Regardless of alteplase dose received, lacunar AIS participants had favorable functional (mRS 2-6, adjusted odds ratio [95% confidence interval] 0.60 [0.47-0.77]) and other clinical or safety outcomes compared to participants with nonlacunar AIS. Low-dose alteplase (versus standard) had no differential effect on functional outcomes (mRS 2-6, 1.04 [0.87-1.24]) but reduced the risk of symptomatic ICH in all included participants. There were no differential treatment effects of low- vs standard-dose alteplase on all outcomes across lacunar and nonlacunar AIS (all 
  
  ≥0.07).
 
  We found no evidence from the ENCHANTED trial that low-dose alteplase had any advantages over standard dose for definite/probable lacunar AIS.
 
  This study provides Class II evidence that for patients with lacunar AIS, low-dose alteplase had no additional benefit or safety over standard-dose alteplase.
 
  Clinicaltrials.gov identifier NCT01422616.
 Clinicaltrials.gov identifier NCT01422616.
  To determine the association of dementia-related psychosis (DRP) with death and use of long-term care (LTC); we hypothesized that DRP would be associated with increased risk of death and use of LTC in patients with dementia.
 
  A retrospective cohort study was performed. Medicare claims from 2008 to 2016 were used to define cohorts of patients with dementia and DRP. Outcomes were LTC, defined as nursing home stays of >100 consecutive days, and death. Patients with DRP were directly matched to patients with dementia without psychosis by age, sex, race, number of comorbid conditions, and dementia index year. Association of DRP with outcomes was evaluated using a Cox proportional hazard regression model.
 
  We identified 256,408 patients with dementia. Within 2 years after the dementia index date, 13.9% of patients developed DRP and 31.9% had died. Corresponding estimates at 5 years were 25.5% and 64.0%. Mean age differed little between those who developed DRP (83.8 ± 7.9 years) and those who did not (83.1 ± 8.7 years). Patients with DRP were slightly more likely to be female (71.0% vs 68.3%) and white (85.7% vs 82.0%). Within 2 years of developing DRP, 16.1% entered LTC and 52.0% died; corresponding percentages for patients without DRP were 8.4% and 30.0%, respectively. In the matched cohort, DRP was associated with greater risk of LTC (hazard ratio [HR] 2.36, 2.29-2.44) and death (HR 2.06, 2.02-2.10).
 
  DRP was associated with a more than doubling in the risk of death and a nearly 2.5-fold increase in risk of the need for LTC.
 DRP was associated with a more than doubling in the risk of death and a nearly 2.5-fold increase in risk of the need for LTC.Genetically identical cells in a tissue can respond differently to perturbations in their environment or "stress." Such stresses can be physicochemical, mechanical, or infectious or may come from competition with other cells in the tissue. Here, I discuss how the varying responses to stress influence the decision of a cell to repair or die, and how one cell's response can have effects on surrounding cells. Such responses control the health and fitness of single cells and how they compete with other genetically identical cells.See related article on p. 129.Inhibitory killer cell immunoglobulin-like receptors (iKIR) tolerize natural killer cells and some T cells upon detecting classical HLA class I molecules. In this issue, Bhatt and colleagues identify the B7 family member HHLA2 as an unanticipated ligand for a peculiar iKIR family member, KIR3DL3. These data establish a new inhibitory checkpoint pathway that may protect HHLA2+ tumor cells from immune attack.See article by Bhatt et al., p. 156.Acute respiratory distress syndrome (ARDS) is a devastating critical illness that can be triggered by a wide range of insults and remains associated with a high mortality of around 40%. The search for targeted treatment for ARDS has been disappointing, possibly due to the enormous heterogeneity within the syndrome. In this perspective from the European Respiratory Society research seminar on "Precision medicine in ARDS", we will summarise the current evidence for heterogeneity, explore the evidence in favour of precision medicine and provide a roadmap for further research in ARDS. There is evident variation in the presentation of ARDS on three distinct levels 1) aetiological; 2) physiological and 3) biological, which leads us to the conclusion that there is no typical ARDS. The lack of a common presentation implies that intervention studies in patients with ARDS need to be phenotype aware and apply a precision medicine approach in order to avoid the lack of success in therapeutic trials that we faced in recent decades.  https://www.selleckchem.com/products/gpr84-antagonist-8.html  Deeper phenotyping and integrative analysis of the sources of variation might result in identification of additional treatable traits that represent specific pathobiological mechanisms, or so-called endotypes.
  Globally, radon is the leading risk factor for lung cancer in never-smokers (LCINS). In this study, we systematically reviewed and meta-analysed the evidence of the risk of LCINS associated with residential radon exposure.
 
  Medline and Embase databases were searched using predefined inclusion and exclusion criteria to identify relevant studies published from 1 January 1990 to 5 March 2020 focused on never-smokers. We identified four pooled collaborative studies (incorporating data from 24 case-control studies), one case-control study and one cohort study for systematic review. Meta-analysis was performed on the results of the four pooled studies due to different measures of effect and outcome reported in the cohort study and insufficient information reported for the case-control study. In a 
  analysis, the corresponding risk for ever-smokers was also examined.
 
  Risk estimates of lung cancer from residential radon exposure were pooled in the meta-analysis for 2341 never-smoker cases, 8967 never-smoker controls, 9937 ever-smoker cases and 12 463 ever-smoker controls. Adjusted excess relative risks (aERRs) per 100 Bq·m
  of radon level were 0.15 (95% CI 0.06-0.25) for never-smokers and 0.09 (95% CI 0.03-0.16) for ever-smokers, and the difference between them was statistically insignificant (p=0.32). The aERR per 100 Bq·m
  was higher for men (0.46; 95% CI 0.15-0.76) than for women (0.09; 95% CI -0.02-0.20) among never-smokers (p=0.027).
 
  This study provided quantified risk estimates for lung cancer from residential radon exposure among both never-smokers and ever-smokers. Among never-smokers in radon-prone areas, men were at higher risk of lung cancer than women.
 This study provided quantified risk estimates for lung cancer from residential radon exposure among both never-smokers and ever-smokers. Among never-smokers in radon-prone areas, men were at higher risk of lung cancer than women.