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( A ) Succinct overview of PRV quiescent infection in N2a cells. ( B ) Fluorescence microscopy images depicting N2a cells infected with different doses of HuBXY/2018-mCherry with or without <t>ACV</t> <t>and</t> <t>IFN-α</t> treatments. The images were acquired on 8 dpi. ( C ) Fluorescence intensity of N2a cells infected with different doses of HuBXY/2018-mCherry with or without ACV and IFN-α treatments. ( D ) LAT transcript levels in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 and 0.005 MOI. ( E ) Relative mRNA transcription levels of the early genes IE180 and the LAT in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 MOI (694× indicates that LAT transcription levels are approximately 694-fold higher than those of IE180 transcription). These levels were normalized to the internal reference gene 28 S RNA and calculated using the 2 -ΔΔCt method (Livak method). ( F to I ) Fluorescence microscopy images obtained from HuBXY/2018-mCherry quiescent cells infected with G. parasuis –CF7066, G. parasuis –Nagasaki, and G. parasuis –SH0165 (F); S. suis –SC19, S. suis –P1/7, and S. suis –43 (G); ETEC- C83549 , ETEC-E66, and ETEC-10667 (H); and ExPEC-RS218, ExPEC-PCN033, and medium control (I). Scale bars, 100 μm. All data were analyzed using t test; *** P < 0.001 indicates significant differences.
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( A ) Succinct overview of PRV quiescent infection in N2a cells. ( B ) Fluorescence microscopy images depicting N2a cells infected with different doses of HuBXY/2018-mCherry with or without <t>ACV</t> <t>and</t> <t>IFN-α</t> treatments. The images were acquired on 8 dpi. ( C ) Fluorescence intensity of N2a cells infected with different doses of HuBXY/2018-mCherry with or without ACV and IFN-α treatments. ( D ) LAT transcript levels in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 and 0.005 MOI. ( E ) Relative mRNA transcription levels of the early genes IE180 and the LAT in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 MOI (694× indicates that LAT transcription levels are approximately 694-fold higher than those of IE180 transcription). These levels were normalized to the internal reference gene 28 S RNA and calculated using the 2 -ΔΔCt method (Livak method). ( F to I ) Fluorescence microscopy images obtained from HuBXY/2018-mCherry quiescent cells infected with G. parasuis –CF7066, G. parasuis –Nagasaki, and G. parasuis –SH0165 (F); S. suis –SC19, S. suis –P1/7, and S. suis –43 (G); ETEC- C83549 , ETEC-E66, and ETEC-10667 (H); and ExPEC-RS218, ExPEC-PCN033, and medium control (I). Scale bars, 100 μm. All data were analyzed using t test; *** P < 0.001 indicates significant differences.
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( A ) Succinct overview of PRV quiescent infection in N2a cells. ( B ) Fluorescence microscopy images depicting N2a cells infected with different doses of HuBXY/2018-mCherry with or without <t>ACV</t> <t>and</t> <t>IFN-α</t> treatments. The images were acquired on 8 dpi. ( C ) Fluorescence intensity of N2a cells infected with different doses of HuBXY/2018-mCherry with or without ACV and IFN-α treatments. ( D ) LAT transcript levels in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 and 0.005 MOI. ( E ) Relative mRNA transcription levels of the early genes IE180 and the LAT in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 MOI (694× indicates that LAT transcription levels are approximately 694-fold higher than those of IE180 transcription). These levels were normalized to the internal reference gene 28 S RNA and calculated using the 2 -ΔΔCt method (Livak method). ( F to I ) Fluorescence microscopy images obtained from HuBXY/2018-mCherry quiescent cells infected with G. parasuis –CF7066, G. parasuis –Nagasaki, and G. parasuis –SH0165 (F); S. suis –SC19, S. suis –P1/7, and S. suis –43 (G); ETEC- C83549 , ETEC-E66, and ETEC-10667 (H); and ExPEC-RS218, ExPEC-PCN033, and medium control (I). Scale bars, 100 μm. All data were analyzed using t test; *** P < 0.001 indicates significant differences.
