Endovascular repair of urgent TAAA using the t-Branch is a feasible treatment option with acceptable 30-day mortality and morbidity in terms of SCI and renal function impairment. Adherence to the IFU prolonged procedure time but had no effect on outcomes. Increased experience of such cases over time may improve outcomes.
The implantation of the t-Branch device in urgent cases achieved accurate apposition without rotational deviation between the target vessels and the position of the endograft branches. Gender may have an impact on orientation of the device. The t-Branch appears to have a "forgiving" nature for higher malorientation with no effect on procedure time, target vessel revascularization, or early branch patency.
Hepatocellular carcinoma (HCC) ranks among the five most common cancer entities worldwide and leads to hundred-thousands of deaths every year. Despite some groundbreaking therapeutical revelations during the last years, the overall prognosis remains poor. Although the immune system fights malignant transformations with a robust anti-tumor response, certain immune mediators have also been shown to promote cancer development. For example, interleukin (IL)-22 has been associated with HCC progression and worsened prognosis in multiple studies. However, the underlying mechanisms of the pathological role of IL-22-signaling as well as the role of its natural antagonist IL-22 binding protein (IL-22BP) in HCC remain elusive. Here, we corroborate the pathogenic role of IL-22 in HCC by taking advantage of two mouse models. Moreover, we observed a protective role of IL-22BP during liver carcinogenesis. While IL-22 was mainly produced by CD4+ T cells in HCC, IL-22BP was abundantly expressed by neutrophils during liver carcinogenesis. Hepatocytes could be identified as a major target of this pathological IL-22-signaling. Moreover, abrogation of IL-22 signaling in hepatocytes in IL22ra1flox/flox × AlbCre+ mice reduced STEAP4 expression-a known oncogene-in HCC in vivo. Likewise, STEAP4 expression correlated with IL22 levels in human HCC samples, but not in healthy liver specimens. In conclusion, these data encourage the development of therapeutical approaches that target the IL-22–IL-22BP axis in HCC.
Electrocardiographic abnormalities in patients with massive pulmonary embolism are common and unspecific. An 80-year-old woman was admitted to our department with severe respiratory insufficiency and hemodynamic instability. Abnormal high-sensitivity cardiac troponin I and ST-segmental elevation in II, III, aVF, and V3–V6 were present on admission. Segmental motion abnormalities of the left ventricular wall were not detectable in echocardiography. Instead, the presence of a right ventricular strain raised the suspicion of a lung artery embolization. The diagnosis was confirmed by a computed tomography of the chest, and a thrombolytic therapy with 100 mg recombinant tissue plasminogen activator (rt-PA) was administered. Though respiratory and hemodynamic stability were established, electromechanical disassociation suddenly occurred 30 hours later and the patient died. Electrocardiographic changes mimicking a myocardial infarction may occur after a massive pulmonary embolism and constitute a diagnostic challenge for clinicians being active in the field of emergency medicine and intensive care.
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