Cardiac haemangiomas are rare cases and can be seen at any age of life. A 49-year-old woman was admitted to our hospital with chest pain. A well-circumscribed soft tissue mass extending from the pulmonary artery truncus to the left ventricular inferior neighborhood. FSEN1 Following surgical resection, the patient was discharged 4 days after surgery. The restraint water immersion stress (RWIS) model includes both psychological and physical stimulation, which may lead to gastrointestinal disorders and cause gastric mucosal damage. The ventrolateral periaqueductal gray (VLPAG) contributes to gastrointestinal function, but whether it is involved in RWIS-induced gastric mucosal damage has not yet been reported. The expression of glial fibrillary acidic protein (GFAP), neuronal c-Fos and phosphorylated extracellular signal regulated kinase 1/2 (p-ERK1/2) in the VLPAG after RWIS was assessed using western blotting and immunocytochemical staining methods. Lateral ventricle injection of astrocytic toxin L-a-aminoadipate (L-AA) and treatment with ERK1/2 signaling pathway inhibitor PD98059 were further used to study protein expression and distribution in the VLPAG after RWIS. The expression of c-Fos, GFAP, and p-ERK1/2 in the VLPAG significantly increased following RWIS and peaked at 1h after RWIS. Lateral ventricle injection of the astrocytic toxin L-AA significantly alleviated gastric mucosal injury and decreased the activation of neurons and astrocytes. Treatment with the ERK1/2 signaling pathway inhibitor PD98059 obviously suppressed gastric mucosal damage as well as the RWIS-induced activation of neurons and astrocytes in the VLPAG. These results suggested that activation of VLPAG neurons and astrocytes induced by RWIS through the ERK1/2 signaling pathway may play a critical role in RWIS-induced gastric mucosa damage.These results suggested that activation of VLPAG neurons and astrocytes induced by RWIS through the ERK1/2 signaling pathway may play a critical role in RWIS-induced gastric mucosa damage.Oesophageal schwannomas are extremely rare tumours arising from Schwann cells of the neural sheath, with less than 115 cases reported in the English literature. These tumours are usually sporadic and account for about 2% of all stromal oesophageal tumours. Diagnosis is usually confirmed by the presence of positive immunohistochemical marker S-100 and absence of CD117, CD34, smooth muscle actine and Desmin. Treatment can vary from enucleation to oesophagectomy. Herein, we report a case of a 61-year-old woman who presented with progressive dysphagia. Computerized tomography scan revealed a 5 × 3 cm mass extending proximal to the azygos arch. Oesophagogastroduodenoscopy showed a submucosal mass at 20-24 cm from the incisors. Endoscopic ultrasound showed a 6 × 3 cm well-circumscribed mass originating from the fourth layer, suspicious for a gastrointestinal stromal tumour. The patient underwent thoracoscopic enucleation of the tumour in a semi-prone position. Final pathology was consistent with a completely resected benign oesophageal schwannoma, positive for S-100. Radioiodine-refractory thyroid cancers have poor outcomes and limited therapeutic options (tyrosine kinase inhibitors) due to transient efficacy and toxicity of treatments. Therefore, combinatorial treatments with new therapeutic approaches are needed. Many studies link G protein-coupled receptors (GPCRs) to cancer cell biology. To perform a specific atlas of GPCR expression in progressive and refractory thyroid cancer to identify potential targets among GPCRs aiming at drug repositioning. We analyzed samples from tumor and normal thyroid tissues from 17 patients with refractory thyroid cancer (12 papillary thyroid cancers [PTCs] and 5 follicular thyroid cancers [FTCs]). We assessed GPCR mRNA expression using NanoString technology with a custom panel of 371 GPCRs. The data were compared with public repositories and pharmacological databases to identify eligible drugs. The analysis of prognostic value of genes was also performed with TCGA datasets. With our transcriptomic analysis, 4 receptors were found to be downregulated in FTC (VIPR1, ADGRL2/LPHN2, ADGRA3, and ADGRV1). In PTC, 24 receptors were deregulated, 7 of which were also identified by bioinformatics analyses of publicly available datasets on primary thyroid cancers (VIPR1, ADORA1, GPRC5B, P2RY8, GABBR2, CYSLTR2, and LPAR5). Among all the differentially expressed genes, 22 GPCRs are the target of approved drugs and some GPCRs are also associated with prognostic factors. For the first time, we performed GPCR mRNA expression profiling in progressive and refractory thyroid cancers. These findings provide an opportunity to identify potential therapeutic targets for drug repositioning and precision medicine in radioiodine-refractory thyroid cancer.For the first time, we performed GPCR mRNA expression profiling in progressive and refractory thyroid cancers. These findings provide an opportunity to identify potential therapeutic targets for drug repositioning and precision medicine in radioiodine-refractory thyroid cancer. Clinical onset of type 1 diabetes (Stage 3 T1D) is preceded by a pre-symptomatic phase characterized by multiple islet autoantibodies with normal glucose tolerance (Stage 1 T1D). The metabolic phenotypes of beta-cell function and insulin sensitivity and clearance were explored in normoglycemic youth with Stage 1 T1D and compared to healthy non-related peers during a 3-h oral glucose tolerance test (OGTT). Twenty-eight lean youth, 14 with ≥2 islet autoantibodies (cases) and 14 healthy controls underwent a 3-h 9-point OGTT with measurement of glucose, C-peptide and insulin. The oral minimal model was used to quantitate β-cell responsiveness (φtotal) and insulin sensitivity (SI), allowing assessment of β-cell function by the disposition index (DI= φtotal x SI). Fasting insulin clearance (CL0) was calculated as the ratio between the fasting insulin secretion rate (ISR) and plasma insulin levels (ISR0/I0), while post-load clearance (CL180) was estimated by the ratio of AUC of ISR over the plasma insulin AUC for the 3-h OGTT (ISRAUC/IAUC).