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strain ss1  (ATCC)


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    Structured Review

    ATCC strain ss1
    Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain <t>SS1</t> following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.
    Strain Ss1, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 269 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/strain ss1/product/ATCC
    Average 95 stars, based on 269 article reviews
    strain ss1 - by Bioz Stars, 2026-03
    95/100 stars

    Images

    1) Product Images from "In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles"

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    Journal: Frontiers in Microbiology

    doi: 10.3389/fmicb.2025.1750216

    Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.
    Figure Legend Snippet: Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.

    Techniques Used: Inhibition

    Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).
    Figure Legend Snippet: Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).

    Techniques Used: Gene Expression, Activity Assay, Control, Expressing

    Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.
    Figure Legend Snippet: Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.

    Techniques Used: In Vitro, Control



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    ATCC clinical strain ss1
    Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain <t>SS1</t> following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.
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    Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain <t>SS1</t> following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.
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    ATCC mouse adapted ss1 strain
    Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain <t>SS1</t> following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.
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    ATCC pylori reference strain ss1
    Immune protection induced by minicell-based H. pylori vaccines. Thirty-two female BALB/c mice (6–8 weeks old) were randomly assigned to four groups (n=8 per group). On Day 0, mice were orally immunized with 100 μL of PBS, or PBS containing 2×10 8 of TA-1m, TA-2m, or Apt-TA-2m, followed by booster doses on Days 14 and 28. Two weeks after the final immunization (Day 42), all groups were orally challenged with 1×10 9 CFU of wild-type H. pylori <t>SS1,</t> administered four times over one week. Mice were sacrificed two weeks after the final challenge (Day 63), at which point the stomachs were collected for bacterial load quantification by plate counting, urease activity assessment via ELISA, and histopathological evaluation. (A) Schematic overview of the immunization and challenge timeline. (B) H. pylori colonization levels in stomach tissues. (C) Urease concentration in the stomach. (D) Histopathological changes in the gastric mucosa. In panel (D) , black arrows indicate epithelial cell necrosis; blue arrows indicate gastric gland necrosis; red arrows show mild inflammatory cell infiltration, and yellow arrows denote areas with more extensive inflammatory infiltration. For all panels involving statistical analysis, significance was determined using One-Way ANOVA and Tukey’s multiple comparison with an adjusted p -value < 0.05. Groups labeled with the same letter (e.g., ‘a’ vs. ‘a’, or ‘a’ vs. ‘ab’) are not significantly different ( p ≥ 0.05), as they share at least one common letter. Conversely, groups labeled with different letters (e.g., ‘a’ vs. ‘b’) are considered significantly different ( p < 0.05).
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    Nikon pylori ss1 strains
    H. pylori <t>SS1</t> luxS mutants do not produce AI-2 and do not have colonization defects in vivo. ( A ) Relative light units (RLUs) indicative of AI-2 amounts in the cell-free culture supernatant of H. pylori SS1 WT or luxS grown in BB10 media overnight. AI-2 RLU was measured by exposing the AI-2 bioluminescent reporter V. harveyi TL26 to H. pylori cell-free media supernatant from WT or luxS mutant or a negative control of media alone. Each point represents technical replicates from a representative biological replicate of three biological replicates, and error bars indicate standard deviation. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. ( B ) Female C57Bl6/N mice were infected with H. pylori SS1 strains for 6 months. The total number of bacteria in the corpus and antrum of the stomach of infected mice was quantified by homogenizing tissue and plating for colony forming units (CFU) and normalized to the weight of the tissue. Each point represents tissue from one mouse, and error bars represent the standard error of the mean. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as ns = not significant.
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    ATCC pylori sydney strain 1 ss1
    H. pylori <t>SS1</t> luxS mutants do not produce AI-2 and do not have colonization defects in vivo. ( A ) Relative light units (RLUs) indicative of AI-2 amounts in the cell-free culture supernatant of H. pylori SS1 WT or luxS grown in BB10 media overnight. AI-2 RLU was measured by exposing the AI-2 bioluminescent reporter V. harveyi TL26 to H. pylori cell-free media supernatant from WT or luxS mutant or a negative control of media alone. Each point represents technical replicates from a representative biological replicate of three biological replicates, and error bars indicate standard deviation. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. ( B ) Female C57Bl6/N mice were infected with H. pylori SS1 strains for 6 months. The total number of bacteria in the corpus and antrum of the stomach of infected mice was quantified by homogenizing tissue and plating for colony forming units (CFU) and normalized to the weight of the tissue. Each point represents tissue from one mouse, and error bars represent the standard error of the mean. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as ns = not significant.
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    ATCC pylori atcc ss1 strain
    H. pylori <t>SS1</t> luxS mutants do not produce AI-2 and do not have colonization defects in vivo. ( A ) Relative light units (RLUs) indicative of AI-2 amounts in the cell-free culture supernatant of H. pylori SS1 WT or luxS grown in BB10 media overnight. AI-2 RLU was measured by exposing the AI-2 bioluminescent reporter V. harveyi TL26 to H. pylori cell-free media supernatant from WT or luxS mutant or a negative control of media alone. Each point represents technical replicates from a representative biological replicate of three biological replicates, and error bars indicate standard deviation. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. ( B ) Female C57Bl6/N mice were infected with H. pylori SS1 strains for 6 months. The total number of bacteria in the corpus and antrum of the stomach of infected mice was quantified by homogenizing tissue and plating for colony forming units (CFU) and normalized to the weight of the tissue. Each point represents tissue from one mouse, and error bars represent the standard error of the mean. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as ns = not significant.
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    Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.

