Society: DDW

LIVE STREAM SESSION

Fig 1. Liver DE-miRs and DEGs identification in Mdr2^-/- mice compared to corresponding WT controls, target prediction and analysis of these DE-miRs and DEGs, and the overlapping miRNAs in cholestatic liver injury.
(A) Liver DE-miRs expression profiles between male Mdr2^-/- and WT controls. (B) Liver DE-miRs expression profiles between female Mdr2^-/- and WT controls. (C) Liver DEGs expression profiles between Mdr2^-/- and WT controls. (D) The top 50 hug genes of the PPI network of upregulated DEGs and the top 50 hug genes of the PPI network of downregulated DEGs. (E) Predicted network of miRNAs – 100 identified hug genes of DEGs between Mdr2^-/- and WT controls. (F) Identification of 11 overlapping upregulated miRNAs in cholestatic liver injury. FC, fold change; miR, micro RNA. DE, differentially expressed, Mdr2^-/- , multidrug resistance 2 gene knockout; WT, wild type.

Fig 2. Exosome DE-miRs identification in Mdr2^-/- mice compared to corresponding WT controls, the overlapping DE-miRs in the liver and serum exosomes, and comparison of the expression levels of these DE-miRs and target genes between normal and CHOL samples in TCGA CCA database.
(A) Exosome DE-miRs expression profiles between female Mdr2^-/- and WT controls. (B) Identification of 2 overlapping upregulated DE-miRs in the serum exosomes which may contribute to cholestatic liver injury. (C) The expression levels of these 2 overlapping upregulated DE-miRs between normal and CHOL samples. (D) Heat map, the expression levels of these target hug genes of 2 overlapping upregulated DE-miRs between normal and CHOL samples.

Fig 1. Liver DE-miRs and DEGs identification in Mdr2^-/- mice compared to corresponding WT controls, target prediction and analysis of these DE-miRs and DEGs, and the overlapping miRNAs in cholestatic liver injury.
(A) Liver DE-miRs expression profiles between male Mdr2^-/- and WT controls. (B) Liver DE-miRs expression profiles between female Mdr2^-/- and WT controls. (C) Liver DEGs expression profiles between Mdr2^-/- and WT controls. (D) The top 50 hug genes of the PPI network of upregulated DEGs and the top 50 hug genes of the PPI network of downregulated DEGs. (E) Predicted network of miRNAs – 100 identified hug genes of DEGs between Mdr2^-/- and WT controls. (F) Identification of 11 overlapping upregulated miRNAs in cholestatic liver injury. FC, fold change; miR, micro RNA. DE, differentially expressed, Mdr2^-/- , multidrug resistance 2 gene knockout; WT, wild type.

Fig 2. Exosome DE-miRs identification in Mdr2^-/- mice compared to corresponding WT controls, the overlapping DE-miRs in the liver and serum exosomes, and comparison of the expression levels of these DE-miRs and target genes between normal and CHOL samples in TCGA CCA database.
(A) Exosome DE-miRs expression profiles between female Mdr2^-/- and WT controls. (B) Identification of 2 overlapping upregulated DE-miRs in the serum exosomes which may contribute to cholestatic liver injury. (C) The expression levels of these 2 overlapping upregulated DE-miRs between normal and CHOL samples. (D) Heat map, the expression levels of these target hug genes of 2 overlapping upregulated DE-miRs between normal and CHOL samples.

Fig 1. Liver DE-miRs and DEGs identification in Mdr2^-/- mice compared to corresponding WT controls, target prediction and analysis of these DE-miRs and DEGs, and the overlapping miRNAs in cholestatic liver injury.
(A) Liver DE-miRs expression profiles between male Mdr2^-/- and WT controls. (B) Liver DE-miRs expression profiles between female Mdr2^-/- and WT controls. (C) Liver DEGs expression profiles between Mdr2^-/- and WT controls. (D) The top 50 hug genes of the PPI network of upregulated DEGs and the top 50 hug genes of the PPI network of downregulated DEGs. (E) Predicted network of miRNAs – 100 identified hug genes of DEGs between Mdr2^-/- and WT controls. (F) Identification of 11 overlapping upregulated miRNAs in cholestatic liver injury. FC, fold change; miR, micro RNA. DE, differentially expressed, Mdr2^-/- , multidrug resistance 2 gene knockout; WT, wild type.