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Dose-dependent effects of capecitabine, acyclovir and lamivudine on cell viability analyzed via non-linear regression. Cell viability (%) following treatment with (A) capecitabine, (B) acyclovir and (C) lamivudine. (D) Non-linear regression curves were used to determine the association between cell activity (%) and capecitabine, <t>aciclovir</t> and lamivudine concentration [Log (µM)].
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Multivariate statistical analyses and volcano plot of differential <t>metabolites</t> in HFS-positive vs. HFS-negative groups. (A) PCA score plot for HFS-positive and HFS-negative groups. (B) PLS-DA score plot between the two groups. (C) OPLS-DA score plot comparing the two groups. (D) A volcano plot was used to compare the upregulated and downregulated metabolites between HFS-positive and HFS-negative groups. PCA, principal component analysis; HFS, hand-foot syndrome; PLS-DA, least partial squares discriminant analysis; OPLS-DA, orthogonal least partial squares discriminant analysis; VIP, variable importance in the projection.
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Multivariate statistical analyses and volcano plot of differential <t>metabolites</t> in HFS-positive vs. HFS-negative groups. (A) PCA score plot for HFS-positive and HFS-negative groups. (B) PLS-DA score plot between the two groups. (C) OPLS-DA score plot comparing the two groups. (D) A volcano plot was used to compare the upregulated and downregulated metabolites between HFS-positive and HFS-negative groups. PCA, principal component analysis; HFS, hand-foot syndrome; PLS-DA, least partial squares discriminant analysis; OPLS-DA, orthogonal least partial squares discriminant analysis; VIP, variable importance in the projection.
Virmen Software Matlab 2015b, supplied by MathWorks Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Multivariate statistical analyses and volcano plot of differential <t>metabolites</t> in HFS-positive vs. HFS-negative groups. (A) PCA score plot for HFS-positive and HFS-negative groups. (B) PLS-DA score plot between the two groups. (C) OPLS-DA score plot comparing the two groups. (D) A volcano plot was used to compare the upregulated and downregulated metabolites between HFS-positive and HFS-negative groups. PCA, principal component analysis; HFS, hand-foot syndrome; PLS-DA, least partial squares discriminant analysis; OPLS-DA, orthogonal least partial squares discriminant analysis; VIP, variable importance in the projection.
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( A ) Succinct overview of PRV quiescent infection in N2a cells. ( B ) Fluorescence microscopy images depicting N2a cells infected with different doses of HuBXY/2018-mCherry with or without ACV and IFN-α treatments. The images were acquired on 8 dpi. ( C ) Fluorescence intensity of N2a cells infected with different doses of HuBXY/2018-mCherry with or without ACV and IFN-α treatments. ( D ) LAT transcript levels in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 and 0.005 MOI. ( E ) Relative mRNA transcription levels of the early genes IE180 and the LAT in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 MOI (694× indicates that LAT transcription levels are approximately 694-fold higher than those of IE180 transcription). These levels were normalized to the internal reference gene 28 S RNA and calculated using the 2 -ΔΔCt method (Livak method). ( F to I ) Fluorescence microscopy images obtained from HuBXY/2018-mCherry quiescent cells infected with G. parasuis –CF7066, G. parasuis –Nagasaki, and G. parasuis –SH0165 (F); S. suis –SC19, S. suis –P1/7, and S. suis –43 (G); ETEC- C83549 , ETEC-E66, and ETEC-10667 (H); and ExPEC-RS218, ExPEC-PCN033, and medium control (I). Scale bars, 100 μm. All data were analyzed using t test; *** P < 0.001 indicates significant differences.