    Journal: Frontiers in Microbiology

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    doi: 10.3389/fmicb.2025.1750216

    Figure Lengend Snippet: Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.

    Article Snippet: The standard strain ATCC 700392 and the clinical strain SS1 were exposed to NBP and NBP-NPs solutions at concentrations of 2 × MIC, 1 × MIC, and 0.5 × MIC under microaerophilic conditions at 37 °C with shaking at 150 rpm for 3 days.

    Techniques: Inhibition

    Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).

    Journal: Frontiers in Microbiology

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    doi: 10.3389/fmicb.2025.1750216

    Figure Lengend Snippet: Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).

    Article Snippet: The standard strain ATCC 700392 and the clinical strain SS1 were exposed to NBP and NBP-NPs solutions at concentrations of 2 × MIC, 1 × MIC, and 0.5 × MIC under microaerophilic conditions at 37 °C with shaking at 150 rpm for 3 days.

    Techniques: Gene Expression, Activity Assay, Control, Expressing

    Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.

    Journal: Frontiers in Microbiology

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    doi: 10.3389/fmicb.2025.1750216

    Figure Lengend Snippet: Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.

    Article Snippet: The standard strain ATCC 700392 and the clinical strain SS1 were exposed to NBP and NBP-NPs solutions at concentrations of 2 × MIC, 1 × MIC, and 0.5 × MIC under microaerophilic conditions at 37 °C with shaking at 150 rpm for 3 days.

    Techniques: In Vitro, Control

    Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.

    Journal: Frontiers in Microbiology

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    doi: 10.3389/fmicb.2025.1750216

    Figure Lengend Snippet: Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.

    Article Snippet: As shown in – , both NBP and NBP-NPs exhibited clear inhibitory effects on the standard strain ATCC 700392 and clinical strain SS1.

    Techniques: Inhibition

    Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).

    Journal: Frontiers in Microbiology

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    doi: 10.3389/fmicb.2025.1750216

    Figure Lengend Snippet: Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).

    Article Snippet: As shown in – , both NBP and NBP-NPs exhibited clear inhibitory effects on the standard strain ATCC 700392 and clinical strain SS1.

    Techniques: Gene Expression, Activity Assay, Control, Expressing

    Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.

