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Background: Critical illness is likely associated with an increased risk of dementia, but the magnitude remains uncertain.Methods: The cohort was a random 2.5% sample of Medicare beneficiaries who received intensive care in 2005 and survived to hospital discharge. Patients were matched with general population controls (age, sex, and race) with 3 yr of follow-up. The authors used an extended Cox model to assess the risk of a diagnosis of dementia, adjusting for the known risk factors for dementia, and the competing risk of death.Results: Among 10,348 intensive care patients who survived to hospital discharge, dementia was newly diagnosed in 1,648 (15.0%) over the 3 yr of follow-up versus 12.2% in controls (incidence per 1,000 person-years, 73.6; 95% CI, 70.0 to 77.1 vs. 45.8; 95% CI, 43.2 to 48.3; hazard ratio [HR], 1.61; 95% CI, 1.50 to 1.74; P < 0.001). After accounting for the known risk factors in the year before the index hospitalization, the risk of receiving a diagnosis of dementia remained increased in patients who received intensive care (adjusted HR, 1.43; 95% CI, 1.32 to 1.54; P < 0.001). Inclusion of identifiable risk factors accrued during the quarter of critical illness accounted for almost all of the increased risks (adjusted HR, 1.09; 95% CI, 1.00 to 1.20; P = 0.06).Conclusions: Elderly critical care survivors have a 60% increased relative risk, but only 3% increased absolute risk, of receiving a diagnosis of dementia in the subsequent 3 yr compared with the general population. This increased risk is not accounted for by risk factors preexisting the critical illness. Surveillance bias, which increases the likelihood of receiving a diagnosis of dementia, could account for some or all of these additional risks. [ABSTRACT FROM AUTHOR]

Objectives: Preventing rehospitalizations for patients with serious chronic illnesses is a focus of national quality initiatives. Although 8 million people are admitted yearly to an ICU, the frequency of rehospitalizations (readmissions to the hospital after discharge) is unknown. We sought to determine the frequency of rehospitalization after an ICU stay, outcomes for rehospitalized patients, and factors associated with rehospitalization. Design: Retrospective cohort study using the New York Statewide Planning and Research Cooperative System, an administrative database of all hospital discharges in New York State. Setting: ICUs in New York State. Patients: ICU patients who survived to hospital discharge in 2008-2010. Interventions: None. Measurements and Main Results: Primary outcome was the cumulative incidence of first early rehospitalization (within 30 days of discharge), and secondary outcome was the cumulative incidence of late rehospitalization (between 31 and 180 d). Factors associated with rehospitalization within both time periods were identified using competing risk regression models. Of 492,653 ICU patients, 79,960 had a first early rehospitalization (cumulative incidence, 16.2%) and an additional 73,250 late rehospitalizations (cumulative incidence, 18.9%). Over one quarter of all rehospitalizations (28.6% for early; 26.7% for late) involved ICU admission. Overall hospital mortality for rehospitalized patients was 7.6% for early and 4.6% for late rehospitalizations. Longer index hospitalization (adjusted hazard ratio, 1.61; 95% CI, 1.57-1.66 for 7-13 d vs < 3 d), discharge to a skilled nursing facility versus home (adjusted hazard ratio, 1.54; 95% CI, 1.51-1.58), and having metastatic cancer (adjusted hazard ratio, 1.46; 95% CI, 1.41-1.51) were associated with the greatest hazard of early rehospitalization. Conclusions: Approximately 16% of ICU survivors were rehospitalized within 30 days of hospital discharge; rehospitalized patients had high rates of ICU admission and hospital mortality. Few characteristics were strongly associated with rehospitalization, suggesting that identifying high-risk individuals for intervention may require additional predictors beyond what is available in administrative databases. [ABSTRACT FROM AUTHOR]

Background: Although use of mechanical circulatory support is increasing, it is unclear how providing such care affects clinicians' moral distress., Objective: To measure moral distress among intensive care unit clinicians who commonly care for patients receiving mechanical circulatory support., Methods: In this prospective study, the Moral Distress Scale-Revised was administered to physicians, nurses, and advanced practice providers from 2 intensive care units in an academic medical center. Linear regression was used to assess whether moral distress was associated with clinician type, burnout, or desire to leave one's job. Clinicians' likelihood of reporting frequent moral distress when caring for patients receiving mechanical circulatory support vs other critically ill patients also was assessed., Results: The sample comprised 102 clinicians who had a mean (SD) score of 100.5 (51.6) on the Moral Distress Scale- Revised. After adjustment for clinician characteristics, moral distress was significantly higher in registered nurses than physicians/advanced practice providers (115.9 vs 71.0, P < .001), clinicians reporting burnout vs those who did not (114.7 vs 83.1, P = .003), and those considering leaving vs those who were not (121.1 vs 89.2, P = .001). Clinicians were more likely to report experiencing frequent moral distress when caring for patients receiving mechanical circulatory support (26.5%) than when caring for patients needing routine care (10.8%; P = .004), but less likely than when caring for patients with either chronic critical illness (57.8%) or multisystem organ failure (56.9%; both P < .001)., Conclusion: Moral distress was high among clinicians who commonly care for patients receiving mechanical circulatory support, suggesting that use of this therapy may affect well-being among intensive care unit clinicians., (©2021 American Association of Critical-Care Nurses.)

Chemotherapy efficacy is limited by intrinsic and acquired resistance in glioblastoma (GBM); hence, novel tactics are crucial. Survivin has been demonstrated as a key resistant factor in GBM because of its function in inhibiting apoptosis, regulating autophagy, and in promoting G₂/M cell cycle transition. Parthenolide has been reported to be an effective antitumor agent in a variety of tumor cells and decreases survivin level in leukemia cells. But the effect of parthenolide on survivin and the cell death process in GBM is still unknown. The aim of this study was to examine whether parthenolide had the potential to inhibit cell proliferation in the GBM cell line U373. The parthenolide-induced effects in relation to survivin suppression and cell death were further investigated. Our results showed that parthenolide substantially inhibited cell viability with IC₅₀ values of approximate 16 μM. Treatment with parthenolide at the dose of 16 μM led to considerable downregulation of survivin, G₂/M cell cycle arrest and Chk2 upregulation in cells. Parthenolide induced apoptosis in only a few cells and a slight increase in activated caspases 3 levels. By contrast, parthenolide induced a significant increase of intracellular autophagosomes and the expression of autophagy related proteins, including ULK1 and LC3 I/LC3 II, in the treated cells. These results suggested that parthenolide induced survivin inhibition, G₂/M cell cycle arrest, and triggered cell death through autophagic cell death in the GBM cell line.

Microwave radiations can be encountered regularly in daily lives. When WHO announced that microwave radiations were a kind of environmental energy which interfere with the physiological functions of the human body, great concerns have been raised over the damages microwave frequencies can do to human physiology. The immunological performance and the activities of the cellular inflammatory factor NFκB have been closely related in monocyte. Due to the effect of phorbol 12-myristate 13-acetate (PMA) on THP-1 monocytes, THP-1 monocytes would differentiate into macrophages and would then react with lipopolysaccharides (LPS), and the amount of NFκB increased in the THP-1 monocytes. Expression of cytokine is affected when cells are exposed to a frequency of 2450 MHz and at 900 W. Thus, in our experiments, an observation was made when THP-1 monocytes were stimulated with PMA and LPS to differentiate into macrophage, the amount of NFκB in cells increased exponentially, and the levels of NFκB expression were decreased by the exposure of microwave radiation. In conclusion, microwave radiations were found to inhibit the activity functions of THP-1 monocytes stimulated with PMA and LPS.