protocol.

Techniques: Derivative Assay

Journal: Journal of Epilepsy Research

Article Title: Effect of Valproate on Serum BDNF and MMP-9 in Pediatric Epilepsy

doi: 10.14581/jer.25012

Figure Lengend Snippet: Effect of valproate on serum BDNF levels (mean±standard deviation) following 16 weeks of treatment in responders. BDNF, brain-derived neurotrophic factor. * p <0.001 (between groups at baseline); ** p <0.001 (within valproate group between baseline and week 16).

Article Snippet: Serum BDNF levels were estimated using a commercially available human BDNF ELISA kit (GENLISA TM ; KRISHGEN BioSystems, Cerritos, CA, USA) according to the manufacturer’s protocol.

Techniques: Standard Deviation, Derivative Assay

Journal: Journal of Epilepsy Research

Article Title: Effect of Valproate on Serum BDNF and MMP-9 in Pediatric Epilepsy

doi: 10.14581/jer.25012

Figure Lengend Snippet: (A) Correlation between serum BDNF levels and social quotient (SQ; VSMS) in children with epilepsy (ρ=0.710; p <0.001). (B) Correlation between serum BDNF levels and developmental quotient (DST) in children with epilepsy (ρ=0.507; p <0.001). (C) Correlation between serum MMP-9 levels and SQ (VSMS) in children with epilepsy (ρ=-0.646; p <0.001). (D) Correlation between serum MMP-9 levels and developmental quotient (DST) in children with epilepsy (ρ=-0.585; p <0.001). VSMS, vineland social maturity scale; BDNF, brain-derived neurotrophic factor; DST, developmental screening test; MMP-9, matrix metalloproteinase-9.

Article Snippet: Serum BDNF levels were estimated using a commercially available human BDNF ELISA kit (GENLISA TM ; KRISHGEN BioSystems, Cerritos, CA, USA) according to the manufacturer’s protocol.

Techniques: Derivative Assay

Journal: Experimental and Therapeutic Medicine

Article Title: Panax notoginsenoside Rb1 ameliorates Alzheimer’s disease by upregulating brain-derived neurotrophic factor and downregulating Tau protein expression

doi: 10.3892/etm.2013.1215

Figure Lengend Snippet: qPCR analysis of the relative levels of brain-derived neurotrophic factor (BDNF) and Tau mRNA, modulated by Panax notoginsenoside Rb1 (PNRb1). Values of the blank control group were taken as one unity to calculate the fold increase. mRNA levels were normalized by glyceraldehyde 3-phosphate dehydrogenase mRNA, whose level did not change during culture with PNRb1. Results are the means of at least three experiments. Values are the mean ± SE.

Article Snippet: Subsequently, the blots were blocked with normal goat serum antibody, incubated in rabbit anti-rat phosphorylated Tau protein and BDNF polyclonal antibody (1:1,000 and 1:600, respectively; Boster, Wuhan, China) at 4°C overnight, then washed in phosphate-buffered saline with 0.1% Triton X-100, three times for 15 min each.

Techniques: Derivative Assay, Control

Journal: Experimental and Therapeutic Medicine

Article Title: Panax notoginsenoside Rb1 ameliorates Alzheimer’s disease by upregulating brain-derived neurotrophic factor and downregulating Tau protein expression

doi: 10.3892/etm.2013.1215

Figure Lengend Snippet: Immunoblot analysis of the relative expression levels of brain-derived neurotrophic factor (BDNF) and phosphorylated Tau protein, modulated by Panax notoginsenoside Rb1 (PNRb1). Values of untreated astrocytes (blank control group) were taken as one unity to calculate the fold increase. Protein levels were normalized by β-tubulin, whose level did not change during culture with PNRb1. Results are the means of at least three experiments. Values are the mean ± SE.

Article Snippet: Subsequently, the blots were blocked with normal goat serum antibody, incubated in rabbit anti-rat phosphorylated Tau protein and BDNF polyclonal antibody (1:1,000 and 1:600, respectively; Boster, Wuhan, China) at 4°C overnight, then washed in phosphate-buffered saline with 0.1% Triton X-100, three times for 15 min each.

Techniques: Western Blot, Expressing, Derivative Assay, Control

Journal: Experimental and Therapeutic Medicine

Article Title: Panax notoginsenoside Rb1 ameliorates Alzheimer’s disease by upregulating brain-derived neurotrophic factor and downregulating Tau protein expression

doi: 10.3892/etm.2013.1215

Figure Lengend Snippet: Correlation between the relative expression of (A) brain-derived neurotrophic factor (BDNF) or (B) phosphorylated Tau protein and Panax notoginsenoside (PNRb1) concentration. The AD tissues were treated with 240 μm PNRb1 for 4 h. Statistical analysis was performed using the Spearman’s rank correlation test. Values of rho between 1 and 0.5 indicate a strong positive correlation, while values between −1 and −0.5 imply a strong negative correlation.

