Long-term Care Financing: Inserting Politics and Resource Allocation in the Debate; Comment on “Financing Long-term Care: Lessons From Japan”

The ageing of the countries’ populations, and in particular the growing number of the very old, is increasing the need for long-term care (LTC). Not surprisingly, therefore, the financing of LTC systems has become a crucial topic across the Organisation for Economic Co-operation and Development (OECD). In the last three decades, various financing policies have been carried out in different countries and the related international debate has grown. The latter has so far focused mostly on the different alternatives to collect economic resources to pay for care. The international debate needs now to focus also on other issues, so far less discussed. One is the politics of LTC: the degree and nature of the political interest in LTC, that affects the size and profile of public financing. The other is resource allocation: how different services and benefits are distributed among people with different care needs, that determines if resources made available are optimized. If we do not pay more attention to these issues – inextricably connected to policies aimed to collect funds – our understanding of LTC financing will remain inevitably limited

The mixed economy of long-term care in England, Germany, Italy, and Spain

This paper is based on a European Commission-funded study of future long-term care expenditure in Germany, Italy, Spain and the United Kingdom. It investigates how sensitive long-term care expenditure is to assumptions about demographic trends, future dependency rates, care arrangements, and real inflation. Macro-simulation projection models for each country reflecting the national characteristics of the care system were used to make comparable projections based on a set of common assumptions. This central case was then used as a point of comparison in order to explore the sensitivity of the models to alternative scenarios about key determinants of future expenditure. The proportion of GDP spent on longterm care is projected to more than double between 2000 and 2050 in each country under the central case. However, projections are highly sensitive to changes in the above assumptions. -- Der Beitrag beruht auf einer EU-finanzierten Studie zur zukünftigen Entwicklung der Ausgaben für Langzeitpflege in Deutschland, Italien, Spanien und dem Vereinigten Königreich. Untersucht wird die Sensitivität der Ausgabenentwicklung hinsichtlich unterschiedlicher Annahmen zur demographischen Entwicklung, zur Pflegebedürftigkeit, zur Pflegeform und zu den Kosten der Pflege. Mittels nationaler Makrosimulationsmodelle, die die länderspezifischen Pflegesysteme berücksichtigen, wird ein auf gemeinsamen Annahmen basierendes Grundmodell berechnet, das den Referenzpunkt der nachfolgenden Sensitivitätsanalyse darstellt. Im Ergebnis zeigt sich in allen Untersuchungsländern, dass sich der Anteil des BIP, der für Pflegeleistungen aufgewandt wird, von 2000 bis 2050 mehr als verdoppelt. Allerdings sind diese Ergebnisse sehr sensitiv in bezug auf Veränderungen der genannten Annahmen.

Establishing the Middle Sea: The Late Bronze Age of Mediterranean Europe (1700–900 BC)

The Late Bronze Age (1700–900 BC) represents an extremely dynamic period for Mediterranean Europe. Here, we provide a comparative survey of the archaeological record of over half a millennium within the entire northern littoral of the Mediterranean, from Greece to Iberia, incorporating archaeological, archaeometric, and bioarchaeological evidence. The picture that emerges, while certainly fragmented and not displaying a unique trajectory, reveals a number of broad trends in aspects as different as social organization, trade, transcultural phenomena, and human mobility. The contribution of such trends to the processes that caused the end of the Bronze Age is also examined. Taken together, they illustrate how networks of interaction, ranging from the short to the long range, became a defining aspect of the “Middle Sea” during this time, influencing the lives of the communities that inhabited its northern shore. They also highlight the importance of research that crosses modern boundaries for gaining a better understanding of broad comparable dynamics

The mixed economy of long-term care in England, Germany, Italy, and Spain

"This paper is based on a European Commission-funded study of future long-term care expenditure in Germany, Italy, Spain and the United Kingdom. It investigates how sensitive long-term care expenditure is to assumptions about demographic trends, future dependency rates, care arrangements, and real inflation. Macro-simulation projection models for each country reflecting the national characteristics of the care system were used to make comparable projections based on a set of common assumptions. This central case was then used as a point of comparison in order to explore the sensitivity of the models to alternative scenarios about key determinants of future expenditure. The proportion of GDP spent on longterm care is projected to more than double between 2000 and 2050 in each country under the central case. However, projections are highly sensitive to changes in the above assumptions." (author's abstract)"Der Beitrag beruht auf einer EU-finanzierten Studie zur zukünftigen Entwicklung der Ausgaben für Langzeitpflege in Deutschland, Italien, Spanien und dem Vereinigten Königreich. Untersucht wird die Sensitivität der Ausgabenentwicklung hinsichtlich unterschiedlicher Annahmen zur demographischen Entwicklung, zur Pflegebedürftigkeit, zur Pflegeform und zu den Kosten der Pflege. Mittels nationaler Makrosimulationsmodelle, die die länderspezifischen Pflegesysteme berücksichtigen, wird ein auf gemeinsamen Annahmen basierendes Grundmodell berechnet, das den Referenzpunkt der nachfolgenden Sensitivitätsanalyse darstellt. Im Ergebnis zeigt sich in allen Untersuchungsländern, dass sich der Anteil des BIP, der für Pflegeleistungen aufgewandt wird, von 2000 bis 2050 mehr als verdoppelt. Allerdings sind diese Ergebnisse sehr sensitiv in bezug auf Veränderungen der genannten Annahmen." (Autorenreferat

City data ecosystems between theory and practice: A qualitative exploratory study in seven European cities

The exponential growth of data collection opens possibilities for analyzing data to address political and societal challenges. Still, European cities are not utilizing the potential of data generated by its citizens, industries, academia, and public authorities for their public service mission. The reasons are complex and relate to an intertwined set of organizational, technological, and legal barriers, although good practices exist that could be scaled, sustained, and further developed. The article contributes to research on data-driven innovation in the public sector comparing high-level expectations on data ecosystems with actual practices of data sharing and innovation at the local and regional level. Our approach consists in triangulating the analysis of in-depth interviews with representatives of the local administrations with documents obtained from the cities. The interviews investigated the experiences and perspectives of local administrations regarding establishing a local or regional data ecosystem. The article examines experiences and obstacles to data sharing within seven administrations investigating what currently prevents the establishment of data ecosystems. The findings are summarized along three main lines. First, the limited involvement of private sector organizations as actors in local data ecosystems through emerging forms of data sharing became evident. Second, we observed the concern over technological aspects and the lack of attention on social or organizational issues. Third, a conceptual decision to apply a centralized and not a federated digital infrastructure is noteworthy

An integrated care pathway for cancer patients with diabetes: A proposal from the Italian experience

Diabetes and cancer frequently coexist in the same subject, often with relevant clinical effects on the management and prognosis of the comorbid patient. The existing guidelines, however, do not appropriately address many clinical issues in this setting. Although collaboration between diabetologists and oncologists should play an important role in achieving appropriate levels of care, close coordination or agreement between these specialists is seldom offered. There is an urgent need for greater interdisciplinary integration between all specialists involved in this setting, for a shared approach ensuring that organisational silos are overcome. To this end, the Italian Associations of Medical Diabetologists (AMD) and the Italian Association of Medical Oncology (AIOM) recently established a dedicated Working Group on 'Diabetes and Cancer'. The working group outlined a diagnostic and therapeutic clinical pathway dedicated to hospitalised patients with diabetes and cancer. In this article, we describe the Italian proposal including some suggested measures to assess, monitor and improve blood glucose control in the hospital setting, to integrate different specialists from both areas, as well as to ensure discharge planning and continuity of care from the hospital to the territory

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease