Neuroinflammation after ischemic stroke involves INPP5D expression mediated by the TMPO-AS1-PU.1 complex.

OBJECTIVES: This study aims to explore the role of lncRNA TMPO-AS1 in ischemic stroke and corresponding mechanism. METHODS: Adult male C57BL/6 J mice were subjected to a middle cerebral artery occlusion (MCAO) model of ischemic stroke, then TMPO-AS1 shRNA lentivirus were injected into ipsilateral striatum of mice. The neurological score and cerebral infarction volume were evaluatedHypoxia/glucose deprivation/reoxygenation (OGD/R)-induced BV2 cells were transfected with TMPO-AS1 shRNA (sh-TMPO-AS1) or together with pcDNA-INPP5D, as well as transfected with sh-PU.1 or together with pcDNA-INPP5D, then TMPO-AS1 level, the expression of PU.1 and INPP5D proteins, the secretion of inflammatory factors (TNF-α, IL-6 and IL-1ß), the levels of iNOS, CD68,Arg1 and CD206 mRNA were detected. RIP and PNA-pull down assays were used to detect the binding of TMPO-AS1 and PU.1, luciferase reporter gene and chromatin immunoprecipitation (ChIP) assays were used to detect the binding activity of PU.1 and INPP5D. RESULTS: TMPO-AS1 level was increased in peripheral blood of ischemic stroke patients , brain tissues of MCAO/R model mice and OGD/R-induced BV2 cells. TMPO-AS1 interference inhibited the inflammation of OGD/R-induced BV2 cells. TMPO-AS1 also enhanced the nuclear accumulation of PU.1 by binding to the transcription factor PU.1, and promoted the transcriptional activation of INPP5D. The anti-inflammatory effects of TMPO-AS1 interference were reversed by INPP5D overexpression. In addition, TMPO-AS1 interference improved the infarct volume of MCAO mice, and improved sensorimotor and cognitive functions. CONCLUSION: INPP5D underexpression mediated by TMPO-AS1-PU.1 complex alleviated neuroinflammation after ischemic stroke.

Two case reports of chorea-acanthocytosis and review of literature.

BACKGROUND: Chorea-acanthocytosis (ChAc), as the most common subtype of neuroacanthocytosis syndrome, is characterized by the presence of acanthocytes and neurological symptoms. It is thought to be caused by the VPS13A (vacuolar protein sorting-associated protein 13A) mutations. This article reports two confirmed cases of ChAc and summarizes some suggestive features, which provide direction for the diagnosis and treatment of acanthocytosis in the future. CASE PRESENTATION: Here, we present two cases of ChAc diagnosed based on typical clinical symptoms, neuroimaging features, genetic findings of VPS13A, and response to the symptomatic treatment. CONCLUSIONS: Chorea-acanthocytosis is a rare neurodegenerative disease with various early clinical manifestations. The final diagnosis of the ChAc can be established by either genetic analysis or protein expression by Western blotting. Supportive treatments and nursing are helpful to improve the quality of the patient's life. Nevertheless, it is imperative to investigate the impact of neuroimaging and neuropathological diagnosis in a larger group of ChAc in future studies.

Brain abscess due to listeria monocytogenes: A case report and literature review.

RATIONALE: Listeria monocytogenes infective encephalitis is a rare phenomenon, which is more common in people with changed eating habits and immunodeficiency. To the best of our knowledge, listeria brain abscess is even more rare. In this case report, we summarized the clinical characteristics of listeria brain abscess, in order to explore the diagnosis and treatment of Listeria brain abscess, and raise awareness and attention to the disease. PATIENT CONCERNS: A 64-years-old female patient presented to our institution with 4 days of right arm and leg weakness, the salient past history of the patient was nephrotic syndrome, membranous nephropathy diagnosed 6 months prior, for which she was prescribed glucocorticoids and cyclophosphamide. DIAGNOSIS: Listeria monocytogenes was cultured in the blood of the patient. Comprehensive medical history and imaging features, she was diagnosed as listeria brain abscess. INTERVENTIONS: The patient underwent ampicillin combined with meropenem but not surgery. OUTCOMES: The patient recovered without complications. At a 3-month follow-up visit, the condition was better than that before treatment. LESSONS: Listeria brain abscess is an unusual form of listeriosis, its clinical manifestations lack specificity. Early accurate diagnosis and standardized treatment can effectively promote the recovery of neurological function as well as reduce the morbidity and mortality and improve the prognosis.