Journal: Science Advances

Article Title: Transition of pseudorabies virus from latency to reactivation state selectively triggered by pathogenic bacteria

doi: 10.1126/sciadv.adw4206

Figure Lengend Snippet: ( A ) Succinct overview of PRV quiescent infection in N2a cells. ( B ) Fluorescence microscopy images depicting N2a cells infected with different doses of HuBXY/2018-mCherry with or without ACV and IFN-α treatments. The images were acquired on 8 dpi. ( C ) Fluorescence intensity of N2a cells infected with different doses of HuBXY/2018-mCherry with or without ACV and IFN-α treatments. ( D ) LAT transcript levels in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 and 0.005 MOI. ( E ) Relative mRNA transcription levels of the early genes IE180 and the LAT in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 MOI (694× indicates that LAT transcription levels are approximately 694-fold higher than those of IE180 transcription). These levels were normalized to the internal reference gene 28 S RNA and calculated using the 2 -ΔΔCt method (Livak method). ( F to I ) Fluorescence microscopy images obtained from HuBXY/2018-mCherry quiescent cells infected with G. parasuis –CF7066, G. parasuis –Nagasaki, and G. parasuis –SH0165 (F); S. suis –SC19, S. suis –P1/7, and S. suis –43 (G); ETEC- C83549 , ETEC-E66, and ETEC-10667 (H); and ExPEC-RS218, ExPEC-PCN033, and medium control (I). Scale bars, 100 μm. All data were analyzed using t test; *** P < 0.001 indicates significant differences.

Article Snippet: Subsequently, the infective medium was removed, and the infected cells were cultured in a medium containing ACV (MedChemExpress, NJ, USA) and IFN-α2a human recombinant (IFN-α, PROSPEC, Rehovot, Israel) for 8 days.

Techniques: Infection, Fluorescence, Microscopy, Control

( A ) Differentially expressed genes in N2a cells upon ExPEC-induced reactivation of quiescent HuBXY/2018-mCherry. ( B ) Read counts and qPCR validation of CXCL1 transcriptional alteration. ( C ) mRNA transcriptional changes of CXCL1 in N2a cells during ExPEC-induced HuBXY/2018-mCherry reactivation. Data were analyzed using the 2 −ΔΔ C t method. ( D ) CXCL1 transcript levels in each group at 6 and 96 hpi. Data were analyzed using the 2 −ΔΔ C t method. ( E ) Differential transcription of IE180 and LAT in N2a-WT and CXCL1 -KO cells during establishment of HuBXY/2018-mCherry quiescence. ( F ) Fluorescence microscopy and bright-field imaging confirmed ExPEC-induced reactivation of quiescent HuBXY/2018-mCherry in N2a-WT cells, but no reactivation was observed in CXCL1 -KO cells. mCherry fluorescence indicates reactivated HuBXY/2018-mCherry within cells. Scale bar, 100 μm. ( G ) Quantification of HuBXY/2018-mCherry reactivation in N2a-WT and CXCL1 -KO cells by gE copy number ( n = 6). ( H ) Proliferation of HuBXY/2018-mCherry during quiescent infection (ACV + IFN-α) in N2a-WT and CXCL1 -KO cells, assessed by qPCR of gE genome copies. Infected cells were sampled from 0 to 11 dpi. Analyses were performed using t-test (** P < 0.01; *** P < 0.001; ns, P > 0.05). ( I ) Proliferation of HuBXY/2018-mCherry during natural infection in N2a-WT and CXCL1 -KO cells. Samples were collected from 0 to 11 dpi. Analyses were performed using t test (*** P < 0.001; ns, P > 0.05). ( J ) Effect of pEGFP-CXCL1 and pEGFP-vector on HuBXY/2018-mCherry reactivation in CXCL1 -KO cells. Scale bar, 100 μm. ( K ) Quantification of HuBXY/2018-mCherry gE copies in CXCL1 -KO cells transfected with pEGFP-CXCL1 or pEGFP-vector. Analyses were performed using t test (*** P < 0.001; ns, P > 0.05).

