A Case of Endovascular Treatment for In-Hospital Stroke with COVID-19 under Protected Code Stroke.

Objective: Coronavirus disease 2019 (COVID-19) is characterized by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and presents with respiratory symptoms. Overall, 5.7% of COVID-19 patients with severe respiratory status have been reported to develop acute cerebrovascular diseases (CVDs), and 41.3% of COVID-19 cases were considered nosocomial infections. Therefore, Protected Code Stroke, which is a guideline for acute stroke management that takes into account the safety of healthcare workers, has been developed. We created an operational manual for COVID-19 in the endovascular treatment center of our hospital and report our experience treating acute stroke in a COVID-19 patient. Case Presentation: A 67-year-old man presented with a 5-day history of fever. Chest CT showed ground glass opacity (GGO) on admission, and the polymerase chain reaction (PCR) test for COVID-19 was positive. Dysarthria, right-sided hemiparesis, and aphasia were discovered on the morning of the third day after hospitalization. MRI showed an acute ischemic stroke at the left corona radiata and occlusion of the left middle cerebral artery (MCA). Progression of right-sided hemiparesis and exacerbation of respiratory status developed after the MRI. Tracheal intubation was performed, and the patient was treated with intravenous alteplase and mechanical thrombectomy (MT). Recanalization of blood flow was not obtained, and the neurological deficits remained. Conclusion: MT was performed for large-vessel occlusion (LVO) in a COVID-19 patient during the COVID-19 pandemic. Safety for healthcare workers and appropriate rapid treatment for acute stroke patients are both vital in the current environment.

Sex differences in immunohistochemical expression and capillary density in pancreatic solid pseudopapillary neoplasm.

Solid pseudopapillary neoplasm (SPN) is a rare and low-grade malignant pancreatic neoplasm. Solid pseudopapillary neoplasm is rare in men, and most SPN cases are in young women. This study aimed to investigate sex differences in SPN clinical histopathology including capillary density and expression of immunochemical markers, including glypican 3. A total of 22 resected tumors from pancreatic SPN patients, including 16 women (73%) and 6 men (27%), were analyzed histopathologically and immunohistochemically for synaptophysin, ß-catenin, estrogen receptor, progesterone receptor, Ki-67, CD10, CD31, and glypican 3. The median age was 52.5 years in men and 24 years in women (P = .046). The median tumor size was 22.5 mm in men and 40 mm in women (P = .337). In 11 of the 16 women (69%), but in none of the men, tumors showed complete or incomplete fibrous cap`sules (P = .006). Cholesterol clefts were observed in tumors from 10 women (63%) but in none from the men (P = .012). No significant sex differences were noted in tumor characteristics, including size, macroscopic cystic degeneration, necrosis, lymphovascular involvement, and perineural invasion. The SPNs were weakly positive for glypican 3, although there was no significant difference between sexes. Capillary density tended to be lower in tumors from men than in those from women, but not significantly. Thus, except for the fibrous capsule and cholesterol clefts often found in tumors and the younger age of the women, there were no significant sex differences in histopathologic or immunohistochemical features of SPN, despite its markedly higher occurrence in women.

Gene expression of the TGF-beta family in rat brain infected with Borna disease virus.

CRNP5, a variant of Borna disease virus (BDV), has stronger pathogenesis in rats than the related variant CRP3, although only 4 amino acids in the whole genome are different. As a first step to clarify the differential pathogenesis between the variants, the present study focused on examining the expression of the transforming growth factor (TGF)-beta family in the brain of rats infected with BDV. The main results were as follows. (1) BDV infection, irrespective of the variant, up-regulates TGF-beta1 expression in the brain, (2) the expressions of signal receptors for TGF-beta1 are also increased, (3) the expression of brain inhibin/activin betaE is up-regulated by BDV infection, and (4) the expression of brain inhibin/activin betaC tends to be higher in rats exhibiting severe Borna disease. These results indicate that members of the TGF-beta family are involved in neuronal disorders induced by BDV infection in a ligand-dependent manner. In particular, up-regulation of inhibin/activin betaC may be a key event responsible for induction of the stronger pathogenesis of the CRNP5 variant of BDV.