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Mattioli, Stefano,Curti, Stefania,De Fazio, Rocco,Mt Cooke, Robin,Zanardi, Francesca,Bonfiglioli, Roberta,Farioli, Andrea,Violante, Francesco S. Occupational Safety and Health Research Institute 2012 Safety and health at work Vol.3 No.1
Objectives: Lifting heavy weights involves the Valsalva manoeuvre, which leads to intraocular pressure spikes. We used data from a case-control study to further investigate the hypothesis that occupational lifting is a risk factor for retinal detachment. Methods: The study population included 48 cases (patients operated for retinal detachment) and 84 controls (outpatients attending an eye clinic). The odds ratios (OR) of idiopathic retinal detachment were estimated with a logistic regression model (adjusted for age, sex and body mass index). Three indexes were used to examine exposure to lifting; 1) maximum load lifted, 2) average weekly lifting, 3) lifelong cumulative lifting. Results: For all indexes, the most exposed subjects showed an increased risk of retinal detachment compared with the unexposed (index 1: OR 3.57, 95% confidence interval [CI] 1.21-10.48; index 2: OR 3.24, 95% CI 1.32-7.97; index 3: OR 2.23, 95% CI 1.27-8.74) and dose-response relationships were apparent. Conclusion: These results reinforce the hypothesis that heavy occupational lifting may be a relevant risk factor for retinal detachment.
Codeine Precipitating Serotonin Syndrome in a Patient in Therapy with Antidepressant and Triptan
Giulia Milano,Werner Maria Natta,Alfredo Bello,Antonietta Martelli,Francesca Mattioli 대한정신약물학회 2017 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.15 No.3
The serotonin syndrome is a serioius medical condition due due to an intensive stimulation of setonin receptors. It is a rare, but severe, consequence of interaction between serotomimetic agents. This is a report of a 70-year-old woman steadily in therapy with venlafaxine and rizatriptan for migraine and major depressive syndrome. She was admitted to neurology unit for decreased light reflex with miotic pupils, global hyperreflexia, tremor, anxiety, ataxia and incoordination. The patient was diagnosed as a probable case of serotonin syndrome due to a pharmacological interaction between venlafaxine and rizatriptan trigged by opioid intake. In this paper, the development of syntomatology, the clinical examination and the possible pharmacokinetics explanation were carefully discussed and analysed.
Giovanna Lattanzi,Camilla Pellegrini,Marta Columbaro,Elisa Schena,Sabino Prencipe,Davide Andrenacci,Patricia Iozzo,Maria Angela Guzzardi,Cristina Capanni,Elisabetta Mattioli,Manuela Loi,David Araujo-V 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Type-2 Familial Partial Lipodystrophy is caused by LMNA mutations. Patients gradually lose subcutaneous fat from the limbs, while they accumulate adipose tissue in the face and neck. Several studies have demonstrated that autophagy is involved in the regulation of adipocyte differentiation and the maintenance of the balance between white and brown adipose tissue. We identified deregulation of autophagy in laminopathic preadipocytes before induction of differentiation. Moreover, in differentiating white adipocyte precursors, we observed impairment of large lipid droplet formation, altered regulation of adipose tissue genes, and expression of the brown adipose tissue marker UCP1. Conversely, in lipodystrophic brown adipocyte precursors induced to differentiate, we noticed activation of autophagy, formation of enlarged lipid droplets typical of white adipocytes, and dysregulation of brown adipose tissue genes. In agreement with these in vitro results indicating conversion of FPLD2 brown preadipocytes toward the white lineage, adipose tissue from FPLD2 patient neck, an area of brown adipogenesis, showed a white phenotype reminiscent of its brown origin. Moreover, in vivo morpho-functional evaluation of fat depots in the neck area of three FPLD2 patients by PET/CT analysis with cold stimulation showed the absence of brown adipose tissue activity. These findings highlight a new pathogenetic mechanism leading to improper fat distribution in lamin A-linked lipodystrophies and show that both impaired white adipocyte turnover and failure of adipose tissue browning contribute to disease.