Journal: Science Advances

Article Title: Transition of pseudorabies virus from latency to reactivation state selectively triggered by pathogenic bacteria

doi: 10.1126/sciadv.adw4206

Figure Lengend Snippet: ( A ) Differentially expressed genes in N2a cells upon ExPEC-induced reactivation of quiescent HuBXY/2018-mCherry. ( B ) Read counts and qPCR validation of CXCL1 transcriptional alteration. ( C ) mRNA transcriptional changes of CXCL1 in N2a cells during ExPEC-induced HuBXY/2018-mCherry reactivation. Data were analyzed using the 2 −ΔΔ C t method. ( D ) CXCL1 transcript levels in each group at 6 and 96 hpi. Data were analyzed using the 2 −ΔΔ C t method. ( E ) Differential transcription of IE180 and LAT in N2a-WT and CXCL1 -KO cells during establishment of HuBXY/2018-mCherry quiescence. ( F ) Fluorescence microscopy and bright-field imaging confirmed ExPEC-induced reactivation of quiescent HuBXY/2018-mCherry in N2a-WT cells, but no reactivation was observed in CXCL1 -KO cells. mCherry fluorescence indicates reactivated HuBXY/2018-mCherry within cells. Scale bar, 100 μm. ( G ) Quantification of HuBXY/2018-mCherry reactivation in N2a-WT and CXCL1 -KO cells by gE copy number ( n = 6). ( H ) Proliferation of HuBXY/2018-mCherry during quiescent infection (ACV + IFN-α) in N2a-WT and CXCL1 -KO cells, assessed by qPCR of gE genome copies. Infected cells were sampled from 0 to 11 dpi. Analyses were performed using t-test (** P < 0.01; *** P < 0.001; ns, P > 0.05). ( I ) Proliferation of HuBXY/2018-mCherry during natural infection in N2a-WT and CXCL1 -KO cells. Samples were collected from 0 to 11 dpi. Analyses were performed using t test (*** P < 0.001; ns, P > 0.05). ( J ) Effect of pEGFP-CXCL1 and pEGFP-vector on HuBXY/2018-mCherry reactivation in CXCL1 -KO cells. Scale bar, 100 μm. ( K ) Quantification of HuBXY/2018-mCherry gE copies in CXCL1 -KO cells transfected with pEGFP-CXCL1 or pEGFP-vector. Analyses were performed using t test (*** P < 0.001; ns, P > 0.05).

Article Snippet: Subsequently, the infective medium was removed, and the infected cells were cultured in a medium containing ACV (MedChemExpress, NJ, USA) and IFN-α2a human recombinant (IFN-α, PROSPEC, Rehovot, Israel) for 8 days.

Techniques: Biomarker Discovery, Fluorescence, Microscopy, Imaging, Infection, Plasmid Preparation, Transfection

Dose-dependent effects of capecitabine, acyclovir and lamivudine on cell viability analyzed via non-linear regression. Cell viability (%) following treatment with (A) capecitabine, (B) acyclovir and (C) lamivudine. (D) Non-linear regression curves were used to determine the association between cell activity (%) and capecitabine, aciclovir and lamivudine concentration [Log (µM)].

Journal: Molecular Medicine Reports

Article Title: Identification of metabolites associated with capecitabine-induced hand-foot syndrome using untargeted metabolomics in patients with cancer

doi: 10.3892/mmr.2025.13568

Figure Lengend Snippet: Dose-dependent effects of capecitabine, acyclovir and lamivudine on cell viability analyzed via non-linear regression. Cell viability (%) following treatment with (A) capecitabine, (B) acyclovir and (C) lamivudine. (D) Non-linear regression curves were used to determine the association between cell activity (%) and capecitabine, aciclovir and lamivudine concentration [Log (µM)].

Article Snippet: Metabolites included aciclovir (cat. no. HY-17422; MedChemExpress), genistein (cat. no. HY-14596; MedChemExpress), Lamivudine (cat. no. HY-B0250; MedChemExpress) and Lomerizine (cat. no. HY-B0768A; MedChemExpress).

Techniques: Activity Assay, Concentration Assay

Multivariate statistical analyses and volcano plot of differential metabolites in HFS-positive vs. HFS-negative groups. (A) PCA score plot for HFS-positive and HFS-negative groups. (B) PLS-DA score plot between the two groups. (C) OPLS-DA score plot comparing the two groups. (D) A volcano plot was used to compare the upregulated and downregulated metabolites between HFS-positive and HFS-negative groups. PCA, principal component analysis; HFS, hand-foot syndrome; PLS-DA, least partial squares discriminant analysis; OPLS-DA, orthogonal least partial squares discriminant analysis; VIP, variable importance in the projection.

