Effects of health-information-based diabetes shared care program participation on preventable hospitalizations in Taiwan.

BACKGROUND: Taiwan's Diabetes Shared Care Program has been implemented since 2012, and the health information system plays a vital role in supporting most services of this program. However, little is known regarding the effectiveness of this information-based program. Therefore, this study investigated the effects of the participation of the Diabetes Shared Care Program on preventable hospitalizations. METHODS: This longitudinal study examined the data of health-care claims from 2011 to 2014 obtained from the diabetes mellitus health database. Patients with diabetes aged ≥18 years were included. Preventable hospitalizations were identified on the basis of prevention quality indicators developed for administrative data by the US Agency for Healthcare Research and Quality. A multilevel logistic regression was performed to examine the effects of the participation of the Diabetes Shared Care Program on preventable hospitalizations after adjustment for other variables. Analyses were conducted in late 2018. RESULTS: A medium level of participation (p = 0.05), age between 40 and 64 years(p < 0.0001), and absence of a catastrophic illness(p < 0.0001) were associated with a lower probability of having a preventable hospitalization. Male sex(p < 0.0001), age ≥ 65 years(p = 0.0203), low income level(p < 0.0001), living in the Southern division(p = 0.0106), and presence of many comorbidities(p < 0.0001) were associated with a higher probability of having a preventable hospitalization after adjustment for characteristics at the individual and county levels. CONCLUSIONS: The health information system records patients' medical history, monitors quality of care, schedules patient follow-ups, and reminds case managers to provide timely health education. This health-information-based Diabetes Shared Care Program is associated with better quality care of ambulatory, so it should be promoted on a broader scale.

Nanoceria restrains PM2.5-induced metabolic disorder and hypothalamus inflammation by inhibition of astrocytes activation related NF-κB pathway in Nrf2 deficient mice.

Increasing studies demonstrated that air pollution (PM2.5) plays a significant role in metabolic and neurological diseases. Unfortunately, there is no direct testimony of this, and yet the molecular mechanism by which the occurrence remains unclear. In this regard, we investigated the role of NF-κB and Nrf2 signaling in PM2.5-induced metabolic disorders and neuroinflammation, and further confirmed whether Nrf2 deficiency promoted PM2.5-induced inflammatory response by up regulating astrocytes activation and nerve injury via modulating NF-κB signaling pathways. Present results found that, indeed, PM2.5 challenges results in glucose tolerance, insulin resistance, dysarteriotony, peripheral inflammation, nerve injury and hypothalamus oxidative stress through astrocytes activation related NF-κB pathway in Nrf2 deficient mice. Moreover, in vitro study, we confirmed that activated astrocytes induced by PM2.5 were involved in pathogenesis of hypothalamic inflammation, which were significantly associated with NF-κB signaling. Nanoceria as potential anti-inflammatory and anti-oxidant stress biomaterial has gained increasing attention. Moderate nanoceria treatment is able to restrain PM2.5-induced metabolic syndrome and inflammation. Inhibition of astrocytes activation related NF-κB and enhancement of Nrf2 by cerium oxide were observed in vivo and in vitro, suggesting cerium oxide inhibited hypothalamic inflammation and nerve injury by altering hypothalamic neuroendocrine alterations and decreasing glial cells activation. In addition, NF-κB inhibitor pyrollidine dithiocarbamate (PDTC) treated primary astrocytes directly determined Nrf2 pathway could be up regulated by dose-dependent nanoceria. These results suggest a new therapeutic approach or target to protect against air pollution related diseases by cerium oxide treatment.