Lichen planus (LP) is an inflammatory skin condition with characteristic clinical and histopathological findings. Classic LP typically presents as pruritic, polygonal, violaceous flat-topped papules and plaques; many variants in morphology and location also exist, including oral, nail, linear, annular, atrophic, hypertrophic, inverse, eruptive, bullous, ulcerative, lichen planus pigmentosus, lichen planopilaris, vulvovaginal, actinic, lichen planus-lupus erythematosus overlap syndrome, and lichen planus pemphigoides. Clinical presentation of the rarer variant lesions may be largely dissimilar to classic LP and therefore difficult to diagnose based solely on clinical examination. However, histopathological examination of LP and LP-variant lesions reveal similar features, aiding in the proper diagnosis of the disease. Management of LP and LP variants aims to control symptoms and to decrease time from onset to resolution; it often involves topical corticosteroids, but varies depending on the severity and location of the lesion. The literature contains an array of reports on the variations in presentation and successful management of LP and its variants. A familiarity with LP and its variants is important in achieving timely recognition and management of the disease.

Social isolation (SI) is increasingly recognized as a risk factor for stroke. Individuals with lack of social support systems have an increased incidence of stroke, poorer recovery, and greater functional decline after injury compared to individuals with social support. Attesting to the importance of social factors in stroke outcome is that these same effects can be reproducibly demonstrated in animals; social interaction improves behavioral deficits and reduces damage after experimental stroke, whereas SI enhances injury. The mechanism by which SI exacerbates injury is unclear. We investigated the role of nuclear factor-kappaB (NF-κB) signaling in male mice that were pair housed (PH) with an ovariectomized female prior to random assignment into continued PH or SI for 7 days prior to middle cerebral artery occlusion. The effects of SI on infarct volume and functional recovery were assessed at 72 h post-stroke. Nuclear NF-κB levels and activity were assessed by Western blot and transcriptional assays. SI significantly exacerbated infarct size in both male and female mice compared to PH mice. SI mice had delayed functional recovery compared to PH mice. An elevation of systemic IL-6 levels, increased nuclear NF-κB transcriptional activity, and enhanced nuclear translocation of NF-κB was seen in SI stroke animals. Interference with NF-κB signaling using either a pharmacological inhibitor or genetically engineered NF-κB p50 knockout mice abolished the detrimental effects of SI on both infarct size and functional recovery. This suggests that NF-κB mediates the detrimental effects of SI.

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BackgroundGlobalised and 24/7 business operations have fuelled demands for people to work long hours and weekends. Research on the mental health effects of these intensive temporal work patterns is sparse, contradictory or has not considered gender differences. Our objective was to examine the relationship between these work patterns and depressive symptoms in a large nationally representative sample of working men and women in the UK.MethodThe current study analysed data from Understanding Society, the UK Household Longitudinal Study, of 11 215 men and 12 188 women in employment or self-employment at the time of the study. Ordinary least squares regression models, adjusted for potential confounders and psychosocial work factors, were used to estimate depressive symptoms across categories of work hours and weekend work patterns.ResultsRelative to a standard 35–40 hours/week, working 55 hours/week or more related to more depressive symptoms among women (ß=0.75, 95% CI 0.12 to 1.39), but not for men (ß=0.24, 95% CI −0.10 to 0.58). Compared with not working weekends, working most or all weekends related to more depressive symptoms for both men (ß=0.34, 95% CI 0.08 to 0.61) and women (ß=0.50, 95% CI 0.20 to 0.79); however, working some weekends only related to more depressive symptoms for men (ß=0.33, 95% CI 0.11 to 0.55), not women (ß=0.17, 95% CI −0.09 to 0.42).ConclusionIncreased depressive symptoms were independently linked to working extra-long hours for women, whereas increased depressive symptoms were associated with working weekends for both genders, suggesting these work patterns may contribute to worse mental health.

Background: Ischemic stroke is a devastating disease, often resulting in death or permanent neurological deficits. EMMPRIN/CD147 is a plasma membrane protein that induces the production of matrix metalloproteinases (MMPs), which contribute to secondary damage after stroke by disrupting the blood brain barrier (BBB) and facilitating peripheral leukocyte infiltration into the brain. Results: CD147 surface expression increased significantly after stroke on infiltrating leukocytes, astrocytes and endothelial cells, but not on resident microglia. Inhibition of CD147 reduced MMP levels, decreased ischemic damage, and improved functional, cognitive and histological outcomes after experimental ischemic stroke in both young and aged mice. In stroke patients, high levels of serum CD147 24 hours after stroke predicted poor functional outcome at 12 months. Brain CD147 levels were correlated with MMP-9 and secondary hemorrhage in post-mortem samples from stroke patients. Conclusions: Acute inhibition of CD147 decreases levels of MMP-9, limits tissue loss, and improve long-term cognitive outcomes following experimental stroke in aged mice. High serum CD147 correlate with poor outcomes in stroke patients. This study identifies CD147 as a novel, clinically relevant target in ischemic stroke.