    Journal: Frontiers in Microbiology

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    doi: 10.3389/fmicb.2025.1750216

    Figure Lengend Snippet: Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.

    Article Snippet: As shown in – , both NBP and NBP-NPs exhibited clear inhibitory effects on the standard strain ATCC 700392 and clinical strain SS1.

    Techniques: In Vitro, Control

    Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.

    Journal: Frontiers in Microbiology

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    doi: 10.3389/fmicb.2025.1750216

    Figure Lengend Snippet: Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.

    Article Snippet: Urease activity assays showed that NBP dose-dependently reduced urease activity in both ATCC 700392 and SS1 strains.

    Techniques: Inhibition

    Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).

    Journal: Frontiers in Microbiology

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    doi: 10.3389/fmicb.2025.1750216

    Figure Lengend Snippet: Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).

    Article Snippet: Urease activity assays showed that NBP dose-dependently reduced urease activity in both ATCC 700392 and SS1 strains.

    Techniques: Gene Expression, Activity Assay, Control, Expressing

    Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.

    Journal: Frontiers in Microbiology

    Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

    doi: 10.3389/fmicb.2025.1750216

    Figure Lengend Snippet: Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.

    Article Snippet: Urease activity assays showed that NBP dose-dependently reduced urease activity in both ATCC 700392 and SS1 strains.

    Techniques: In Vitro, Control

    Immune protection induced by minicell-based H. pylori vaccines. Thirty-two female BALB/c mice (6–8 weeks old) were randomly assigned to four groups (n=8 per group). On Day 0, mice were orally immunized with 100 μL of PBS, or PBS containing 2×10 8 of TA-1m, TA-2m, or Apt-TA-2m, followed by booster doses on Days 14 and 28. Two weeks after the final immunization (Day 42), all groups were orally challenged with 1×10 9 CFU of wild-type H. pylori SS1, administered four times over one week. Mice were sacrificed two weeks after the final challenge (Day 63), at which point the stomachs were collected for bacterial load quantification by plate counting, urease activity assessment via ELISA, and histopathological evaluation. (A) Schematic overview of the immunization and challenge timeline. (B) H. pylori colonization levels in stomach tissues. (C) Urease concentration in the stomach. (D) Histopathological changes in the gastric mucosa. In panel (D) , black arrows indicate epithelial cell necrosis; blue arrows indicate gastric gland necrosis; red arrows show mild inflammatory cell infiltration, and yellow arrows denote areas with more extensive inflammatory infiltration. For all panels involving statistical analysis, significance was determined using One-Way ANOVA and Tukey’s multiple comparison with an adjusted p -value < 0.05. Groups labeled with the same letter (e.g., ‘a’ vs. ‘a’, or ‘a’ vs. ‘ab’) are not significantly different ( p ≥ 0.05), as they share at least one common letter. Conversely, groups labeled with different letters (e.g., ‘a’ vs. ‘b’) are considered significantly different ( p < 0.05).

    Journal: Frontiers in Immunology

    Article Title: Construction and evaluation of a Salmonella minicell-based dendritic cell-targeted multi-epitope vaccine against Helicobacter pylori

    doi: 10.3389/fimmu.2025.1595096

    Figure Lengend Snippet: Immune protection induced by minicell-based H. pylori vaccines. Thirty-two female BALB/c mice (6–8 weeks old) were randomly assigned to four groups (n=8 per group). On Day 0, mice were orally immunized with 100 μL of PBS, or PBS containing 2×10 8 of TA-1m, TA-2m, or Apt-TA-2m, followed by booster doses on Days 14 and 28. Two weeks after the final immunization (Day 42), all groups were orally challenged with 1×10 9 CFU of wild-type H. pylori SS1, administered four times over one week. Mice were sacrificed two weeks after the final challenge (Day 63), at which point the stomachs were collected for bacterial load quantification by plate counting, urease activity assessment via ELISA, and histopathological evaluation. (A) Schematic overview of the immunization and challenge timeline. (B) H. pylori colonization levels in stomach tissues. (C) Urease concentration in the stomach. (D) Histopathological changes in the gastric mucosa. In panel (D) , black arrows indicate epithelial cell necrosis; blue arrows indicate gastric gland necrosis; red arrows show mild inflammatory cell infiltration, and yellow arrows denote areas with more extensive inflammatory infiltration. For all panels involving statistical analysis, significance was determined using One-Way ANOVA and Tukey’s multiple comparison with an adjusted p -value < 0.05. Groups labeled with the same letter (e.g., ‘a’ vs. ‘a’, or ‘a’ vs. ‘ab’) are not significantly different ( p ≥ 0.05), as they share at least one common letter. Conversely, groups labeled with different letters (e.g., ‘a’ vs. ‘b’) are considered significantly different ( p < 0.05).