Article Snippet: Subsequently, the blots were blocked with normal goat serum antibody, incubated in rabbit anti-rat phosphorylated Tau protein and BDNF polyclonal antibody (1:1,000 and 1:600, respectively; Boster, Wuhan, China) at 4°C overnight, then washed in phosphate-buffered saline with 0.1% Triton X-100, three times for 15 min each.

Techniques: Expressing, Derivative Assay, Concentration Assay

Journal: Molecular Psychiatry

Article Title: Inhibition of colony stimulating factor 1 receptor corrects maternal inflammation-induced microglial and synaptic dysfunction and behavioral abnormalities

doi: 10.1038/s41380-020-0671-2

Figure Lengend Snippet: a Gene ontology (GO) biological processes pathway analysis shows that MIA microglia increase synaptogenic functions while repopulated microglia recover homeostatic functions. Left (red): Top significantly enriched GO biological process terms increased by MIA and decreased by repopulation. Right (purple): Top significantly enriched GO biological process terms decreased by MIA and increased by repopulation. These GO findings were verified using GORILLA. b IPA of genes with differential expression in microglia between MIA versus Saline (RNA-seq data). Pathway analysis reveals MIA-induced upregulation of neuritogenic gene expression, specifically in developmental stages, based on activation z -score. Red denotes pathway activated in E17 MIA microglia. c Genes in “neuritogenesis/formation of cellular protrusions” function. Hierarchal clustering of gene sets based on relative expression values; red: high relative expression, blue: low relative expression. Cluster 1 represents genes increased in adult MIA microglia but reduced in MIA + MG-REP including Ctnnd2, Ncam2, and Ntrk2 . Cluster 2 represents genes increased in immature MIA microglia including Ncam2, Ntn, Ptn and Wnt5a . Cluster3 represents genes decreased in immature MIA microglia including Plau. In situ hybridization (ISH) and immunofluorescence of E17 Saline or MIA offspring in the cortical plate region. d mRNA of cellular protrusion/ neuritogenic genes ( Ctnnd2, Ncam2, Ntn, Ptn, and Wnt5a ) were detected by florescent-labeled antisense cRNA probes (red) but not by scramble cRNA probe (not detected: N.D.), and the sections were immunostained for IBA1 (green) and DAPI (blue). e The number of IBA1 + cells expressing the cellular protrusion/neuritogenic genes were quantified in the cortical plate region. n = (4–5/2) male mice/ litters per molecule for Saline and MIA, n = 3 for scramble control probe. * p < 0.05, ** p < 0.01, ns denotes no significance, by unpaired Student t test. Graphs indicate mean ± s.e.m. ELISA verification of selected RNA-seq molecules: CTNND2 ( f ), NCAM2 ( g ), NTRK2 ( h ), NTN ( i) , PTN ( j ) and WNT5A ( k ) in acutely isolated microglia. MIA increases protein expression of cellular protrusion/neuriotgenic molecules in microglia that were normalized via repopulation. n = (6/4, 6/3, 5/3, 6/3) female mice/litters for P60 Saline + CTRL, MIA + CTRL, Saline + MG-REP and MIA + MG-REP. CTNND2: Prenatal treatment effect, F (1,19) = 157.1, p < 0.0001, Drug effect, F (1,19) = 262.7, p < 0.0001, Interaction effect, F (1,19) = 201, p < 0.0001, NCAM2: Prenatal treatment effect, F (1,19) = 23.76, p = 0.0001, Drug effect, F (1,19) = 26.29, p < 0.0001, Interaction effect, F (1,19) = 17.63, p = 0.0005, NTRK2: Prenatal treatment effect, F (1,18) = 13.99, p = 0.0015, Drug effect, F (1,18) = 12.45, p = 0.0024, Interaction effect, F (1,18) = 0.06203, p = 0.8061, NTN: Prenatal treatment effect, F (1,19) = 0.01669, p = 0.8986, Drug effect, F (1,19) = 0.8, p = 0.3823, Interaction effect, F (1,19) = 6.121, p = 0.0230, PTN: Prenatal treatment effect, F (1,19) = 10.31, p = 0.0046, Drug effect, F (1,19) = 52.02, p < 0.0001, Interaction effect, F (1,19) = 0.002927 p = 0.9574, WNT5A: Prenatal treatment effect, F (1,19) = 5.581, p = 0.0290, Drug effect, F (1,19) = 1.550, p = 0.2282, Interaction effect, F (1,19) = 0.0834 p = 0.7799, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 as determined by 2-way ANOVA (alpha = 0.05) with Tukey’s post-hoc. # p < 0.05 for main effect of MIA. Graphs indicate mean ± s.e.m.

