Typically, right coronary artery (RCA) occlusion causes ST-segment elevation in inferior leads. However, it is rarely observed that RCA occlusion causes ST-segment elevation only in precordial leads. In general, an electrocardiogram is considered to be the most important method for determining the infarct-related artery, and recognizing this is helpful for timely discrimination of the culprit artery for reperfusion therapy. In this case, an elderly woman presented with chest pain showing dynamic changes in precordial ST-segment elevation with RCA occlusion.
 
  A 96-year-old woman presented with acute chest pain showing precordial ST-segment elevation with dynamic changes. Myocardial injury markers became positive. Coronary angiography indicated acute total occlusion of the proximal nondominant RCA, mild atherosclerosis of left anterior descending artery and 75% stenosis in the left circumflex coronary artery. Percutaneous coronary intervention was conducted for the RCA. Repeated manual thrombus aspiration was performed, and fresh thrombus was aspirated. A 2 mm × 15 mm balloon was used to dilate the RCA with an acceptable angiographic result. The patient's chest pain was relieved immediately. A postprocedural electrocardiogram showed alleviation of precordial ST-segment elevation. The diagnosis of acute isolated right ventricular infarction caused by proximal nondominant RCA occlusion was confirmed. Echocardiography indicated normal motion of the left ventricular anterior wall and interventricular septum (ejection fraction of 54%), and the right ventricle was slightly dilated. The patient was asymptomatic during the 9-mo follow-up period.
 
  Cardiologists should be conscious that precordial ST-segment elevation may be caused by occlusion of the nondominant RCA.
 Cardiologists should be conscious that precordial ST-segment elevation may be caused by occlusion of the nondominant RCA.
  Gastroesophageal varices are a rare complication of essential thrombocythemia (ET). ET is a chronic myeloproliferative neoplasm (MPN) characterized by an increased number of blood platelets.
 
  A 46-year-old woman, who denied a history of liver disease, was admitted to our hospital on presentation of hematemesis. Laboratory examination revealed a hemoglobin level of 83 g/L, and a platelet count of 397 × 10
  /L. The appearance of gastric and esophageal varices with red colored signs as displayed by an urgent endoscopy was followed by endoscopic variceal ligation and endoscopic tissue adhesive. Abdominal computed tomography revealed cirrhosis, marked splenomegaly, portal vein thrombosis and portal hypertension. In addition, bone marrow biopsy and evidence of mutated Janus kinase 2, substantiated the onset of ET. The patient was asymptomatic with regular routine blood testing during the 6-mo follow-up period. Therefore, in this case, gastroesophageal varices were induced by ET.
 
  MPN should be given considerable attention when performing differential diagnoses in patients with gastroesophageal varices. An integrated approach such as laboratory tests, radiological examination, and pathological biopsy, should be included to allow optimal decisions and management.
 MPN should be given considerable attention when performing differential diagnoses in patients with gastroesophageal varices. An integrated approach such as laboratory tests, radiological examination, and pathological biopsy, should be included to allow optimal decisions and management.
  Intradural osteoma is very rarely located in the subdural or subarachnoid space.  https://www.selleckchem.com/products/liraglutide.html  Unfortunately, intradural osteoma lacks specificity in clinical manifestations and imaging features and there is currently no consensus on its diagnosis method or treatment strategy. Moreover, the pathogenesis of osteoma without skull structure involvement remains unclear.
 
  We describe two cases of intradural osteomas located in the subdural and subarachnoid spaces, respectively. The first case involved a 47-year-old woman who presented with a 3-year history of intermittent headache and dizziness. Intraoperatively, a bony hard mass was found in the left frontal area, attached to the inner surface of the dura mater and compressing the underlying arachnoid membrane and brain. The second case involved a 56-year-old woman who had an intracranial high-density lesion isolated under the right greater wing of the sphenoid. Intraoperatively, an arachnoid-covered bony tumor was found in the sylvian fissure. The pathological diagnosis for both patients was osteoma.
 
  Surgery and pathological examination are required for diagnosis of intradural osteomas, and craniotomy is a safe and effective treatment.
 Surgery and pathological examination are required for diagnosis of intradural osteomas, and craniotomy is a safe and effective treatment.
  Craniometaphyseal dysplasia (CMD) is a rare genetic disorder. Autosomal dominant CMD (AD-CMD) is caused by mutations in the 
  gene. Affected individuals typically have distinctive facial features including progressive thickening of the craniofacial bones. Treatment for AD-CMD primarily consists of surgical intervention to release compression of the cranial nerves and the brain stem/spinal cord. To alleviate progression of the clinical course and improve the quality of life in children waiting to undergo the necessary surgery, we investigated clinical changes in a diagnosed patient with AD-CMD over three years.
 
  A 17-mo-old boy presented with progressive nasal obstruction, snoring and hearing loss symptoms. Physical examination showed enlargement of the head circumference and clinical features such as wide nasal bridge, paranasal bossing, widely spaced eyes with an increased bizygomatic width, and a prominent mandible. The patient underwent otolaryngological examination, endoscopy, hearing test, laboratoryafter dietary intervention indicating that a low-calcium diet may be applied in pediatric AD-CMD patients with ANKH mutations to help alleviate phenotypic manifestations and improve the quality of life before surgical intervention. Further large scale studies are needed to replicate these findings and to establish the appropriate timing for nutritional and surgical interventions.