Fig 2. Exosome DE-miRs identification in Mdr2^-/- mice compared to corresponding WT controls, the overlapping DE-miRs in the liver and serum exosomes, and comparison of the expression levels of these DE-miRs and target genes between normal and CHOL samples in TCGA CCA database.
(A) Exosome DE-miRs expression profiles between female Mdr2^-/- and WT controls. (B) Identification of 2 overlapping upregulated DE-miRs in the serum exosomes which may contribute to cholestatic liver injury. (C) The expression levels of these 2 overlapping upregulated DE-miRs between normal and CHOL samples. (D) Heat map, the expression levels of these target hug genes of 2 overlapping upregulated DE-miRs between normal and CHOL samples.

Fig 1. Liver DE-miRs and DEGs identification in Mdr2^-/- mice compared to corresponding WT controls, target prediction and analysis of these DE-miRs and DEGs, and the overlapping miRNAs in cholestatic liver injury.
(A) Liver DE-miRs expression profiles between male Mdr2^-/- and WT controls. (B) Liver DE-miRs expression profiles between female Mdr2^-/- and WT controls. (C) Liver DEGs expression profiles between Mdr2^-/- and WT controls. (D) The top 50 hug genes of the PPI network of upregulated DEGs and the top 50 hug genes of the PPI network of downregulated DEGs. (E) Predicted network of miRNAs – 100 identified hug genes of DEGs between Mdr2^-/- and WT controls. (F) Identification of 11 overlapping upregulated miRNAs in cholestatic liver injury. FC, fold change; miR, micro RNA. DE, differentially expressed, Mdr2^-/- , multidrug resistance 2 gene knockout; WT, wild type.

Fig 2. Exosome DE-miRs identification in Mdr2^-/- mice compared to corresponding WT controls, the overlapping DE-miRs in the liver and serum exosomes, and comparison of the expression levels of these DE-miRs and target genes between normal and CHOL samples in TCGA CCA database.
(A) Exosome DE-miRs expression profiles between female Mdr2^-/- and WT controls. (B) Identification of 2 overlapping upregulated DE-miRs in the serum exosomes which may contribute to cholestatic liver injury. (C) The expression levels of these 2 overlapping upregulated DE-miRs between normal and CHOL samples. (D) Heat map, the expression levels of these target hug genes of 2 overlapping upregulated DE-miRs between normal and CHOL samples.

Fig 1. Liver DE-miRs and DEGs identification in Mdr2^-/- mice compared to corresponding WT controls, target prediction and analysis of these DE-miRs and DEGs, and the overlapping miRNAs in cholestatic liver injury.
(A) Liver DE-miRs expression profiles between male Mdr2^-/- and WT controls. (B) Liver DE-miRs expression profiles between female Mdr2^-/- and WT controls. (C) Liver DEGs expression profiles between Mdr2^-/- and WT controls. (D) The top 50 hug genes of the PPI network of upregulated DEGs and the top 50 hug genes of the PPI network of downregulated DEGs. (E) Predicted network of miRNAs – 100 identified hug genes of DEGs between Mdr2^-/- and WT controls. (F) Identification of 11 overlapping upregulated miRNAs in cholestatic liver injury. FC, fold change; miR, micro RNA. DE, differentially expressed, Mdr2^-/- , multidrug resistance 2 gene knockout; WT, wild type.

Fig 2. Exosome DE-miRs identification in Mdr2^-/- mice compared to corresponding WT controls, the overlapping DE-miRs in the liver and serum exosomes, and comparison of the expression levels of these DE-miRs and target genes between normal and CHOL samples in TCGA CCA database.
(A) Exosome DE-miRs expression profiles between female Mdr2^-/- and WT controls. (B) Identification of 2 overlapping upregulated DE-miRs in the serum exosomes which may contribute to cholestatic liver injury. (C) The expression levels of these 2 overlapping upregulated DE-miRs between normal and CHOL samples. (D) Heat map, the expression levels of these target hug genes of 2 overlapping upregulated DE-miRs between normal and CHOL samples.

