Numerous studies have increasingly suggested that medical history and lifestyle factors could be involved in the increase of cancer risk in adults. The issue whether psychological factors can influence the development of cancer has been discussed for many years. In the field of brain cancer, psychological stress has not so far been investigated. We conducted a French case-control pilot study with 122 adult incident cases and 122 controls free of any cancer diagnosis, matched for age and gender, to investigate links between malignant primitive brain tumours (MPBT) and medical history, private habits and psychological stress. Data were collected through self-administered questionnaires, and person-to-person interviews. To complete the psychological stress assessment, 100-mm visual analog scales were used. After adjustment for confounders, we found no significant effect of head trauma, aspartame, tobacco or alcohol consumption, place (rural or urban) of residence, sociodemographic data, and experience of psychological stress at work/home. Our results showed a significant association between MPBT risk and major life events over the past 5 years before diagnosis (OR = 1.90, 95% CI 1.13-3.20), family histories of cancer (OR = 1.90, 95% CI 1.12-3.22), fresh vegetable and fruit intake (OR = 0.29, 95% CI 0.09-0.95), and skipped meals several times per week (OR = 0.35, 95% CI 0.16-0.77). The present study suggests the role of genetic factors in glioma risk, and also suggests that an acute and sudden psychological stress might influence MPBT appearance. Additional large clinical studies are needed to confirm these findings.

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We report 77 cases of occupational exposures for 57 healthcare workers at the Ebola Treatment Center in Conakry, Guinea, during the Ebola virus disease outbreak in 2014−2015. Despite the high incidence of 3.5 occupational exposures/healthcare worker/year, only 18% of workers were at high risk for transmission, and no infections occurred.

Colchicine, a microtubule polymerization inhibitor, can very occasionally induce myopathy. We report two cases of colchicine myopathy. Both patients presented with myalgia and proximal muscle weakness. The first patient, an 80-year-old woman, had chronic renal failure related to renal amyloidosis. She had been treated by colchicine for 4 months. The second, a 75-year-old man with normal renal function, suffering from gout, was treated by colchicine for 3 weeks. Muscle biopsies displayed the same alterations, but the degree of severity was different. Conventional histology revealed vacuolar changes characterized by acid phosphatase-positive vacuoles and myofibrillar disarray foci. The lesions were selective for type I fibers. Ultrastructural study demonstrated autophagic vacuoles. Most of the vacuoles expressed dystrophin but not merosin. Several fibers reacted with anti-MHC class I antibody and granular deposits of membrane attack complex were observed on the surface of numerous myofibers. Anti-alphaB-crystallin antibody strongly reacted with vacuolar content. Physiopathologically, microtubules are primordial for vesicle movements and colchicine induces autophagic vacuole accumulation by preventing their fusion with lysosomes. The selective type I involvement is probably due to the higher tubulin amount in type I fibers. AlphaB-crystallin overexpression is related to its microtubule protection properties. Moreover, we suggest that vacuoles randomly floating in sarcoplasm might occasionally meet the plasma membrane and open in the extracellular space, leading to complement activation. Accurate diagnosis of colchicine myopathy is relevant because the treatment is based on colchicine interruption.