From co-design to co-production: Approaches, enablers, and constraints in developing a public health, capacity-building solution.

Introduction: Investigating how co-designed knowledge can be translated to co-produce a public health capacity-building solution for difficult-to-engage population groups drawing on the co-production experience of a prevention-focused, capacity-building mental health solution targeting primary producers.

Design: A qualitative study undertaken in rural and regional Victoria involving members of the design working group including project team (7px), digital design team (5px), marketing team (3px), and funding partner representatives. The study design involved reflective practice to collect data to identify the phases of co-production and assess the design working group members' experiences.

Development of a Synthetic Population Model for Assessing Excess Risk for Cardiovascular Disease Death.

Importance: Evaluating the association of social determinants of health with chronic diseases at the population level requires access to individual-level factors associated with disease, which are rarely available for large populations. Synthetic populations are a possible alternative for this purpose.

Objective: To construct and validate a synthetic population that statistically mimics the characteristics and spatial disease distribution of a real population, using real and synthetic data.

Cigarette smoke and decreased oxygen tension inhibit pulmonary claudin-6 expression.

Purpose: Chronic obstructive pulmonary disease is a condition involving perturbed barrier integrity coincident with both emphysema and inflammation of the airways, and smoking is considered a major risk factor. Claudins (Cldns) stabilize barriers and contribute to tight junctions by preventing paracellular transport of extracellular fluid constituents.

Methods: To determine Cldn6 was differentially influenced by tobacco smoke, Cldn6 was evaluated in cells and tissues by q-PCR, immunoblotting, and immunohistochemistry following exposure.

Decreased activation of placental mTOR family members is associated with the induction of intrauterine growth restriction by secondhand smoke in the mouse.

Cigarette smoke is known to be a risk for the development of intrauterine growth restriction (IUGR). Our objective was to assess the effects of secondhand smoke (SHS) during pregnancy and to what extent it regulates the activation of mTOR family members and murine trophoblast invasion. Mice were treated to SHS for 4 days.