Table 1. Cardiovascular outcomes between the Users of GLP-1RA vs. SGLT2 in patients with NAFLD and type 2 diabetes

Sex Adjusted Incidence Rate of Celiac Disease by Age groups between 2000-2021

Sex Adjusted Incidence Rate of Celiac Disease by Age groups between 2000-2021

Sex Adjusted Incidence Rate of Celiac Disease by Age groups between 2000-2021

Figure 1. Post-inflammatory female mice exhibit increased visceral pain. Visceral hypersensitivity was measured by evaluating the VMR to CRD. Data expressed as mean ± SEM, n=10-12 animals/group. Two-way analysis of variance, Tukey post hoc test; p=0.003 at 60mmHg.

Figure 2. Differential abundance of amplicon sequence variants (ASV) in post-inflammatory male vs post-inflammatory female mice. Log2 fold change of which ASV abundance significantly increased (right) and decreased (left) in males compared to females after 5 weeks of recovery. DESeq2; Wald test.

Figure. Annual median colorectal cancer screening rates in Federally Qualified Health Centers in the United States (blue), in California State (orange), and in Los Angeles County (gray) from 2014 to 2021.

Table. Clinic-level factors associated with colorectal cancer (CRC) screening rate change from 2020 to 2021 at Federally Qualified Health Centers (FQHCs) in the United States and California, based on mixed effects linear regression.

Figure. Annual median colorectal cancer screening rates in Federally Qualified Health Centers in the United States (blue), in California State (orange), and in Los Angeles County (gray) from 2014 to 2021.

Table. Clinic-level factors associated with colorectal cancer (CRC) screening rate change from 2020 to 2021 at Federally Qualified Health Centers (FQHCs) in the United States and California, based on mixed effects linear regression.

Percent of patients with symptoms pre- and post-treatment for eosinophilic esophagitis with corresponding P-values. Circles indicate the median peak eosinophil count at baseline and triangles indicate the median peak eosinophil count at follow-up among patients presenting with that symptom.

Proportion of patients achieving histologic remission (defined by peak eosinophil count < 15 per high power field) by EoE treatment.

Percent of patients with symptoms pre- and post-treatment for eosinophilic esophagitis with corresponding P-values. Circles indicate the median peak eosinophil count at baseline and triangles indicate the median peak eosinophil count at follow-up among patients presenting with that symptom.

Proportion of patients achieving histologic remission (defined by peak eosinophil count < 15 per high power field) by EoE treatment.

Percent of patients with symptoms pre- and post-treatment for eosinophilic esophagitis with corresponding P-values. Circles indicate the median peak eosinophil count at baseline and triangles indicate the median peak eosinophil count at follow-up among patients presenting with that symptom.

Proportion of patients achieving histologic remission (defined by peak eosinophil count < 15 per high power field) by EoE treatment.

Table 1. Results of Multivariable Logistic Regression for an Association Between Autoantibodies and SARS-CoV-2 Antibody Status (n=4717)

Percent of patients with symptoms pre- and post-treatment for eosinophilic esophagitis with corresponding P-values. Circles indicate the median peak eosinophil count at baseline and triangles indicate the median peak eosinophil count at follow-up among patients presenting with that symptom.

Proportion of patients achieving histologic remission (defined by peak eosinophil count < 15 per high power field) by EoE treatment.

Table 1. Results of Multivariable Logistic Regression for an Association Between Autoantibodies and SARS-CoV-2 Antibody Status (n=4717)

Percent of patients with symptoms pre- and post-treatment for eosinophilic esophagitis with corresponding P-values. Circles indicate the median peak eosinophil count at baseline and triangles indicate the median peak eosinophil count at follow-up among patients presenting with that symptom.

Proportion of patients achieving histologic remission (defined by peak eosinophil count < 15 per high power field) by EoE treatment.

Table 1. Results of Multivariable Logistic Regression for an Association Between Autoantibodies and SARS-CoV-2 Antibody Status (n=4717)

Figure 1. Beta diversity-based principal coordinate analysis of SI contents of mice gavaged with human SI aspirates (purple) and human stool (yellow) and the original human input sample (human SI, green and human stool, grey).

Figure 2. SI dysbiosis induces visceral hypersensitivity. The visceromotor response of mice, gavaged with SI aspirates from patients with abdominal pain, was increased at distension pressures of 30, 45 and 60 mmHg when compared to mice, gavaged with SI aspirates from healthy controls. Repeated measurements Two-Way ANOVA with Bonferroni post-hoc correction to account for multiple mice colonized with the same donor sample: *p<0.05, **p<0.01.

