Deaths from suicides, drug poisonings, and alcohol-related diseases (‘deaths of despair’) are well-documented among working-age Americans, and have been hypothesized to be largely specific to the U.S. However, support for this assertion–and associated policies to reduce premature mortality–requires tests concerning these deaths in other industrialized countries, with different institutional contexts. We tested whether the concentration and accumulation of health and social disadvantage forecasts deaths of despair, in New Zealand and Denmark.

We used nationwide administrative data. Our observation period was 10 years (NZ = July 2006–June 2016, Denmark = January 2007–December 2016). We identified all NZ-born and Danish-born individuals aged 25–64 in the last observation year (NZ = 1 555 902, Denmark = 2 541 758). We ascertained measures of disadvantage (public-hospital stays for physical- and mental-health difficulties, social-welfare benefit-use, and criminal convictions) across the first nine years. We ascertained deaths from suicide, drugs, alcohol, and all other causes in the last year.

Deaths of despair clustered within a population segment that disproportionately experienced multiple disadvantages. In both countries, individuals in the top 5% of the population in multiple health- and social-service sectors were at elevated risk for deaths from suicide, drugs, and alcohol, and deaths from other causes. Associations were evident across sex and age.

Deaths of despair are a marker of inequalities in countries beyond the U.S. with robust social-safety nets, nationwide healthcare, and strong pharmaceutical regulations. These deaths cluster within a highly disadvantaged population segment identifiable within health- and social-service systems.

Startup companies in the healthcare sector often fail because they lack sufficient entrepreneurial, regulatory, and business development expertise. Maturity models provide useful frameworks to assess the state of business elements more systematically than heuristic assessments. However, previous models were developed primarily to characterize the business state of larger nonmedical companies. A maturity index designed specifically for startup companies in the medical product sector could help to identify areas in which targeted interventions could assist business development.

A novel MedTech Startup Maturity Index (SMI) was developed by a collaborative team of academic and industry experts and refined through feedback from external stakeholders. Pediatric medical device startups associated with the West Coast Consortium for Technology & Innovation in Pediatrics (CTIP) were scored and ranked according to the SMI following semi-structured interviews. The CTIP executive team independently ranked the maturity of each company based on their extensive experiences with the same companies.

SMI scores for 16 companies ranged from 1.2 to 3.8 out of 4. These scores were well aligned with heuristic CTIP rankings for 14 out of 16 companies, reflected by strong correlations between the two datasets (Spearman’s rho = 0.721, P = 0.002, and Kendall’s tau-b = 0.526, P = 0.006).

The SMI yields maturity scores that correlate well with expert rankings but can be assessed without prior company knowledge and can identify specific areas of concern more systematically. Further research is required to generalize and validate the SMI as a pre-/post-evaluation tool.

Barriers to research participation by racial and ethnic minority group members are multi-factorial, stem from historical social injustices and occur at participant, research team, and research process levels. The informed consent procedure is a key component of the research process and represents an opportunity to address these barriers. This manuscript describes the development of the Strengthening Translational Research in Diverse Enrollment (STRIDE) intervention, which aims to improve research participation by individuals from underrepresented groups.

We used a community-engaged approach to develop an integrated, culturally, and literacy-sensitive, multi-component intervention that addresses barriers to research participation during the informed consent process. This approach involved having Community Investigators participate in intervention development activities and using community engagement studios and other methods to get feedback from community members on intervention components.

The STRIDE intervention has three components: a simulation-based training program directed toward clinical study research assistants that emphasizes cultural competency and communication skills for assisting in the informed consent process, an electronic consent (eConsent) framework designed to improve health-related research material comprehension and relevance, and a “storytelling” intervention in which prior research participants from diverse backgrounds share their experiences delivered via video vignettes during the consent process.

The community engaged development approach resulted in a multi-component intervention that addresses known barriers to research participation and can be integrated into the consent process of research studies. Results of an ongoing study will determine its effectiveness at increasing diversity among research participants.

