Abstract Background The coronavirus disease 2019 (COVID-19) pandemic and associated lockdown could be considered a ‘perfect storm’ for increases in emotional distress. Such increases can only be identified by studies that use data collected before and during the pandemic. Longitudinal data are also needed to examine (1) the roles of previous distress and stressors in emotional distress during the pandemic and (2) how COVID-19-related stressors and coping strategies are associated with emotional distress when pre-pandemic distress is accounted for. Methods Data came from a cohort study (N = 768). Emotional distress (perceived stress, internalizing symptoms, and anger), COVID-19-related stressors, and coping strategies were measured during the pandemic/lockdown when participants were aged 22. Previous distress and stressors were measured before COVID-19 (at age 20). Results On average, participants showed increased levels of perceived stress and anger (but not internalizing symptoms) during the pandemic compared to before. Pre-COVID-19 emotional distress was the strongest predictor of during-pandemic emotional distress, followed by during-pandemic economic and psychosocial stressors (e.g. lifestyle and economic disruptions) and hopelessness, and pre-pandemic social stressors (e.g. bullying victimization and stressful life events). Most health risks to self or loved ones due to COVID-19 were not uniquely associated with emotional distress in final models. Coping strategies associated with reduced distress included keeping a daily routine, physical activity, and positive reappraisal/reframing. Conclusions In our community sample, pre-pandemic distress, secondary consequences of the pandemic (e.g. lifestyle and economic disruptions), and pre-pandemic social stressors were more consistently associated with young adults' emotional distress than COVID-19-related health risk exposures.

Rationale Adolescents and young adults were identified internationally as a group with potentially low compliance rates with public health measures aimed at curbing the spread of coronavirus disease 2019 (COVID-19). Although non-compliance research during pandemics has typically focused on concurrent correlates, less is known about how prior social and psychological risk factors are associated with non-compliance during pandemics. Objective This paper leverages a prospective-longitudinal cohort study with data before and during the pandemic to describe patterns of non-compliance with COVID- 19 related public health measures in young adults and to identify which characteristics increase the risk of non-compliance. Methods Data came from an ongoing cohort study in Zurich, Switzerland (n=737). Non-compliance with public health measures and concurrent correlates were measured at age 22. Antecedent sociodemographic, social, and psychological factors were measured at ages 15-20. Young adults generally complied with COVID-19 public health measures, although non-compliance with some measures (e.g., cleaning/disinfecting mobile phones, standing 1.5-2 meters apart) was relatively higher. Results Non-compliance, especially with hygiene-related measures, was more prevalent in males, and in individuals with higher education, higher SES, and a nonmigrant background. Non-compliance was higher in young adults who had previously scored high on indicators of “antisocial potential,” including low acceptance of moral rules, pre-pandemic legal cynicism, low shame/guilt, low self-control, engagement in delinquent behaviors, and association with delinquent peers. Young adults with low trust, including in the government’s measures for fighting the virus, also complied less. Conclusions In order to increase voluntary compliance with COVID-19 measures, public health campaigns should implement strategies that foster moral obligation and trust in authorities, or leverage trustworthy individuals in the community to disseminate information. For young adults with low self-control, self-monitoring, environmental restructuring, or nudging may increase compliance. Long-term investments into integrating youth with antisocial potential into society may decrease rule-breaking behaviors, including during pandemics when compliance saves lives.

Two seemingly-associated demographic trends have generated considerable interest: income stagnation and rising premature mortality from suicides, drug poisoning, and alcoholic liver disease among U.S. white non-Hispanics with low education. Economists interpret these population-level trends to indicate that despair, induced by financial stressors, is a shared pathway to these causes of death. Although we now have the catchy term “deaths of despair” (DoD), we have yet to study its central empirical claim: that conceptually defined and empirically assessed “despair” is indeed a common pathway to several causes of death. At the level of the person, despair comprises cognitive, emotional, behavioral, and biological domains. Despair can also permeate social relationships, networks, institutions, and communities. Extant longitudinal datasets feature repeated measures of despair—before, during, and after the Great Recession—offering resources to test the role of economic decline-induced despair in premature morbidity/mortality. Such tests must also focus on protective factors that could shield individuals. DoD is more than a phrase; it is a hypothesis that deserves conceptual mapping and empirical study with longitudinal, multi-level data.