    Article Snippet: The H. pylori reference strain SS1 was purchased from American Type Culture Collection (ATCC).

    Techniques: Vaccines, Activity Assay, Enzyme-linked Immunosorbent Assay, Concentration Assay, Comparison, Labeling

    H. pylori SS1 luxS mutants do not produce AI-2 and do not have colonization defects in vivo. ( A ) Relative light units (RLUs) indicative of AI-2 amounts in the cell-free culture supernatant of H. pylori SS1 WT or luxS grown in BB10 media overnight. AI-2 RLU was measured by exposing the AI-2 bioluminescent reporter V. harveyi TL26 to H. pylori cell-free media supernatant from WT or luxS mutant or a negative control of media alone. Each point represents technical replicates from a representative biological replicate of three biological replicates, and error bars indicate standard deviation. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. ( B ) Female C57Bl6/N mice were infected with H. pylori SS1 strains for 6 months. The total number of bacteria in the corpus and antrum of the stomach of infected mice was quantified by homogenizing tissue and plating for colony forming units (CFU) and normalized to the weight of the tissue. Each point represents tissue from one mouse, and error bars represent the standard error of the mean. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as ns = not significant.

    Journal: Microbiology Spectrum

    Article Title: Helicobacter pylori luxS mutants cause hyperinflammatory responses during chronic infection

    doi: 10.1128/spectrum.01073-24

    Figure Lengend Snippet: H. pylori SS1 luxS mutants do not produce AI-2 and do not have colonization defects in vivo. ( A ) Relative light units (RLUs) indicative of AI-2 amounts in the cell-free culture supernatant of H. pylori SS1 WT or luxS grown in BB10 media overnight. AI-2 RLU was measured by exposing the AI-2 bioluminescent reporter V. harveyi TL26 to H. pylori cell-free media supernatant from WT or luxS mutant or a negative control of media alone. Each point represents technical replicates from a representative biological replicate of three biological replicates, and error bars indicate standard deviation. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. ( B ) Female C57Bl6/N mice were infected with H. pylori SS1 strains for 6 months. The total number of bacteria in the corpus and antrum of the stomach of infected mice was quantified by homogenizing tissue and plating for colony forming units (CFU) and normalized to the weight of the tissue. Each point represents tissue from one mouse, and error bars represent the standard error of the mean. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as ns = not significant.

    Article Snippet: H. pylori SS1 strains were prepared by growing to between mid-exponential phase (OD 600 = ~0.3) to late exponential phase (OD600 = ~0.75) in BB10 overnight and were checked for GFP fluorescence and motility using a Nikon Eclipse E600 phase-contrast microscope at 400× magnification with a LED illuminator (pE-300white, CoolLED) with a fluorescent filter for GFP.