Smoking prevalence is higher amongst individuals with schizophrenia and depression compared with the general population. Mendelian randomisation (MR) can examine whether this association is causal using genetic variants identified in genome-wide association studies (GWAS).

We conducted two-sample MR to explore the bi-directional effects of smoking on schizophrenia and depression. For smoking behaviour, we used (1) smoking initiation GWAS from the GSCAN consortium and (2) we conducted our own GWAS of lifetime smoking behaviour (which captures smoking duration, heaviness and cessation) in a sample of 462690 individuals from the UK Biobank. We validated this instrument using positive control outcomes (e.g. lung cancer). For schizophrenia and depression we used GWAS from the PGC consortium.

There was strong evidence to suggest smoking is a risk factor for both schizophrenia (odds ratio (OR) 2.27, 95% confidence interval (CI) 1.67–3.08, p < 0.001) and depression (OR 1.99, 95% CI 1.71–2.32, p < 0.001). Results were consistent across both lifetime smoking and smoking initiation. We found some evidence that genetic liability to depression increases smoking (β = 0.091, 95% CI 0.027–0.155, p = 0.005) but evidence was mixed for schizophrenia (β = 0.022, 95% CI 0.005–0.038, p = 0.009) with very weak evidence for an effect on smoking initiation.

These findings suggest that the association between smoking, schizophrenia and depression is due, at least in part, to a causal effect of smoking, providing further evidence for the detrimental consequences of smoking on mental health.

Prior research has documented shared heritable contributions to non-suicidal self-injury (NSSI) and suicidal ideation (SI) as well as NSSI and suicide attempt (SA). In addition, trauma exposure has been implicated in risk for NSSI and suicide. Genetically informative studies are needed to determine common sources of liability to all three self-injurious thoughts and behaviors, and to clarify the nature of their associations with traumatic experiences.

Multivariate biometric modeling was conducted using data from 9526 twins [59% female, mean age = 31.7 years (range 24–42)] from two cohorts of the Australian Twin Registry, some of whom also participated in the Childhood Trauma Study and the Nicotine Addiction Genetics Project.

The prevalences of high-risk trauma exposure (HRT), NSSI, SI, and SA were 24.4, 5.6, 27.1, and 4.6%, respectively. All phenotypes were moderately to highly correlated. Genetic influences on self-injurious thoughts and behaviors and HRT were significant and highly correlated among men [rG = 0.59, 95% confidence interval (CI) (0.37–0.81)] and women [rG = 0.56 (0.49–0.63)]. Unique environmental influences were modestly correlated in women [rE = 0.23 (0.01–0.45)], suggesting that high-risk trauma may confer some direct risk for self-injurious thoughts and behaviors among females.

Individuals engaging in NSSI are at increased risk for suicide, and common heritable factors contribute to these associations. Preventing trauma exposure may help to mitigate risk for self-harm and suicide, either directly or indirectly via reductions in liability to psychopathology more broadly. In addition, targeting pre-existing vulnerability factors could significantly reduce risk for life-threatening behaviors among those who have experienced trauma.

Mental health disorders commonly co-occur, even between conceptually distinct syndromes, such as internalizing and externalizing disorders. The current study investigated whether phenotypic, genetic, and environmental variance in negative emotionality and behavioral control account for the covariation between major depressive disorder (MDD) and alcohol use disorder (AUD).

A total of 3623 members of a national twin registry were administered structured diagnostic telephone interviews that included assessments of lifetime histories of MDD and AUD, and were mailed self-report personality questionnaires that assessed stress reactivity (SR) and behavioral control (CON). A series of biometric models were fitted to partition the proportion of covariance between MDD and AUD into SR and CON.

A statistically significant proportion of the correlation between MDD and AUD was due to variance specific to SR (men = 0.31, women = 0.27) and CON (men = 0.20, women = 0.19). Further, genetic factors explained a large proportion of this correlation (0.63), with unique environmental factors explaining the rest. SR explained a significant proportion of the genetic (0.33) and environmental (0.23) overlap between MDD and AUD. In contrast, variance specific to CON accounted for genetic overlap (0.32), but not environmental overlap (0.004). In total, SR and CON accounted for approximately 70% of the genetic and 20% of the environmental covariation between MDD and AUD.