Figure 1. Beta diversity-based principal coordinate analysis of SI contents of mice gavaged with human SI aspirates (purple) and human stool (yellow) and the original human input sample (human SI, green and human stool, grey).

Figure 2. SI dysbiosis induces visceral hypersensitivity. The visceromotor response of mice, gavaged with SI aspirates from patients with abdominal pain, was increased at distension pressures of 30, 45 and 60 mmHg when compared to mice, gavaged with SI aspirates from healthy controls. Repeated measurements Two-Way ANOVA with Bonferroni post-hoc correction to account for multiple mice colonized with the same donor sample: *p<0.05, **p<0.01.

Figure 1. Beta diversity-based principal coordinate analysis of SI contents of mice gavaged with human SI aspirates (purple) and human stool (yellow) and the original human input sample (human SI, green and human stool, grey).

Figure 2. SI dysbiosis induces visceral hypersensitivity. The visceromotor response of mice, gavaged with SI aspirates from patients with abdominal pain, was increased at distension pressures of 30, 45 and 60 mmHg when compared to mice, gavaged with SI aspirates from healthy controls. Repeated measurements Two-Way ANOVA with Bonferroni post-hoc correction to account for multiple mice colonized with the same donor sample: *p<0.05, **p<0.01.

Figure 1. Beta diversity-based principal coordinate analysis of SI contents of mice gavaged with human SI aspirates (purple) and human stool (yellow) and the original human input sample (human SI, green and human stool, grey).

Figure 2. SI dysbiosis induces visceral hypersensitivity. The visceromotor response of mice, gavaged with SI aspirates from patients with abdominal pain, was increased at distension pressures of 30, 45 and 60 mmHg when compared to mice, gavaged with SI aspirates from healthy controls. Repeated measurements Two-Way ANOVA with Bonferroni post-hoc correction to account for multiple mice colonized with the same donor sample: *p<0.05, **p<0.01.

Table 1. Baseline characteristics of RYGB patients with weight regain who underwent endoscopic gastric bypass revision (EGBR).

Figure 1. An anatomy-based algorithm for the treatment of weight regain following Roux-en-Y gastric bypass. APC: argon plasma coagulation; S-TORe: suturing transoral outlet reduction; P-TORe: plication transoral outlet reduction; %TWL: percent total weight loss at 12 months. Bold font with * indicates statistical significance.

Table 1. Baseline characteristics of RYGB patients with weight regain who underwent endoscopic gastric bypass revision (EGBR).

Figure 1. An anatomy-based algorithm for the treatment of weight regain following Roux-en-Y gastric bypass. APC: argon plasma coagulation; S-TORe: suturing transoral outlet reduction; P-TORe: plication transoral outlet reduction; %TWL: percent total weight loss at 12 months. Bold font with * indicates statistical significance.

Table 1. Baseline characteristics of RYGB patients with weight regain who underwent endoscopic gastric bypass revision (EGBR).

Figure 1. An anatomy-based algorithm for the treatment of weight regain following Roux-en-Y gastric bypass. APC: argon plasma coagulation; S-TORe: suturing transoral outlet reduction; P-TORe: plication transoral outlet reduction; %TWL: percent total weight loss at 12 months. Bold font with * indicates statistical significance.

Table 1. Baseline characteristics of RYGB patients with weight regain who underwent endoscopic gastric bypass revision (EGBR).

Figure 1. An anatomy-based algorithm for the treatment of weight regain following Roux-en-Y gastric bypass. APC: argon plasma coagulation; S-TORe: suturing transoral outlet reduction; P-TORe: plication transoral outlet reduction; %TWL: percent total weight loss at 12 months. Bold font with * indicates statistical significance.

Table 1. Baseline characteristics of RYGB patients with weight regain who underwent endoscopic gastric bypass revision (EGBR).

Figure 1. An anatomy-based algorithm for the treatment of weight regain following Roux-en-Y gastric bypass. APC: argon plasma coagulation; S-TORe: suturing transoral outlet reduction; P-TORe: plication transoral outlet reduction; %TWL: percent total weight loss at 12 months. Bold font with * indicates statistical significance.