The Effect of Fucoidan on Cellular Oxidative Stress and the CatD-Bax Signaling Axis in MN9D Cells Damaged by 1-Methyl-4-Phenypyridinium.

Background: The purpose of this study was to investigate the impact of fucoidan (FUC) on the oxidative stress response and lysosomal apoptotic pathways in the Parkinson disease (PD) cell model. Methods: The Dopaminergic nerve precursor cell line(MN9D) cells that served as a PD model in this study underwent damage induced by 100 µM 1-methyl-4-phenyl pyridine (MPP+). Cell viability was assessed after FUC treatment and intracellular SOD GSH was measured via immunofluorescence assay. Cellular changes in cathepsin D, Autophagy marker Light Chain 3-II (LC3-II), and apoptotic protein Bax were assessed by Western blot. The expression of Cat D, LC3-II, and B cell lymphoma-2-associated x protein (Bax) was also measured after addition of the cathepsin inhibitor, pepstatin A. Results: The results indicated that MN9D cell viability decreased by 50% within 24 h after 100 µM MPP+ induced toxicity. Pretreatment with 100 µM Fucoidan reduced cellular expression of LC3-II and CatD in 3 h and suppressed the induction of Bax protein. After pepstatin A treatment, Bax expression was significantly downregulated.FUC reversed the reduction of superoxide dismutase (SOD) L-Glutathione(GSH), decreased cell viability, and apoptosis induced by MPP+ in 6 h, suggesting that Fucoidan can attenuate damage to MN9D cells induced by MPP+. Conclusions: Fucoidan protected lysosomes, reduced the expression of LC3-II, inhibited the expression of CatD-Bax and the oxidative stress response, suppressed apoptosis, and thus conferred protective effects for dopaminergic neural cells. FUC may have neuroprotective effects on PD and further research is needed.

Misdiagnosis of a Patient with Internal Carotid Artery Fenestration: A Case Report and Literature Review.

BACKGROUND: Internal carotid artery fenestration is a rare congenital cerebrovascular condition and can be misdiagnosed as carotid artery dissection. CASE REPORT: A patient was initially misdiagnosed with carotid artery dissection. This initial diagnosis was made using a carotid vascular computed angiography and magnetic resonance angiography. A digital subtraction angiography examination revealed a fenestration in the terminal C1 segment of the right internal carotid artery. Previous literature related to carotid artery fenestration was reviewed and analyzed. CONCLUSIONS: Fenestration of the carotid artery combined with aneurysm at the external segment of the internal carotid artery or from the starting position of the carotid artery remains rare in elderly patients, can be misdiagnosed as artery dissection.

Viral encephalitis complicated by acute retinal necrosis syndrome: A case report.

Acute retinal necrosis syndrome (ARN) is a viral infection characterized by focal retinal necrosis. Viral meningitis complicated by ARN is relatively rare. In the present case study, a 44-year-old male presented with fever, headache and mental disorder. After four days, the patient developed blurred vision. The patient was diagnosed with viral encephalitis complicated by bilateral ARN, based on the examination results. After treatment with antivirals and systemic glucocorticoids, the symptoms of the patient improved. Viral encephalitis may be an important risk factor for ARN. For a patient with viral encephalitis who experiences decreased visual acuity or vitreous opacification, the possibility of ARN should be considered.