Journal: Molecular Medicine Reports

Article Title: Identification of metabolites associated with capecitabine-induced hand-foot syndrome using untargeted metabolomics in patients with cancer

doi: 10.3892/mmr.2025.13568

Figure Lengend Snippet: Multivariate statistical analyses and volcano plot of differential metabolites in HFS-positive vs. HFS-negative groups. (A) PCA score plot for HFS-positive and HFS-negative groups. (B) PLS-DA score plot between the two groups. (C) OPLS-DA score plot comparing the two groups. (D) A volcano plot was used to compare the upregulated and downregulated metabolites between HFS-positive and HFS-negative groups. PCA, principal component analysis; HFS, hand-foot syndrome; PLS-DA, least partial squares discriminant analysis; OPLS-DA, orthogonal least partial squares discriminant analysis; VIP, variable importance in the projection.

Article Snippet: Metabolites included aciclovir (cat. no. HY-17422; MedChemExpress), genistein (cat. no. HY-14596; MedChemExpress), Lamivudine (cat. no. HY-B0250; MedChemExpress) and Lomerizine (cat. no. HY-B0768A; MedChemExpress).

Techniques:

Comprehensive metabolomic profiling and pathway enrichment of differential metabolites in HFS-positive vs. HFS-negative groups. (A) Heatmap of significantly altered metabolites between the two groups. Red and green represent HFS-positive and HFS-negative groups, respectively. (B) VIP analysis of differential metabolites between the two groups. (C) Differential metabolite correlation analysis. Names of metabolites are in the right and bottom of the figure and metabolite clustering dendrograms are in the left and top of the figure. (D) KEGG indicated the biological functions of metabolites. (E) KEGG metabolic pathways were used to classify differential metabolites into five categories; namely, environmental information processing, genetic information processing, human diseases, metabolism and organismal systems. (F) Enriched KEGG pathways of 193 differential metabolites between the HFS-positive and HFS-negative groups. (G) DA score is indicative of changes in differential metabolites in the metabolite pathway. (H) HMDB compound classification of the differential metabolites. HFS, hand-foot syndrome; VIP, variable importance in the projection; KEGG, Kyoto Encyclopedia of Genes and Genomes; DA, differential abundance; HMDB, Human Metabolome Database.

Journal: Molecular Medicine Reports

Article Title: Identification of metabolites associated with capecitabine-induced hand-foot syndrome using untargeted metabolomics in patients with cancer

doi: 10.3892/mmr.2025.13568

Figure Lengend Snippet: Comprehensive metabolomic profiling and pathway enrichment of differential metabolites in HFS-positive vs. HFS-negative groups. (A) Heatmap of significantly altered metabolites between the two groups. Red and green represent HFS-positive and HFS-negative groups, respectively. (B) VIP analysis of differential metabolites between the two groups. (C) Differential metabolite correlation analysis. Names of metabolites are in the right and bottom of the figure and metabolite clustering dendrograms are in the left and top of the figure. (D) KEGG indicated the biological functions of metabolites. (E) KEGG metabolic pathways were used to classify differential metabolites into five categories; namely, environmental information processing, genetic information processing, human diseases, metabolism and organismal systems. (F) Enriched KEGG pathways of 193 differential metabolites between the HFS-positive and HFS-negative groups. (G) DA score is indicative of changes in differential metabolites in the metabolite pathway. (H) HMDB compound classification of the differential metabolites. HFS, hand-foot syndrome; VIP, variable importance in the projection; KEGG, Kyoto Encyclopedia of Genes and Genomes; DA, differential abundance; HMDB, Human Metabolome Database.

Article Snippet: Metabolites included aciclovir (cat. no. HY-17422; MedChemExpress), genistein (cat. no. HY-14596; MedChemExpress), Lamivudine (cat. no. HY-B0250; MedChemExpress) and Lomerizine (cat. no. HY-B0768A; MedChemExpress).

Techniques: