AimsTo evaluate the role of 17-β-oestradiol, oestrone and total testosterone (TT) deficiency in the pathogenesis of severe evaporative dry eye syndrome (DES), investigating the relationship between tear osmolarity, tear film break-up time (TF-BUT), Schirmer test and serum sex hormones in postmenopausal women. Methods 44 postmenopausal women were recruited for a case-control study: 22 women with severe evaporative DES (Group A) and 22 without DES (Group B). The tests performed included laboratory blood analysis: fasting plasma profile (17-β-oestradiol, oestrone and TT), glucose level and lipid profile. Detailed eye examinations, including corneal and conjunctival staining, tear osmolarity measurement, tear volume and TF-BUT, were performed. The Ocular Surface Disease Index Questionnaire was also administered. Results Values of Schirmer test and TF-BUT in Group A were significantly lower in comparison with Group B ( p<0.001). Serum levels of 17-β-oestradiol, oestrone and TT were significantly lower in Group A compared with Group B ( p<0.05). In women with severe evaporative DES, the levels of 17-β-oestradiol, oestrone and TT were inversely correlated with the tear film osmolarity (r=−0.7, −0.88, −0.81, respectively). Conclusions In postmenopausal women with severe evaporative DES, sex hormone levels are lower than control and that tear osmolarity is negatively correlated with sex hormone levels.

Although it is well known that hypoxemia induces pulmonary vasoconstriction and vascular remodeling, due to the proliferation of both vascular smooth muscle cells and fibroblasts, the effects of hypoxemia on airway smooth muscle cells are not well characterized. The present study was designed to assess the in vitro effects of hypoxia (1 or 3% O(2)) on rat airway smooth muscle cell growth and response to mitogens (PDGF and 5-HT). Cell growth was assessed by cell counting and cell cycle analysis. Compared with normoxia (21% O(2)), there was a 42.2% increase in the rate of proliferation of cells exposed to 3% O(2) (72 h, P = 0.006), as well as an enhanced response to PDGF (13.9% increase; P = 0.023) and to 5-HT (17.2% increase; P = 0.039). Exposure to 1% O(2) (72 h) decreased cell proliferation by 21.0% (P = 0.017) and reduced the increase in cell proliferation induced by PGDF and 5-HT by 16.2 and 15.7%, respectively (P = 0.019 and P = 0.011). A significant inhibition in hypoxia-induced cell proliferation was observed after the administration of bisindolylmaleimide GF-109203X (a specific PKC inhibitor) or downregulation of PKC with PMA. Pretreatment with GF-109203X decreased proliferation by 21.5% (P = 0.004) and PMA by 31.5% (P = 0.005). These results show that hypoxia induces airway smooth muscle cell proliferation, which is at least partially dependent on PKC activation. They suggest that hypoxia could contribute to airway remodeling in patients suffering from chronic, severe respiratory diseases.

Vaccines have represented the breakthrough in the fight against COVID-19. Based on reported headache attacks after vaccination in randomized controlled trials, we focused on the effects of COVID-19 vaccine administration on the migraine population, using an online questionnaire published on Italian Facebook groups oriented to headache patients. We collected data about the demographics and clinical parameters of migraine severity, COVID-19 infection, vaccination, and characteristics of headaches following vaccination. Out of 841 migraine patients filling in the questionnaire, 66.47% and 60.15% patients experienced a headache attack (from 1 hour to 7 days) after the first and the second vaccine dose, respectively. The main finding concerns headaches perceived by 57.60% of patients: attacks following vaccination were referred to as more severe (50.62% of patients), long-lasting (52.80% of patients) and hardwearing (49.69% of patients) compared to the usually experienced migraine attacks. This could be related to the production of inflammatory mediators such as type Iβ interferon. Considering the high prevalence of migraine in the general population, awareness of the possibility of headaches worsening following COVID-19 vaccination in these patients may allow both patients and clinicians to face this clinical entity with conscious serenity, and to reduce the waste of resources towards inappropriate health-care.

Constrictive pericarditis is caused by adhesions between the visceral and parietal layers of the pericardium and progressive pericardial fibrosis that restricts diastolic filling of the heart. Later on, the thickened pericardium may calcify. Despite a better understanding of the pathophysiologic basis of the imaging findings in constrictive pericarditis and the recent advent of magnetic resonance imaging (MRI) technology, which has dramatically improved the visualization of the pericardium, the diagnosis of constrictive pericarditis remains a challenge in many cases. In patients with clinical suspicion of underlying constrictive pericarditis, the most important radiologic diagnostic feature is abnormal pericardial thickening, which can be shown readily by computed tomography (CT) and especially by MRI, and is highly suggestive of constrictive pericarditis. Nevertheless, a thickened pericardium does not always indicate constrictive pericarditis. Furthermore, constrictive pericarditis can occur without pericardial thickening.