Huge gastric plexiform fibromyxoma presenting as pyemia by rupture of tumor: A case report.

BACKGROUND: Plexiform fibromyxoma (PF) is a rare mesenchymal tumor, with limited case reports worldwide. Common clinical symptoms are abdominal discomfort and bleeding signs, which frequently present slow-onset in reported cases. Herein, we report a case of gastric PF presenting as acute onset and with pyemia accom-panying tumor rupture. We resected the tumor as well as the distal gastric, bulbus duodeni and gallbladder for treatment in emergency surgery. Notably, before the onset of the disease, the patient received coronavirus disease 2019 (COVID-19) vaccines. CASE SUMMARY: A 26-year-old man was admitted to our hospital, due to abdominal pain and fever after having received COVID-19 vaccines. Laboratory examination indicated severe sepsis. Computed tomography scan revealed a large mass in the abdomen. Deformation of the gastrointestinal tract was seen during gastroscopy. After failure of anti-infective treatment and symptoms of shock developed, he received an emergency surgery. We found a huge and partly ruptured mass, with thick purulence. Microscopically, the mass was composed of spindle cells with clarified cytoplasm, accompanied by myxoid stroma and arborizing blood vessels. Immunohistochemistry showed the tumor cells as positive for smooth muscle actin and succinate dehydrogenase subunit B but negative for DOG-1 and CD117. Finally, the patient was diagnosed with gastric PF and discharged from the hospital. CONCLUSION: Gastric PF manifesting as tumor rupture combined with pyemia is rare. Timely surgery is critical for optimal prognosis.

Posterior Reversible Encephalopathy Syndrome Associated With Anlotinib: A Case Report and Literature Review.

Posterior reversible encephalopathy syndrome (PRES) is a relatively rare clinical disease, characterized by reversible subcortical vasogenic edema. Here, we present the first reported case of PRES induced by anlotinib, a multi-target tyrosine kinase inhibitor. A 56-year-old female patient with lung adenocarcinoma and bone metastasis experienced hypertension and mental confusion when she received anti-angiogenesis treatment. PRES was diagnosed after magnetic resonance of the patient's brain revealed hyperintensities bilaterally around the cerebellum, pons, fronto-parieto-occipital areas, and corona radiate. Diffusion-weighted imaging showed hyperintensities bilaterally in the parieto-occipital cortical regions. Subsequently, the patient was diagnosed with PRES, and remission was achieved with anti-hypertensive drugs. Six cases of rare adverse effects induced by anlotinib were reviewed in the literature. Since anlotinib has been widely applied as a novel third-line treatment in patients with non-small-cell lung cancer, the association between PRES and anlotinib would benefit neurologists and oncologists in future diagnoses and treatment.

Clinical features and management of coexisting anti-N-methyl-D-aspartate receptor encephalitis and myelin oligodendrocyte glycoprotein antibody-associated encephalomyelitis: a case report and review of the literature.

BACKGROUND: Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis is an autoimmune encephalitis caused by antibodies targeting the GluN1 subunit of NMDA receptors. Myelin oligodendrocyte glycoprotein (MOG) antibody disorders are now widely accepted as peculiar neuroimmunological diseases with specific clinical and pathological features. Some rare cases of overlapping anti-NMDA receptor encephalitis and MOG antibody-associated diseases have been reported, presenting complex clinical symptoms that make the disease more difficult to recognize. METHOD: In accordance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines, the terms "NMDAR" and "MOG," "NMDAR" and "demyelination," and "MOG" and "encephalitis" were searched in PubMed. Clinical cases with dual-positive anti-NMDA cerebrospinal fluid receptors and MOG serum antibodies during the disease course were included in this study. RESULTS: A total of 25 patients were analyzed in this study. The age at onset ranged from 3 to 54 years. The median number of relapses was 2.8. Administration of intravenous methylprednisolone and immunoglobulin was the most widely used treatment strategy (19/25 patients). Second-line treatments such as administration of mycophenolate mofetil, rituximab, interferon-ß, azathioprine, cyclophosphamide, and temozolomide were also reported, followed by good outcomes. CONCLUSIONS: The rates of coexisting anti-NMDA receptor encephalitis and MOG antibody-associated encephalomyelitis may be underestimated. Clinical symptoms such as seizures and cognitive decline accompanied by atypical central nervous system demyelination serve as warning signs of possible coexisting anti-NMDA receptor encephalitis and MOG antibody-associated encephalomyelitis. These patients could achieve good outcomes under proper immunotherapies.

Small Nucleolar RNA Host Gene 18 Acts as a Tumor Suppressor and a Diagnostic Indicator in Hepatocellular Carcinoma.

