A mobile thrombus of the thoracic aorta is a rare entity, which might have serious clinical manifestations, including arterial emboli. Due to its low incidence, there is no consensus regarding the most adequate management of mobile thoracic aorta thrombus. The current case describes a patient with Polycythemia Vera and myeloproliferative neoplasm, who presented with mobile thrombus of the thoracic aorta, manifested by blue toe syndrome and asymptomatic splenic infarct. She was treated conservatively with anti-coagulation and Iloprost alongside the patient’s permanent treatment of Aspirin, Hydrea and Atorvastatin. Under this treatment, the thrombus resolved completely, and the blue toes improved, except for one.
Schizophrenia is a severe psychiatric disorder, with heritability around 80%, but a not fully understood pathophysiology. Signal transduction through the mothers against decapentaplegic (SMADs) are eight different proteins involved in the regulation of inflammatory processes, cell cycle, and tissue patterning. The literature is not consistent regarding the differential expression of SMAD genes among subjects with schizophrenia. In this article, we performed a systematic meta‐analysis of the expression of SMAD genes in 423 brain samples (211 schizophrenia vs. 212 healthy controls), integrating 10 datasets from two public repositories, following the PRISMA guidelines. We found a statistically significant up‐regulation of SMAD1, SMAD4, SMAD5, and SMAD7, and a tendency for up‐regulation of SMAD3 and SMAD9 in brain samples of patients with schizophrenia. Overall, six of the eight genes showed a tendency for up‐regulation, and none of them was found to have a tendency for down‐regulation. SMAD1 and SMAD4 were up‐regulated also in blood samples of 13 individuals with schizophrenia versus eight healthy controls, suggesting the SMAD genes' potential role as biomarkers of schizophrenia. Furthermore, SMAD genes' expression levels were significantly correlated with those of Sphingosine‐1‐phosphate receptor‐1 (S1PR1), which is known to regulate inflammatory processes. Our meta‐analysis supports the involvement of SMAD genes in the pathophysiology of schizophrenia through their role in inflammatory processes, as well as demonstrates the importance of gene expression meta‐analysis for improving our understanding of psychiatric diseases.
Background Intercostal artery aneurysms (ICA) are rare vascular disease. A rupture of ICA is a possible mechanism of intramural aortic hematoma (IH). We report a case with IH and ICAs without clear etiology. Case presentation: A 64-year-old man was admitted to our emergency room with a sudden onset of acute diffused abdominal and chest pain, radiating to the back. Without previous traumatic insult, a computed tomographic angiography scan (CTA) revealed an IH beginning inferior to the left subclavian artery extending to the level of the celiac trunk. Follow-up CTA demonstrated a stable maximal IH thickness diameter of 11 mm, maximal aortic diameter of 40 mm, a new left hemorrhagic pleural effusion, and a focal contrast enhancement at T9 level. Due to these findings, thoracic endovascular aortic repair (TEVAR) was performed. During follow up, T9 focal enhancement continues to grow and an additional one developed. Selective angiography was performed demonstrating a connection to the costal artery and the aortic lumen, confirming ICA. Successful embolization with micro coils was performed. During follow up, additional 2 ICAs developed and treated with embolization. CTA three months later showed a complete resolution of the IH and obliteration of all treated ICAs. Infectious, inflammatory and connective tissue disease investigations were undertaken without a clear etiology. Conclusions: This is a case of IH and ICAs, in the absence of a clear etiology which were successfully treated by endovascular procedures TEVAR and coil embolization. It is not clear whether the hematoma was the source of the ICA or the other way round. Lack of ICAs in the initial CTA might be due to the pressure exerted by the hematoma or that they were too small to be detected but continued to grow on follow up. Rupture of these micro-aneurysms is a possible mechanism of intramural aortic hematoma.
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