OBJECTIVES

Timely access to appropriate levels of care is essential for improving maternal, newborn,
and child health outcomes. To address persistent service delivery fragmentation and strengthen referral systems, the Philippine Department of Health issued Administrative Order 2020-0019 to guide the design of Health Care Provider Networks (HCPNs) under the Universal Health Care Act of 2019. This study assessed the extent to which sixteen municipalities across four provinces in Eastern Visayas comply with the HCPN service delivery guidelines in the context of maternal and newborn care.

METHODS

The study employed a descriptive cross-sectional mixed-methods design, utilizing structured facility checklists to assess compliance with HCPN standards. Qualitative data were gathered through key informant interviews and focus group discussions with purposively selected stakeholders—decision makers, health personnel, and mothers—to contextualize findings. A three-lever framework for integrated care (policy, operational, and cross- cutting) guided the analysis

RESULTS

The findings revealed significant gaps between the current capacities of study health facilities and the requirements outlined in the HCPN guidelines. Major gaps included (1) weak cooperative governance mechanisms to support network-wide coordination; (2) limited systematic linkages between facilities, including fragmented referral protocols and non-interoperable health information systems; (3) inadequate investments in infrastructure, health human resources, and medical commodities; and (4) absence of performance monitoring systems across HCPNs.

CONCLUSION

 

Human ; Information Systems ; Occupational Groups ; Referral And Consultation ; Universal Health Care ; Delivery Of Health Care

Cardiovascular disease is the most common cause of death in diabetic patients. Hyperglycemia is the primary characteristic of diabetes and is associated with many complications. The role of hyperglycemia in the dysfunction of human cardiac progenitor cells that can regenerate damaged cardiac tissue has been investigated, but the exact mechanism underlying this association is not clear. Thus, we examined whether hyperglycemia could regulate mitochondrial dynamics and lead to cardiac progenitor cell dysfunction, and whether blocking glucose uptake could rescue this dysfunction. High glucose in cardiac progenitor cells results in reduced cell viability and decreased expression of cell cycle-related molecules, including CDK2 and cyclin E. A tube formation assay revealed that hyperglycemia led to a significant decrease in the tube-forming ability of cardiac progenitor cells. Fluorescent labeling of cardiac progenitor cell mitochondria revealed that hyperglycemia alters mitochondrial dynamics and increases expression of fission-related proteins, including Fis1 and Drp1. Moreover, we showed that specific blockage of GLUT1 improved cell viability, tube formation, and regulation of mitochondrial dynamics in cardiac progenitor cells. To our knowledge, this study is the first to demonstrate that high glucose leads to cardiac progenitor cell dysfunction through an increase in mitochondrial fission, and that a GLUT1 blocker can rescue cardiac progenitor cell dysfunction and downregulation of mitochondrial fission. Combined therapy with cardiac progenitor cells and a GLUT1 blocker may provide a novel strategy for cardiac progenitor cell therapy in cardiovascular disease patients with diabetes.
Cardiovascular Diseases ; Cause of Death ; Cell Survival ; Cyclin E ; Cyclins ; Diabetic Cardiomyopathies ; Down-Regulation ; Glucose* ; Humans* ; Hyperglycemia ; Mitochondria ; Mitochondrial Dynamics* ; Stem Cells*