Adolescent self-injury is a widespread public health problem, but long-term longitudinal studies from European countries are rare. Self-injury in males and sex differences are poorly understood. This study describes the prevalence, frequency, agerelated course, and recurrence of, and mental health services use related to adolescent self-injury. Data came from a Swiss prospective-longitudinal cohort study (N = 1482). Adolescents (52% male) reported frequency of self-injury and mental health services use (including reasons for and types of services use, hospitalizations) at ages 13, 15, 17, and 20. Between ages 13-20, 27% of adolescents reported self-injury at least once. In males, prevalence decreased from 12 to 5%; in females self-injury peaked at age 15 (16%) and then decreased (11% at age 20). In males, recurrence of self-injury increased after age 15 (from odds ratio [OR] < 3 to OR > 10); in females, recurrence was high from age 13 onwards (OR > 5). Predictors of recurrence included childhood/early adolescent internalizing symptoms and early self-injury onset. Typically, less than half of adolescents with self-injury used mental health services. Males with self-injury used services mainly for externalizing problems, learning difficulties, and attention/concentration problems; females for depression or self-injury, family problems, and victimization. Types of services used changed with age, and adolescents with self-injury had increased rates of hospitalization. There are notable sex differences in the longitudinal course of self-injury and reasons for related mental health services use. Treating early internalizing symptoms could be a promising target for preventing recurrent self-injury. Males are at particular risk of not receiving adequate treatment for self-injury.

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Macrophage migration inhibitory factor (MIF) was originally described as a T-cell-derived lymphokine with the potential to inhibit the random migration of macrophages. However, recent reports have shown a much broader tissue distribution, including the skin. Functionally, MIF appears to act as an antagonist of anti-inflammatory glucocorticoid action. To elucidate the role of MIF in inflammatory skin diseases, we investigated the production and localization of this cytokine in human skin of patients with psoriasis by means of reverse transcription-polymerase chain reaction, immunohistochemistry and Western blot analysis. In normal skin, our results showed a moderate but homogeneous MIF immunoreactivity in all epidermal layers. Endothelial cells and the outer root sheath of hair follicles were also positive for MIF. In lesional psoriatic human skin, a significant increase in MIF immunoreactivity was visible in suprabasal keratinocytes, especially of the spinous layer. In addition, endothelial cells also showed increased immunolabelling for MIF in psoriatic lesions, indicating a cell-specific upregulation of this mediator in untreated psoriasis. Western blot analysis also revealed a clear increase in MIF in homogenates of lesional skin from psoriasis patients. These results suggest a role for MIF in the inflammatory skin disease psoriasis.

The genetic background of extranodal marginal zone B-cell non-Hodgkin's lymphoma (NHL) of mucosa-associated lymphoid tissue (MALT) type is poorly understood. In contrast to most entities of primary nodal lymphomas, few cytogenetic data are available, and gene rearrangements frequently encountered in and highly characteristic of certain entities of systemic NHL are absent in this type of lymphoma. Recently, it was suggested that MALT-type NHLs are associated with certain numerical chromosome aberrations and especially with trisomy 3. We performed an extensive study using a sensitive double (bicolor) fluorescence in situ hybridization technique for the analysis of trisomies for chromosomes 3, 7, 12, and 18 in 60 samples of low-grade and 45 high-grade MALT-type tumors. In the low-grade cases, trisomy 3 was found in a frequency of only 20%. High-grade lymphomas of MALT type were associated with trisomies 3, 7, 12, and 18 in 36, 20, 18, and 13% of the cases, respectively. Whereas no difference was encountered for trisomy 3 in primary and secondary/simultaneous high-grade lymphomas, +7 and +12 were associated with primary lymphomas, and a +18 was predominantly found in secondary/simultaneous high-grade NHL. These results challenge earlier reports describing a high frequency of +3 in low-grade MALT-type NHL and indicate a possibly different genetic evolution pattern of primary and secondary/simultaneous high-grade lymphomas of primary mucosal origin.

Peripheral sensory and autonomic nerves are critically involved in many pathways of the innate and adoptive immune system during allergic and atopic skin diseases. Further dissection of receptor-mediated and intracellular signal pathways will help to develop more effective therapeutic approaches for allergic and inflammatory skin diseases.