Introduction: The nutritional status of children with Attention-Deficit/Hyperactivity Disorder (ADHD) and Down Syndrome (DS) is influenced by multiple food environment determinants. However, the precise relationship between food environment determinants and nutritional outcomes in these children remains unclear. This study aimed to understand the food environment determinants that are associated with the intake and nutritional status of these children in Malaysia, Lao PDR, and Indonesia. Methods: This cross-sectional study involved 7- to 18-year-old students with ADHD and DS in three Southeast Asian countries. Sociodemographic characteristics, dietary habits, and repeated 24-hour food recall data were collected through a structured questionnaire. Anthropometric data were obtained through direct measurements and analysed using the WHO AnthroPlus software. Further analyses were done using descriptive statistics and chi-square tests. Results: Total participants were 284 children, comprised of 37.7% with ADHD and 62.3% with DS; 62.3% of the children were boys and 37.7% were girls. Among the food environment determinants collected during the study, monthly household income and school food assistance status had significant associations (p<0.05) with BMI-for-age z-score category and total energy, protein, zinc, and calcium intakes. While the country, type of residence, and type of school had significant associations with total energy, protein, zinc, and calcium intakes. Conclusions: Food environment determinants, particularly household income and access to school food assistance, significantly influence the nutritional status and intake of children with ADHD and Down Syndrome. Thus, strengthening inclusive nutrition programmes may improve outcomes for this vulnerable group in Southeast Asia.

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.

Objective To investigate the correlation between serum Visfatin, CXC chemokine 12 (CXCL12) and silent information regulator 1 (Sirt1) levels and carotid atherosclerosis (CAS) in patients with type 2 diabetes mellitus (type 2 diabetes mellitus ,T2DM). Methods Four hundred and ninety-five patients with T2DM in the hospital from July 2021 to June 2023 were selected as the observation group, and 50 healthy volunteers were included in the control group. The levels of serum Visfatin, CXCL12 and Sirt1 were detected, and the above levels were compared between groups. The patients in the observation group were divided into simple T2DM group and T2DM with CAS group by means of the results of carotid ultrasound examination, and the clinical data were compared. Multivariate Logistic regression analysis was performed to analyze the factors affecting the occurrence of CAS in T2DM patients. Spearman correlation analysis of serum Visfatin, CXCL12 and Sirt1 levels and severity of CAS was analyzed by Spearman correlation analysis. Results Compared with the control group, the levels of serum Visfatin and CXCL12 in the observation group were higher (t=14.524, t=11.536, all P<0.05) while the level of Sirt1 was lower (t=21.912, P<0.05). There were statistical differences in age, body mass index (BMI), FBG, HbAlc, FINS, TG, LDL-C, Visfatin, CXCL12 and Sirt1 between T2DM with CAS group and simple T2DM group (P<0.05). Multivariate analysis suggested that age (OR=2.155), FBG (OR=2.563), HbAlc (OR=2.472), FINS (OR=0.438), TG (OR=2.492), LDL-C (OR=2.445), Visfatin (OR=2.404), CXCL12 (OR=2.214) and Sirt1 (OR=0.398) were the influencing factors of CAS in patients with T2DM (P<0.05). The levels of serum Visfatin and CXCL12 were positively correlated with the severity of CAS (r=0.574, r=0.530, P<0.05), and the level of Sirt1 was negatively correlated with the severity of CAS (r=-0.621, P<0.05). Conclusion Serum Visfatin, CXCL12 and Sirt1 in T2DM patients are related to the occurrence and severity of CAS. Visfatin, CXCL12 and Sirt1 may be involved in the occurrence and development of CAS in T2DM patients.

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.

Background: Type 1 diabetes (T1D) results in autoreactive T cells chronically destroying pancreatic islets. This often results in irreplaceable loss of insulin-producing beta cells. To reverse course, a combinatorial strategy of employing glucose-responsive insulin restoration coupled with inhibiting autoreactive immune responses is required. Methods: Non-obese diabetic mice received a single intraperitoneal implantation of a novel biomaterial co-seeded with insulin-producing islets and T regulatory cells (Tregs). Controls included biomaterial seeded solely with islets, or biomaterial only groups. Mice were interrogated for changes in inflammation and diabetes progression via blood glucose monitoring, multiplex serum cytokine profiling, flow cytometry and immunohistochemistry assessments. Results: Islet and Tregs co-seeded biomaterial recipients had increased longevity, insulin secretion, and normoglycemia through 180 days post-implantation compared to controls. Serum profile revealed reduced TNFα, IFNγ, IL-1β and increased IL-10, insulin, C-Peptide, PP and PPY in recipients receiving co-seeded biomaterial. Evaluation of the resected co-seeded biomaterial revealed reduced infiltrating autoreactive CD8 + and CD4 + T cells concomitant with sustained presence of Foxp3 + Tregs; further analysis revealed that the few infiltrated resident effector CD4+ or CD8+ T cells were anergic, as measured by low levels of IFNγ and Granzyme-B upon stimulation when compared to controls. Interestingly, studies also revealed increased Tregs in the pancreas. However, there was no restoration of the pancreas beta cell compartment, suggesting normoglycemia and production of insulin levels were largely supported by the implanted co-seeded biomaterial. Conclusion These studies show the efficacy of a combinatorial approach seeding Tregs with pancreatic islets in a novel self-assembling organoid for reversing T1D.