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Background and aim Personality functioning is predictive of drug misuse and relapse, yet little is known about the role of personality in engagement with the treatment process. This study aimed to estimate the extent to which broad‐ and facet‐level characteristic adaptations contribute to or hinder treatment engagement, while controlling for psychosocial indicators. Design Multi‐site cross‐sectional survey. Setting In‐patient treatment units covering 80% of residential treatment entries in Greece. Participants A total of 338 service users, 287 (84.9%) male, 51 (15.1%) female, average age 33.4 years. Measurements Expressions of personality functioning (characteristic adaptations) were assessed using the Severity Indices of Personality Problems (SIPP‐118). Treatment engagement was measured using the Client Evaluation of Self and Treatment, in‐patient version (CEST). Findings Dysfunctional levels of relational capacities predicted counselling rapport [β = 1.50, 95% confidence interval (CI) = 0.326–2.69, P = 0.013], treatment participation (β = 2.09, 95% CI = 1.15–3.11, P < 0.001) and treatment satisfaction (β = 1.65, 95% CI = 0.735–2.57, P < 0.001). Counselling rapport was also predicted by dysfunctional levels in self‐control (β = 1.78, 95% CI = 0.899–2.67, P < 0.001), self‐reflective functioning at the facet‐level (β = 2.24, 95% CI = 1.01–3.46, P < 0.001) and aggression regulation (β = 1.43, 95% CI = 0.438–2.42, P = 0.005). Dysfunctional levels on social concordance (β = −1.90, 95% CI = −2.87 to –0.941, P = 0.001), emotional regulation (β = 1.90, 95% CI = 0.87–2.92, P < 0.001) and intimacy (β = 2.04, 95% CI = 1.31–3.05, P < 0.001) were significant predictors of treatment participation. Treatment readiness and desire for help predicted treatment engagement. Conclusions In people attending substance use treatment services, maladaptive interpersonal patterns and relational intimacy, emotional dysregulation and impulse control may be associated with low levels of counselling rapport and treatment participation. Low frustration tolerance and aggressive impulses also appeared to predict low participation.

To investigate the association between cannabis smoking and lung cancer risk, data on 2,159 lung cancer cases and 2,985 controls were pooled from 6 case-control studies in the US, Canada, UK, and New Zealand within the International Lung Cancer Consortium. Study-specific associations between cannabis smoking and lung cancer were estimated using unconditional logistic regression adjusting for sociodemographic factors, tobacco smoking status and pack-years; odds-ratio estimates were pooled using random effects models. Subgroup analyses were done for sex, histology and tobacco smoking status. The shapes of dose-response associations were examined using restricted cubic spline regression. The overall pooled OR for habitual versus nonhabitual or never users was 0.96 (95% CI: 0.66-1.38). Compared to nonhabitual or never users, the summary OR was 0.88 (95%CI: 0.63-1.24) for individuals who smoked 1 or more joint-equivalents of cannabis per day and 0.94 (95%CI: 0.67-1.32) for those consumed at least 10 joint-years. For adenocarcinoma cases the ORs were 1.73 (95%CI: 0.75-4.00) and 1.74 (95%CI: 0.85-3.55), respectively. However, no association was found for the squamous cell carcinoma based on small numbers. Weak associations between cannabis smoking and lung cancer were observed in never tobacco smokers. Spline modeling indicated a weak positive monotonic association between cumulative cannabis use and lung cancer, but precision was low at high exposure levels. Results from our pooled analyses provide little evidence for an increased risk of lung cancer among habitual or long-term cannabis smokers, although the possibility of potential adverse effect for heavy consumption cannot be excluded.

Objective There is increasing evidence to indicate that genetic factors contribute significantly to radiologic joint damage in rheumatoid arthritis (RA). The aim of the present study was to determine whether genotypes of 10 recently identified RA susceptibility loci are associated with radiologic severity. Methods A 2-stage study was performed using 3 Northern European RA populations: a British cross-sectional population (discovery cohort; n = 885) and the Leiden Early Arthritis Clinic (EAC) cohort (n = 581) and Yorkshire Early Arthritis Register (YEAR) cohort (n = 418) (validation cohorts). Radiologic damage was assessed using a modified Larsen method for scoring radiographs (in the discovery cohort) or modified Sharp/van der Heijde score (in the 2 validation cohorts). A meta-analysis was performed to bring together the evidence from the 3 studies, using data on radiologic severity of joint damage from a single time point. Results An allele-dose association of rs26232 was present in the discovery population (P = 4 × 10−4); the median modified Larsen scores of radiologic joint damage per genotype were 31 (for those with CC), 27 (for those with CT), and 16 (for those with TT). The allele-dose association of rs26232 was replicated in both the Leiden EAC cohort during the initial 7 years of RA (P = 0.04) and the YEAR cohort (P = 0.039). In a fixed-effects meta-analysis of all 3 studies, the per T allele effect on the ratio of radiologic severity scores was 0.90 (95% confidence interval 0.84, 0.96; P = 0.004). Conclusion The variant rs26232, in the first intron of the C5orf30 locus, is associated with the severity of radiologic damage in RA and is independent of established prognostic biomarkers. The biologic activities of C5orf30 are unknown, but our genetic data suggest that it is involved in mediating joint damage in RA.

The cancer experience among 754 first-degree relatives (mothers, fathers, and siblings) of a population-based series of 177 children with soft tissue sarcoma is reported. the current study represents an extension of our earlier work in which the authors found an excess of breast cancer in the mothers of 143 of these children. There were 40 cancers among all first-degree relatives, compared with 24.82 expected (relative risk [RR] 1.61, P = 0.006). There was no excess in fathers, but an excess of borderline significance was seen in mothers (RR 1.67, P = 0.0545), and a significant excess in siblings (RR 4.55, P = 0.0002), mainly due to carcinoma of the breast and pediatric tumors. Results of a step forward Cox multivariate analysis identified three variables in the index child which were independently associated with high cancer risk in relatives, as follows: age younger than 24 months at diagnosis; histologic type, embryonal rhabdomyosarcoma or other and unspecified soft tissue sarcoma; and male sex. It was possible, therefore, to identify a subgroup of children whose relatives are at high risk of early onset cancer (RR in this group 10.14). the pattern of cancers is consistent with the Li-Fraumeni syndrome. the authors conclude that a marked proportion of childhood soft tissue sarcoma has a genetic basis.