BACKGROUND: Noncoding RNAs are crucial regulators acting as either tumor suppressor genes or oncogenes in human cancer progression. The aberrant expression of noncoding RNAs has been confirmed in different kinds of cancers. Hepatocellular carcinoma is one of the most common malignant tumors worldwide, characterized by insidious onset, great malignancy, and high rates of recurrence and metastasis. Due to lack of early predictive markers, numerous patients are diagnosed in the late stages. As therapeutic options for advanced patients are quite limited, great efforts have been made to screen patients at early stages. A previous study reported that small nucleolar RNA host gene 18 played crucial role in glioma. However, its functions and roles in hepatocellular carcinoma are unknown. PURPOSE: To explore its functional role and diagnostic value in hepatocellular carcinoma, we investigated its expression level. METHODS: We performed real-time quantitative polymerase chain reaction in tumor tissues and adjacent noncancerous tissues derived from patients with hepatocellular carcinoma as well as in plasma, including samples from the healthy control, patients with hepatitis B, cirrhosis, and hepatocellular carcinoma. RESULTS: Small nucleolar RNA host gene 18 was downregulated in liver tissues compared to paired adjacent noncancerous tissues ( P < .0001). Meanwhile, plasma small nucleolar RNA host gene 18 showed a relatively high sensitivity and specificity (75.61% and 73.49%) for distinguishing patients with hepatocellular carcinoma whose α-fetoprotein levels were below 200 ng/mL from the healthy controls. CONCLUSION: Our study suggested that small nucleolar RNA host gene 18 might act as a tumor suppressor gene in hepatocellular carcinoma and potentially a diagnostic indicator to distinguish hepatocellular carcinoma from the healthy control and cirrhosis.

Decreased expression of LncRNA SRA1 in hepatocellular carcinoma and its clinical significance.

BACKGROUND: Hepatocellular carcinoma (HCC), is an extremely aggressive malignancy with poor prognosis and high fatality rates worldwide. Accumulating evidence indicated that novel biomarkers are required to get a better understanding of the biological mechanisms of HCC. SRA1, a long non-coding RNA (lncRNA), serves as a critical regulator in several cancers. However, the association between SRA1 expression and tumorigenesis in HCC tissues remains unclear. OBJECTIVE: In the present study, we evaluated the expression of SRA1 in HCC and its clinical association. METHODS: The expression levels of SRA1 in 67 pairs of cancer tissues and adjacent normal tissues from HCC patients were detected using quantitative real-time PCR. Expression of SRA1 in HCC cell lines compared with normal human hepatocyte cell lines was also measured. Finally, the potential associations between its level in HCC tissues and the clinicopathological parameters were analyzed as well. RESULTS: The results indicated that the expression levels of SRA1 in HCC were remarkably decreased, compared with matched normal tissues (P< 0.001). Levels of SRA1 in HCC cell lines were also significantly decreased than that in normal human hepatocyte cell line L-02. Additionally, the levels of SRA1 were significantly associated with tumor size (P= 0.020) and serum GLU level (P= 0.046). CONCLUSIONS: This study highlighted that SRA1 was downregulated in HCC and might serve as a tumor suppressor in HCC, which laid a solid foundation for future research.

Prognostic value of abnormally expressed lncRNAs in ovarian carcinoma: a systematic review and meta-analysis.

Ovarian cancer (OC) is the most deadly gynecological cancer and it is urgently needed to find a new marker for the progress of OC. Many long noncoding RNAs (lncRNAs) have been reported to be aberrantly expressed in ovarian carcinoma, and may serve as prognostic markers. Therefore, we conducted this meta-analysis to gain a better understanding of the prognostic value of lncRNAs in patients with varian carcinoma. We systematically searched PubMed, EMBASE, and Web of Science. A total of 13 eligible studies, including 10 on clinicopathological features, 13 on prognosis were identified. Pooled hazard ratios (HRs) or odds ratios (OR) and 95% confidence intervals (95% CIs) were calculated using random- or fixed-effects models. Our results revealed that the increased expressions of 8 lncRNAs were associated with poor prognosis and the decreased expressions of 5 lncRNAs were related to poor prognosis in ovarian carcinoma. High HOTAIR expression was associated with shorter overall survival in ovarian cancer (pooled HR: 2.05, 95% CI: 1.51-2.77, P < 0.001). In conclusion, our meta-analysis suggested that LncRNAs could function as potential prognostic markers for ovarian cancer patients and high expression HOTAIR was associated with shorter overall survival in ovarian cancer.

Optogenetic activation reveals distinct roles of PIP3 and Akt in adipocyte insulin action.

Glucose transporter 4 (GLUT4; also known as SLC2A4) resides on intracellular vesicles in muscle and adipose cells, and translocates to the plasma membrane in response to insulin. The phosphoinositide 3-kinase (PI3K)-Akt signaling pathway plays a major role in GLUT4 translocation; however, a challenge has been to unravel the potentially distinct contributions of PI3K and Akt (of which there are three isoforms, Akt1-Akt3) to overall insulin action. Here, we describe new optogenetic tools based on CRY2 and the N-terminus of CIB1 (CIBN). We used these 'Opto' modules to activate PI3K and Akt selectively in time and space in 3T3-L1 adipocytes. We validated these tools using biochemical assays and performed live-cell kinetic analyses of IRAP-pHluorin translocation (IRAP is also known as LNPEP and acts as a surrogate marker for GLUT4 here). Strikingly, Opto-PIP3 largely mimicked the maximal effects of insulin stimulation, whereas Opto-Akt only partially triggered translocation. Conversely, drug-mediated inhibition of Akt only partially dampened the translocation response of Opto-PIP3 In spatial optogenetic studies, focal targeting of Akt to a region of the cell marked the sites where IRAP-pHluorin vesicles fused, supporting the idea that local Akt-mediated signaling regulates exocytosis. Taken together, these results indicate that PI3K and Akt play distinct roles, and that PI3K stimulates Akt-independent pathways that are important for GLUT4 translocation.