In the present study, the role of microRNA-663b (miR-663b) in cardiomyocyte injury was examined. Reverse transcription-quantitative PCR (RT-qPCR) was performed to detect miR-663b expression in hypoxia-induced H9c2 cells. The results revealed that miR-663b expression was significantly upregulated in hypoxia-induced H9c2 cells compared with control cells. TargetScan analysis and dual-luciferase reporter assays demonstrated that miR-663b directly targeted the B-cell lymphoma 2 like 1 (BCL2L1) gene. RT-qPCR and western blotting data indicated that BCL2L1 expression was significantly downregulated in hypoxia-induced H9c2 cells compared with control cells. Under hypoxic conditions, H9c2 cells were transfected with miR-663b inhibitor, inhibitor control, miR-663b inhibitor + control small interfering (si)RNA or miR-663b inhibitor + BCL2L1-siRNA for 48 h. ELISA against creatine kinase-muscle/brain (CK-MB) and cardiac troponin 1 (cTnI) demonstrated that the miR-663b inhibitor reduced CK-MD and cTnI release and increased mitochondrial viability when compared with hypoxia-treated cells. Additionally, the miR-663b inhibitor significantly increased H9c2 cell viability and decreased cell apoptosis under hypoxic conditions. The results of ELISA further revealed that the miR-663b inhibitor decreased the release of various inflammatory factors, including tumour necrosis factor α, interleukin (IL) 1β and IL-6 in H9c2 cells under hypoxic conditions. These changes were reversed following BCL2L1 knockdown. In conclusion, miR-663b inhibition protected cardiomyocytes against hypoxia-induced injury by targeting BCL2L1 and may potentially be a novel target for the treatment of patients with myocardial infarction.
Rationale:Autoimmune encephalitis (AE) is a heterogeneous group of recently identified disorders. Despite severe and even prolonged neurologic deficits, dramatic improvements may occur with proper immunotherapy in some patients with AE. Antineuronal antibodies have been discovered in patients’ serum and cerebrospinal fluid (CSF). However, AE with multiple antineuronal antibodies is rare. To date, there are no published reports of AE with both anti-γ-aminobutyric acid B receptor (GABABR) and anticollapsin response-mediator protein 5 (CV2) antibodies.Patient concerns:We describe a 46-year-old man who presented with seizures, working memory deficits, and visual hallucinations. We detected anti-CV2 and anti-GABABR antibodies in his serum and CSF. Brain magnetic resonance imaging (MRI) revealed patchy abnormal signals in his left temporal lobe and hippocampus. The patient's symptoms improved after receiving intravenous immunoglobulin injections and glucocorticoids, but his condition relapsed within 4 months, and he was readmitted to our hospital. Repeated MRI scans revealed new lesions in his right temporal lobe and hippocampus.Diagnosis:The AE diagnosis was established from the results of the preliminary physical examination, the laboratory tests, and the imaging findings.Interventions:The patient received intravenous immunoglobulins and glucocorticoids.Outcomes:We followed the patient for 9 months from the date of the patient's second hospital discharge. He experienced no seizures during this period, but his short-term memory deficits and visual hallucinations were not completely alleviated.Lessons:Coexisting anti-CV2 and anti-GABABR antibodies may have synergistic effects and worsen the clinical syndrome. AE with multiple antineuronal antibodies may be relapse-prone. Further studies investigating the relationship between anti-CV2 and anti-GABABR antibodies are warranted.
Background: Spontaneous thrombolysis of unruptured intracranial aneurysm with spontaneous thrombosis is rare and its significance remains unclear. To date, there are no published reports of spontaneous thrombolysis prior to growth of unruptured intracranial aneurysm with spontaneous thrombosis. Methods: We described a 65-year-old man with a chief complaint of mild weakness and numbness in the left limbs. He had a smoking history of 20 years. Then he was diagnosed having unruptured intracranial aneurysm with spontaneous thrombosis. His cerebrovascular digital subtraction angiography conducted 30 days after his first onset revealed spontaneous thrombolysis of the unruptured intracranial aneurysm. And his following brain computed tomography scan conducted 36 days after his first onset revealed growth of the unruptured intracranial aneurysm. Results: The diagnosis of unruptured right fetal-type posterior cerebral artery aneurysm with spontaneous complete thrombosis was established based on the preliminary physical examination and the imaging findings. The patient underwent embolization of the aneurysm and parent artery. We followed up with the patient for 12 months after his embolization of the aneurysm and parent artery. He experienced neither aneurysm recurrence nor cerebral infarction during this period, but his were not alleviated. Conclusion: Spontaneous thrombolysis after spontaneous thrombosis of unruptured intracranial aneurysm is an urgent indication for isolation of the aneurysm, as it may foreshadow the growth of unruptured intracranial aneurysm.
Internal carotid artery dissection(ICAD) is a series of pathological processes caused by intimal tear of the internal carotid artery. Syncope refers to a transient loss of consciousness caused by transient global brain hypoperfusion. ICAD with syncope is rare. Here we present a case of unilateral ICAD with syncope as the first symptom. We also review the literature and discuss the pathogenesis of syncope in ICAD patients. The main message we want to convey to readers is that unilateral ICAD can have syncope as the first symptom, which should not be ignored in the differential diagnosis of syncope. Furthermore, the pathogenesis of syncope in ICAD is more likely to be that subintimal blood flow can easily increase the mechanical stretch of adventitia, stimulate the baroreceptors and cause hyperactive carotid sinus reflex.
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