This is the first study to demonstrate that negative emotionality and behavioral control confer risk for the co-occurrence of MDD and AUD via genetic factors. These findings are consistent with the aims of NIMH's RDoC proposal to elucidate how transdiagnostic risk factors drive psychopathology.

Catheter-related bloodstream infections (CRBSIs) account for the majority of hemodialysis-related infections. There are no published data on the efficacy of the chlorhexidine-impregnated foam dressing at reducing the rate of CRBSI among patients undergoing hemodialysis.

A prospective, nonblinded, crossover intervention trial to determine the efficacy of a chlorhexidine-impregnated foam dressing to reduce the rate of CRBSI among patients undergoing hemodialysis.

Two outpatient dialysis centers.

A total of 121 patients who underwent dialysis through tunneled central venous catheters received the intervention during the trial.

The primary outcome of interest was the incidence of CRBSI. A nested cohort study of all patients who received the chlorhexidine-impregnated foam dressing was also conducted. Backward stepwise logistic regression analysis was used to determine independent risk factors for development of CRBSI.

Thirty-seven CRBSIs occurred in the intervention group, for an incidence of 6.3 CRBSIs per 1,000 dialysis sessions, and 30 CRBSIs occurred in the control group, an incidence of 5.2 CRBSIs per 1,000 dialysis sessions (risk ratio, 1.22 [95% confidence interval {CI}, 0.75-1.97]; P = .46). The chlorhexidine-impregnated foam dressing was well tolerated, with only 2 patients (<2%) experiencing dermatitis that led to its discontinuation. The only independent risk factor for development of CRBSI was dialysis treatment at one dialysis center (adjusted odds ratio, 4.4 [95% CI, 1.77-13.65]; P = .002). Age of at least 60 years (adjusted odds ratio, 0.28 [95% CI, 0.09-0.82]; P = .02) was associated with lower risk of CRBSI.

The use of a chlorhexidine-impregnated foam dressing did not decrease the incidence of CRBSI among patients with tunneled central venous catheters who were undergoing hemodialysis.

Staphylococcus aureus is an important cause of infection in intensive care unit (ICU) patients. Colonization with methicillin-resistant S. aureus (MRSA) is a risk factor for subsequent S. aureus infection. However, MRSA-colonized patients may have more comorbidities than methicillin-susceptible S. aureus (MSSA)-colonized or noncolonized patients and therefore may be more susceptible to infection on that basis.

To determine whether MRSA-colonized patients who are admitted to medical and surgical ICUs are more likely to develop any S. aureus infection in the ICU, compared with patients colonized with MSSA or not colonized with S. aureus, independent of predisposing patient risk factors.

Prospective cohort study.

A 24-bed surgical ICU and a 19-bed medical ICU of a 1,252-bed, academic hospital.

A total of 9,523 patients for whom nasal swab samples were cultured for S. aureus at ICU admission during the period from December 2002 through August 2007.

Patients in the ICU for more than 48 hours were examined for an ICU-acquired S. aureus infection, defined as development of S. aureus infection more than 48 hours after ICU admission.

S. aureus colonization was present at admission for 1,433 (27.8%) of 5,161 patients (674 [47.0%] with MRSA and 759 [53.0%] with MSSA). An ICU-acquired S. aureus infection developed in 113 (2.19%) patients, of whom 75 (66.4%) had an infection due to MRSA. Risk factors associated with an ICU-acquired S. aureus infection included MRSA colonization at admission (adjusted hazard ratio, 4.70 [95% confidence interval, 3.07-7.21]) and MSSA colonization at admission (adjusted hazard ratio, 2.47 [95% confidence interval, 1.52-4.01]).

ICU patients colonized with S. aureus were at greater risk of developing a S. aureus infection in the ICU. Even after adjusting for patient-specific risk factors, MRSA-colonized patients were more likely to develop S. aureus infection, compared with MSSA-colonized or noncolonized patients.