ObjectivesTo examine national trends in prevalence of serious psychological distress and depression among adults with stroke in the United States (US) from 2004 to 2017, and variations across sociodemographic subgroups.MethodsData were obtained from the household components of the 2004-2017 Medical Expenditure Panel Survey, a nationally representative survey in the US. History of stroke or transient ischemic attack was based on self-report. Psychological distress was measured by the Kessler-6 scale, and depressive symptoms were measured by the 2-item Patient Health Questionnaire. Logistic regression models were used to examine the trends in prevalence of serious psychological distress and depression overall and by age, sex, and race/ethnicity.ResultsAmong 10889 participants with stroke or transient ischemic attack, 60.0% were aged ≥ 65, 54.4% were female, and 72.2% were non-Hispanic white. The prevalence of serious psychological distress decreased from 14.9% in 2004-2005 to 11.3% in 2016-2017, corresponding to 7% lower odds every 2 years (adjusted odds ratio [aOR0.93, 95% confidence interval [CI]=0.89-0.97); and the prevalence of depression decreased from 23.1% in 2004-2005 to 18.3% in 2016-2017, corresponding to 5% lower odds every 2 years (aOR=0.95, 95% CI=0.92-0.98), after adjustment for sociodemographic characteristics, functional limitations, and antidepressant use. The trends varied significantly by age, but not sex and race/ethnicity. The overall decline was mainly driven by older adults above age 64.ConclusionsPrevalence of serious psychological distress and depression among US adults with stroke decreased from 2004 to 2017, but the burden of mental health problems remained high. 相似文献
Ischemia-reperfusion injury (IRI) has been considered as the major cause of acute kidney injury and can result in poor long-term graft function. Functional recovery after IRI is impaired in the elderly. In the present study, we aimed to compare kidney morphology, function, oxidative stress, inflammation, and development of renal fibrosis in young and aged rats after renal IRI.
Materials and methods
Rat models of warm renal IRI were established by clamping left pedicles for 45 min after right nephrectomy, then the clamp was removed, and kidneys were reperfused for up to 12 wk. Biochemical and histologic renal damage were assessed at 12 wk after reperfusion. The immunohistochemical staining of monocyte macrophage antigen-1 (ED-1) and transforming growth factor beta 1 (TGF-β1) and messenger RNA level of TGF-β1 in the kidney were analyzed.
Results
Renal IRI caused significant increases of malondialdehyde and 8-hydroxydeoxyguanosine levels and a decrease of superoxide dismutase activity in young and aged IRI rats; however, these changes were more obvious in the aged rats. IRI resulted in severe inflammation and tubulointerstitial fibrosis with decreased creatinine (Cr) clearance and increased histologic damage in aged rats compared with young rats. Moreover, we measured the ratio of Cr clearance between young and aged IRI rats. It demonstrated that aged IRI rats did have poor Cr clearance compared with the young IRI rats. ED-1 and TGF-β1 expression levels in the kidney were significantly higher in aged rats than in young rats after IRI.
