On the importance of primary and community healthcare in relation to global health and environmental threats: lessons from the COVID-19 crisis.

In the course of the COVID-19 pandemic, it has become clear that primary healthcare systems play a critical role in clinical care, such as patient screening, triage, physical and psychological support and also in promoting good community advice and awareness in coordination with secondary healthcare and preventive care. Because of the role of social and environmental factors in COVID-19 transmission and burden of disease, it is essential to ensure that there is adequate coordination of population-based health services and public health interventions. The COVID-19 pandemic has shown the primary and community healthcare (P&CHC) system's weaknesses worldwide. In many instances, P&CHC played only a minor role, the emphasis being on hospital and intensive care beds. This was compounded by political failures, in supporting local community resilience. Placing community building, social cohesion and resilience at the forefront of dealing with the COVID-19 crisis can help align solutions that provide a vision of 'planetary health'. This can be achieved by involving local well-being and participation in the face of any pervasive health and environmental crisis, including other epidemics and large-scale ecological crises. This paper proposes that P&CHC should take on two critical roles: first, to support local problem-solving efforts and to serve as a partner in innovative approaches to safeguarding community well-being; and second, to understand the local environment and health risks in the context of the global health perspective. We see this as an opportunity of immediate value and broad consequence beyond the control of the COVID-19 pandemic.

Hepatic steatosis, carotid atherosclerosis and metabolic syndrome: the STEATO Study.

PURPOSE: Hepatic steatosis is frequently observed in subjects with metabolic syndrome (MS). In type 2 diabetics, it is independently associated with cardiovascular diseases. In order to confirm and extend this finding, a large group of patients with risk factors for atherosclerosis was studied. METHODS: Carotid atherosclerosis was investigated by echo-Doppler, and hepatic steatosis by ultrasound and transaminase values. Strict exclusion criteria were chosen in order to avoid secondary forms of fatty liver and interference on transaminase values. RESULTS: Among 970 enrolled patients, about 20% were diabetics, half had MS and 76% presented echographic hepatic steatosis. In multivariate analyses, fatty liver and MS were associated with carotid atherosclerosis [odds ratio (95% confidence intervals) 2.15 (1.27-3.63) and 1.72(1.12-2.64), respectively], whereas HOMA index was not. Aspartate aminotransferase and alanine aminotransferase were not independently associated with carotid atherosclerosis, whereas gamma-glutamyl transferase showed a link with atherosclerosis beyond MS and steatosis presence. The analyses of the 780 non diabetics recruited showed similar results. CONCLUSIONS: The results of the present study demonstrate that hepatic steatosis measured by echography is associated with carotid atherosclerosis in a large population mostly carrying cardiovascular or metabolic risk factors, independently of MS, cardiovascular diseases, diabetes mellitus and/or insulin resistance.

MYH9 spectrum of autosomal-dominant giant platelet syndromes: unexpected association with fibulin-1 variant-D inactivation.

The autosomal-dominant giant platelet syndromes (Fechtner, Epstein, and Sebastian platelet syndromes and May-Hegglin anomaly) represent a group of disorders characterized by variable degrees of macrothrombocytopenia with further combinations of neutrophil inclusion bodies and Alport-like syndrome manifestations, namely, deafness, renal disease, and eye abnormalities. The disease-causing gene of these giant platelet syndromes was previously mapped by us to chromosome 22. Following their successful mapping, these syndromes were shown to represent a broad phenotypic spectrum of disorders caused by different mutations in the nonmuscle myosin heavy chain 9 gene (MYH9). In this study, we examined the potential role of another gene, fibulin-1, encoding an extracellular matrix protein as a disease modifier. Eight unrelated families with autosomal-dominant giant platelet syndromes were studied for DNA sequence mutations and expression of the four fibulin-1 splice variants (A-D). A mutation in the splice acceptor site of fibulin-1 exon 19 was found in affected individuals of the Israeli Fechtner family, whereas no MYH9 mutations were identified. Unexpectedly, fibulin-1 variant D expression was absent in affected individuals from all eight families and coupled with expression of a putative antisense RNA. Transfection of the putative antisense RNA into H1299 cells abolished variant D expression. Based on the observation that only affected individuals lack variant D expression and demonstrate antisense RNA overexpression, we suggest that these autosomal-dominant giant platelet syndromes are associated, and may be modified, by aberrant antisense gene regulation of the fibulin-1 gene.