For tumours of 2.1 cm or more in size lobectomy appears to carry the least risk of postoperative complications and death in hospital and best achieves a cancer-free surgical margin.
A 52-year-old woman presenting with shortness of breath and having no related past medical history was diagnosed with takotsubo cardiomyopathy. However, she revealed respiratory failure atypical with takotsubo cardiomyopathy. We diagnosed myasthenia gravis with myasthenic crisis by acetylcholine receptor-binding antibody titer with mediastinal tumor. Physical or emotional stress is well known to trigger the onset of takotsubo cardiomyopathy. Similarly, myasthenia crisis is also triggered by stress. Here, we report a case of simultaneous occurrence of takotsubo cardiomyopathy and myasthenia crisis.
Background: Selective inhibition of cyclooxygenase 2 has been reported to have not only anti-inflammatory effects but also effects on the immune response. We investigated ability of a cyclooxygenase 2 inhibitor to inhibit alloimmune response in a murine cardiac transplantation model. Methods: CBA (H2 k ) mice underwent transplantation of C57BL/10 (H2 b ) hearts. On the day of transplantation, the recipients received either no treatment or single administration of aspirin (a cyclooxygenase 1 and 2 inhibitor) or the selective cyclooxygenase 2 inhibitor NS-398. Naive CBA mice (secondary recipients) underwent adoptive transfer of splenocytes from treated mice with long-surviving grafts (primary recipients) to determine whether regulatory cells developed after NS-398 treatment. Histologic, cell-proliferation, and cytokine studies were also performed.Results: Untreated CBA mice rejected C57BL/10 cardiac grafts acutely (median survival time, 8 days). The majority of recipients given aspirin rejected their grafts within 20 days (median survival time, 11 days). In mice given NS-398, the majority of the grafts survived indefinitely (median survival time, Ͼ100 days). Secondary CBA recipients given CD4 ϩ splenocytes from primary CBA recipients treated with NS-398 also had indefinite survival of C57BL/10 hearts (median survival time, Ͼ60 days). Graft acceptance and proliferative hyporesponsiveness were also confirmed by the histologic and cell-proliferation studies, respectively. Production of interleukin 4 and 10 from splenocytes of the recipients treated with NS-398 were significantly higher than that from untreated recipients.
Conclusions:In our model administration of cyclooxygenase 2 inhibitor induced indefinite survival of fully mismatched cardiac grafts and generated CD4 ϩ regulatory cells. Cyclooxygenase 2 inhibitor could warrant consideration for use as an immunomodulating agent in clinical transplantation.
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