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Mechanical irritation by protruding bone: A possible cause of breast implant rupture
Matthias Michael Aitzetmüller,David Johannes Haslhofer,Raphael Wenny,Manfred Schmidt,Dominik Duscher,Georg Michael Huemer 대한성형외과학회 2018 Archives of Plastic Surgery Vol.45 No.5
Although breast implants have been in clinical use for almost 6 decades and have undergone considerable development during this time, implant rupture is still a dreaded long-term complication. Some obvious external factors, such as trauma, can lead to implant rupture, but many studies have reported a high rate of “spontaneous” implant rupture. Herein, we present two cases with the aim of raising awareness of a new possible cause of “spontaneous” implant rupture: mechanical irritation by bony protrusions.
Mechanical irritation by protruding bone: A possible cause of breast implant rupture
Aitzetmuller, Matthias Michael,Haslhofer, David Johannes,Wenny, Raphael,Schmidt, Manfred,Duscher, Dominik,Huemer, Georg Michael Korean Society of Plastic and Reconstructive Surge 2018 Archives of Plastic Surgery Vol.45 No.5
Although breast implants have been in clinical use for almost 6 decades and have undergone considerable development during this time, implant rupture is still a dreaded long-term complication. Some obvious external factors, such as trauma, can lead to implant rupture, but many studies have reported a high rate of "spontaneous" implant rupture. Herein, we present two cases with the aim of raising awareness of a new possible cause of "spontaneous" implant rupture: mechanical irritation by bony protrusions.
Lena Hell,Kristina Lurger,Lisa-Marie Mauracher,Ella Grilz,Christina Maria Reumiller,Georg Johannes Schmidt,Huriye Ercan,Silvia Koder,Alice Assinger,José Basilio,Johanna Gebhart,Cihan Ay,Ingrid Pabinge 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-
Patients with antiphospholipid syndrome (APS) are at high risk of developing venous and arterial thromboembolism (TE). The role of platelets in the pathogenesis of these prothrombotic conditions is not yet fully understood. The aim of this study was to gain mechanistic insights into the role of platelets in APS by comparing the platelet proteome between lupus anticoagulant (LA)-positive patients with (LA+TE+) and without a history of TE (LA+TE−) and healthy controls. The platelet proteome of 47 patients with LA, 31 with a history of TE and 16 without thrombotic history, and 47 healthy controls was analyzed by two-dimensional differential in-gel electrophoresis and mass spectrometry to identify disease-related proteins. Afterward, selected LA-related platelet proteins were validated by western blot and ELISA. Alterations of 25 proteins were observed between the study groups. STRING pathway analysis showed that LArelated protein profiles were involved in platelet activation, aggregation, and degranulation. For example, protein disulfide isomerase family members, enzymes that promote thrombosis, were upregulated in platelets and plasma of LA+TE+patients. Leukocyte elastase inhibitor (SERPINB1), an antagonist of neutrophil extracellular trap (NET) formation, was decreased in platelets of LA+TE+patients compared to healthy controls. Additionally, citrullinated histone H3, a NET-specific marker, was increased in plasma of LA+TE+patients. These findings suggest that decreased platelet SERPINB1 levels favor prothrombotic NETosis, especially in LA+TE+patients. Our findings reveal protein abundance changes connected to altered platelet function in LA-positive patients, thus suggesting a pathogenic role of platelets in thrombotic complications in APS.