Conclusion
Aged rats are more susceptible to IRI-induced renal failure, which may associate with the increased oxidative stress, increased histologic damage, and increased inflammation and tubulointerstitial fibrosis. Targeting oxidative stress and inflammatory response should improve the kidney recovery after IRI. 相似文献
Background and aimsPremature cardiovascular disease cause excess mortality in type 1 diabetes (T1D). The Steno T1D Risk Engine was developed and validated in northern European countries but its validity in other populations is unknown. We evaluated the performance of the Steno T1D Risk Engine in Italian patients with T1D.Materials and methodsWe included patients with T1D with a baseline visit between July 2013 and April 2014, who were free of cardiovascular disease and had complete information to estimate risk. The estimated cardiovascular risk score was compared with the 5-year rate of cardiovascular events by means of logistic regression.ResultsAmong 223 patients (mean age 43 ± 13 years, 34.5% male, mean duration of diabetes 22 ± 12 years) the mean estimated cardiovascular risk at 5 years was 5.9% (95% C.I. 5.2–6.5%). At baseline, high estimated risk discriminated the presence of asymptomatic atherosclerosis better than microangiopathy, and was not associated with markers of inflammation or endothelial activation. After a mean follow-up of 4.7 ± 0.5 years, only 3 cardiovascular events were observed and nonetheless the risk score was significantly associated with their incidence (OR 1.22; 95% C.I. 1.08–1.39, p = 0.001). However, the observed event rate was significantly lower than the estimated one (3 vs 13; 95% C.I. 12–14; p < 0.001).ConclusionThe Steno T1D Risk Score identified subjects with subclinical atherosclerosis and high cardiovascular risk in an Italian T1D population. However, the absolute risk was significantly overestimated. Further studies in larger population are needed to confirm these results. 相似文献
Background and aimsSelf-monitoring blood glucose (SMBG) remains a widespread tool to monitor blood glucose. The development of diabetes management systems (DMS) allows SMBG to provide additional information as time spent in target range (TIR). This study evaluates the association between HbA1c and TIR, evaluated through DMS, over 2 months, and 2 weeks.Methods and resultsType 1 (T1D) and Type 2 (T2D) insulin-treated patients with diabetes were enrolled. We used the term PIR (Points in Range) instead of TIR, since SMBG provides point-in-time glucose values rather than a continuous trend over time. PIR was calculated in 2-month and 2-week time ranges before available HbA1c measurement.One-hundred ninety-seven patients with T1D and 36 with T2D were recruited. HbA1c and PIR were inversely associated (2 months: R -0.72, 2 weeks R -0.70; p < 0.0001) in all subjects. The relationship did not change when T1D and T2D patients were analyzed separately. For every 10% change of PIR, there was a change of HbA1c by 0.4%.ConclusionsOur study, for the first time, demonstrates a significant correlation between HbA1c and PIR calculated by DMS. DMS offers additional information useful in disease management of patients with T1D and T2D performing SMBG. 相似文献
Osteoclasts are responsible for bone destruction in rheumatoid arthritis (RA), and adipose-derived mesenchymal stromal cells (ADSCs) can inhibit experimental collagen-induced arthritis model. This study aims to determine whether ADSCs also suppresses osteoclastogenesis and bone erosion in collagen-induced arthritis (CIA). Osteoclasts were induced from bone marrow-derived CD11b+ cells with receptor activator of nuclear factor-κ B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) stimulation and assessed with tartrate-resistant acid phosphatase (TRAP) staining. For human cells, osteoclasts were produced from human CD14+ cells. ADSCs were generated and added to cultures with different ratios with CD11b+ cells. Transwell and antibody blockade experiments were performed to define the mechanism of action. NF-κB and RANKL expression were determined by Western blotting and RT-qPCR. About 2 × 106 ADSCs or fibroblast cells were adoptively transferred to DBA1/J mice on day 14 after immunization with type II collagen/complete Freund's adjuvant (CII/CFA) while the onset and severity of the CIA were monitored. Adipose-derived mesenchymal stromal cells but not fibroblast cells completely suppressed osteoclastogenesis in vitro for human and mice. ADSCs injected after immunization and before of onset of CIA significantly suppressed disease development. Treatment with ADSCs dramatically decreased the levels of NF-κB p65/p50 in osteoclasts in vitro and P65/50 and RANKL expression by synovial tissues in vivo. We have demonstrated that ADSCs can inhibit RANKL-induced osteoclasts genesis via CD39 signals. Our findings also suggest that ADSCs can inhibit osteoclasts genesis without the involvement of regulatory T cells. ADSCs might represent a promising strategy for stem cell-based therapies for RA. Thus, manipulation of ADSCs may have therapeutic effects on RA and other bone erosion–related diseases. 相似文献