Figure 1: a, b) brightfield microscopic images of co-cultured InMyoFibs+CaCO2 cells in the lumen of bioprinted tubes at day 4 after seeding CaCO2 cells; c) viability of co-cultured InMyoFibs+CaCO2 cells in the lumen of bioprinted tubes at Day 10 after seeding CaCO2 cells; d, e, f) microscopic images showing the viability of InMyoFibs+InEpCs +CaCO2 cells in the lumen bioprinted tubes at day 7 after addition of 1.5 ug/ml bleomycin, 10 mg/ml for minocycline and 40 ng/ml TGF-beta1, respectively (note that the green color represents live cells, and the red represents dead cells); g, h, i) microscopic images showing immunostained for Collagen-I at Day 7 of 1.5 ug/ml bleomycin, 10 mg/ml for minocycline and 40 ng/ml TGF-beta1, respectively.

Figure 2: Confocal images of the organ-on-a-chip culture showing immunostaining for α-SMA and Collagen-I (Col-I) at day 7 after the addition of 40 ng/ml recombinant TGFB1, and 1000 uM of Sodium Tetradecyl Sulfate (STS).

Table 1. Baseline characteristics of RYGB patients with weight regain who underwent endoscopic gastric bypass revision (EGBR).

Figure 1. An anatomy-based algorithm for the treatment of weight regain following Roux-en-Y gastric bypass. APC: argon plasma coagulation; S-TORe: suturing transoral outlet reduction; P-TORe: plication transoral outlet reduction; %TWL: percent total weight loss at 12 months. Bold font with * indicates statistical significance.

Figure 1: a, b) brightfield microscopic images of co-cultured InMyoFibs+CaCO2 cells in the lumen of bioprinted tubes at day 4 after seeding CaCO2 cells; c) viability of co-cultured InMyoFibs+CaCO2 cells in the lumen of bioprinted tubes at Day 10 after seeding CaCO2 cells; d, e, f) microscopic images showing the viability of InMyoFibs+InEpCs +CaCO2 cells in the lumen bioprinted tubes at day 7 after addition of 1.5 ug/ml bleomycin, 10 mg/ml for minocycline and 40 ng/ml TGF-beta1, respectively (note that the green color represents live cells, and the red represents dead cells); g, h, i) microscopic images showing immunostained for Collagen-I at Day 7 of 1.5 ug/ml bleomycin, 10 mg/ml for minocycline and 40 ng/ml TGF-beta1, respectively.

Figure 2: Confocal images of the organ-on-a-chip culture showing immunostaining for α-SMA and Collagen-I (Col-I) at day 7 after the addition of 40 ng/ml recombinant TGFB1, and 1000 uM of Sodium Tetradecyl Sulfate (STS).

Table 1. Baseline characteristics of RYGB patients with weight regain who underwent endoscopic gastric bypass revision (EGBR).

Figure 1. An anatomy-based algorithm for the treatment of weight regain following Roux-en-Y gastric bypass. APC: argon plasma coagulation; S-TORe: suturing transoral outlet reduction; P-TORe: plication transoral outlet reduction; %TWL: percent total weight loss at 12 months. Bold font with * indicates statistical significance.

Figure 1: a, b) brightfield microscopic images of co-cultured InMyoFibs+CaCO2 cells in the lumen of bioprinted tubes at day 4 after seeding CaCO2 cells; c) viability of co-cultured InMyoFibs+CaCO2 cells in the lumen of bioprinted tubes at Day 10 after seeding CaCO2 cells; d, e, f) microscopic images showing the viability of InMyoFibs+InEpCs +CaCO2 cells in the lumen bioprinted tubes at day 7 after addition of 1.5 ug/ml bleomycin, 10 mg/ml for minocycline and 40 ng/ml TGF-beta1, respectively (note that the green color represents live cells, and the red represents dead cells); g, h, i) microscopic images showing immunostained for Collagen-I at Day 7 of 1.5 ug/ml bleomycin, 10 mg/ml for minocycline and 40 ng/ml TGF-beta1, respectively.

Figure 2: Confocal images of the organ-on-a-chip culture showing immunostaining for α-SMA and Collagen-I (Col-I) at day 7 after the addition of 40 ng/ml recombinant TGFB1, and 1000 uM of Sodium Tetradecyl Sulfate (STS).

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