    Techniques: In Vivo, Mutagenesis, Negative Control, Standard Deviation, Comparison, Infection, Bacteria

    H. pylori luxS mutants recruit more T cells to the stomach of infected mice compared with WT H. pylori female C57/BL6N mice were infected with SS1 WT or SS1 luxS, and lymphocytes from the corpus lamina propria were isolated at 6 months post-infection (n = 5–10). Mice same as shown in . Analysis includes uninfected mice. ( A ) αβ T cells, ( B ) CD4 + T cells, and ( C ) CD8α + T cells were analyzed by flow cytometry using the gating strategy shown in . Error bars represent the standard error of the mean. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: Microbiology Spectrum

    Article Title: Helicobacter pylori luxS mutants cause hyperinflammatory responses during chronic infection

    doi: 10.1128/spectrum.01073-24

    Figure Lengend Snippet: H. pylori luxS mutants recruit more T cells to the stomach of infected mice compared with WT H. pylori female C57/BL6N mice were infected with SS1 WT or SS1 luxS, and lymphocytes from the corpus lamina propria were isolated at 6 months post-infection (n = 5–10). Mice same as shown in . Analysis includes uninfected mice. ( A ) αβ T cells, ( B ) CD4 + T cells, and ( C ) CD8α + T cells were analyzed by flow cytometry using the gating strategy shown in . Error bars represent the standard error of the mean. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: H. pylori SS1 strains were prepared by growing to between mid-exponential phase (OD 600 = ~0.3) to late exponential phase (OD600 = ~0.75) in BB10 overnight and were checked for GFP fluorescence and motility using a Nikon Eclipse E600 phase-contrast microscope at 400× magnification with a LED illuminator (pE-300white, CoolLED) with a fluorescent filter for GFP.

    Techniques: Infection, Isolation, Flow Cytometry, Comparison

    H. pylori luxS mutants recruit more effector and regulatory T cells to the stomach compared with WT H. pylori female C57/BL6N mice infected with H. pylori SS1 WT or SS1 luxS and lymphocytes from the corpus lamina propria were isolated at 6 months post-infection (n = 5–10). Analysis includes uninfected mice. ( A ) CD4 + IFNγ, ( B ) CD4 + IL17α, and ( C ) CD4 + IL10 were analyzed by flow cytometry as shown in . Mice same as shown in . Error bars represent the standard error of the mean. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: Microbiology Spectrum

    Article Title: Helicobacter pylori luxS mutants cause hyperinflammatory responses during chronic infection

    doi: 10.1128/spectrum.01073-24

    Figure Lengend Snippet: H. pylori luxS mutants recruit more effector and regulatory T cells to the stomach compared with WT H. pylori female C57/BL6N mice infected with H. pylori SS1 WT or SS1 luxS and lymphocytes from the corpus lamina propria were isolated at 6 months post-infection (n = 5–10). Analysis includes uninfected mice. ( A ) CD4 + IFNγ, ( B ) CD4 + IL17α, and ( C ) CD4 + IL10 were analyzed by flow cytometry as shown in . Mice same as shown in . Error bars represent the standard error of the mean. Statistical analyses were performed using one-way ANOVA with Tukey’s multiple comparison test, indicated as *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: H. pylori SS1 strains were prepared by growing to between mid-exponential phase (OD 600 = ~0.3) to late exponential phase (OD600 = ~0.75) in BB10 overnight and were checked for GFP fluorescence and motility using a Nikon Eclipse E600 phase-contrast microscope at 400× magnification with a LED illuminator (pE-300white, CoolLED) with a fluorescent filter for GFP.

    Techniques: Infection, Isolation, Flow Cytometry, Comparison

    Bacterial strains

    Journal: Microbiology Spectrum

    Article Title: Helicobacter pylori luxS mutants cause hyperinflammatory responses during chronic infection

    doi: 10.1128/spectrum.01073-24

    Figure Lengend Snippet: Bacterial strains

    Article Snippet: H. pylori SS1 strains were prepared by growing to between mid-exponential phase (OD 600 = ~0.3) to late exponential phase (OD600 = ~0.75) in BB10 overnight and were checked for GFP fluorescence and motility using a Nikon Eclipse E600 phase-contrast microscope at 400× magnification with a LED illuminator (pE-300white, CoolLED) with a fluorescent filter for GFP.

    Techniques: Plasmid Preparation