Article Snippet: For the detection of NTRK2 (TrkB), PTN and NTN1, following commercial ELISA kits were used: Mouse TrkB ELISA kit (Boster Biological Technology, EK0849), Mouse PTN ELISA kit (Biomatik Corporation, EKU06717), Mouse NTN1 ELISA kit (LifeSpan Biosciences, LS-F5882).

Techniques: Quantitative Proteomics, Saline, RNA Sequencing, Gene Expression, Activation Assay, Expressing, In Situ Hybridization, Immunofluorescence, Labeling, Control, Enzyme-linked Immunosorbent Assay, Isolation

Journal: Annals of Diagnostic Pathology

Article Title: Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein ☆

doi: 10.1016/j.anndiagpath.2020.151682

Figure Lengend Snippet: Quantification of biomarkers associated with endothelialopathy of the brains in people who died of COVID-19 and in the mice with IV injection of different spike protein subunits.

Article Snippet: The recombinant spike proteins, all from PROSCI, were: Val16-Arg685 (cat #10-300) = full length S1 subunit; Arg319-Phe541 (10-303) = truncated S1 subunit (contains only the receptor binding domain) and full length S2 subunit = (Ser686–Pro1273 (10-426).

Techniques: IV Injection

Journal: Annals of Diagnostic Pathology

Article Title: Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein ☆

doi: 10.1016/j.anndiagpath.2020.151682

Figure Lengend Snippet: Quantification of cell line data after incubation with different subunits of the SARS-CoV2 spike protein.

Article Snippet: The recombinant spike proteins, all from PROSCI, were: Val16-Arg685 (cat #10-300) = full length S1 subunit; Arg319-Phe541 (10-303) = truncated S1 subunit (contains only the receptor binding domain) and full length S2 subunit = (Ser686–Pro1273 (10-426).

Techniques: Incubation

Journal: Annals of Diagnostic Pathology

Article Title: Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein ☆

doi: 10.1016/j.anndiagpath.2020.151682

Figure Lengend Snippet: Cytologic and molecular correlates of the S1 subunit of the spike protein in cell lines. Panel A shows the cytology of untreated HUVEC cells; these endothelial cells strongly express ACE2 (panel B). Treatment with the S1 subunit of spike protein induced cell aggregation and degeneration (panel C). The S1 subunit was not endocytosed by the RAW cells (panel D) and was evident in the HUVEC cells where it co-localized with caspase 3 as seen in panels F-H. Panel F is the isolated spike data (fluorescent green), panel G the isolated caspase 3 data (fluorescent red) and panel H the merged image with fluorescent yellow marking the co-localization of the two protein. The MN cells likewise showed co-localization of the spike protein and caspase 3 (panel E). The magnifications are 600× (panels A-D) and 1000× (panels E -F) with DAB (brown) signal (panel D). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The recombinant spike proteins, all from PROSCI, were: Val16-Arg685 (cat #10-300) = full length S1 subunit; Arg319-Phe541 (10-303) = truncated S1 subunit (contains only the receptor binding domain) and full length S2 subunit = (Ser686–Pro1273 (10-426).

Techniques: Isolation

Journal: Annals of Diagnostic Pathology

Article Title: Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein ☆

doi: 10.1016/j.anndiagpath.2020.151682

Figure Lengend Snippet: Histologic and molecular results in mice after tail vein injection of different spike subunits. Panel A shows the capillaries of normal mouse brain in which no perivascular space is evident (box). The microvessels of the mice brains after spike S1 subunit injection do show edema (panel B, box). The spike S1 subunit was evident in the capillaries of the brain (panel C) and deep fat of the skin (panel F) as was activated caspase 3 (panel D). However, mice injected with the spike S2 subunit showed no endocytosis in the endothelia in the brain nor caspase-3 activation (panel E). The fluorescent yellow in panel F indicates that the S1 spike subunit did co-localize with caspase-3. As in the human COVID-19 brains, the mouse brains showed increase nNOS after spike S1 subunit injection (panel G) but not S2 subunit injection (panel H). Complement cascade activated, documented by C5b-9 expression, was seen in the capillaries of the brain (panel I) and deep fat of the skin (panel J) after S1 injection. Magnifications are at 600× (panels A, B, G, H) or at 1000× (other panels) with DAB (brown) signal. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The recombinant spike proteins, all from PROSCI, were: Val16-Arg685 (cat #10-300) = full length S1 subunit; Arg319-Phe541 (10-303) = truncated S1 subunit (contains only the receptor binding domain) and full length S2 subunit = (Ser686–Pro1273 (10-426).

Techniques: Injection, Activation Assay, Expressing