Halomonas socia sp. nov., isolated from high salt culture of Dunaliella salina.

A moderately halophilic bacteria designed strain NY-011(T) was isolated from the high salt culture of Dunaliella salina in Chengdu of Sichuan Province, China. The isolate was Gram-negative, nonmotile, rod-shaped and 12.5-21.6 µm in length. Colonies on solid media are circular, wet, smooth and cream. The strain grew optimally at 37 °C, pH 7.0 and in the presence of 8 % NaCl. Acid was produced from glycerol, D-arabinose, glucose, trehalose, inositol, mannose, mannitol, sucrose, maltose and sorbitol. Catalase is produced but not oxidase. The major fatty acids are C18: 1ω7c (37.59 %), C19: 0 cyclo ω8c (18.29 %), C16: 0 (16.05 %) and C6: 0 (12.43 %). The predominant respiratory lipoquinone found in strain NY-011(T) is ubiquinone with nine isoprene units (Q-9). The genomic DNA G + C content of strain NY-011(T) was 62.7 mol%. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strain NY-011(T) belonged to the genus Halomonas. The highest levels of 16S rRNA gene sequence similarity were found between the strain NY-011(T) and H. pantelleriensis (sequence similarity 98.43 %). However, the levels of DNA-DNA relatedness between them were only 23.1 %. In addition, the strain NY-011(T) had a phenotypic profile that readily distinguished it from H. pantelleriensis. The strain NY-011(T) therefore represents a new species of the genus Halomonas, for which the name Halomonas socia sp. nov. is proposed, with NY-011(T) (=CCTCC AB 2011033(T) = KCTC 23671(T)) as the type strain.

Misdiagnosis of an elevated lesion in the esophagus: A case report.

BACKGROUND: Esophageal carcinosarcoma (ECS) is a rare biphasic tumor and a type of esophageal malignancy, which presents as protruding or elevated lesions. ECS patients are often not hospitalized until they have severe dysphagia. ECS is easily misdiagnosed as a benign tumor due to its atypical characteristics under endoscopy. With the popularization of endoscopic treatment, these patients are often referred to endoscopic treatment, such as endoscopic submucosal dissection (ESD). However, there is a lack of consensus on the endoscopic features and therapies for ECS. Here, we report a case of ECS and discuss the value of endoscopic diagnosis and therapeutic strategies. CASE SUMMARY: A 63-year-old man was admitted to the hospital with dysphagia. During the endoscopic examination, an elevated lesion was found with an erosive and hyperemic surface covered with white pseudomembranous inflammation. Endoscopic ultrasonography (EUS), biopsies, and enhanced thoracic computed tomography were performed, suggesting that it was a benign lesion and located within the submucosal layer. This lesion was diagnosed as a fibrovascular polyp with a Paris classification of 0-Ip. The patient was then referred to ESD treatment. However, the post-ESD pathological and immunohistochemical study showed that this lesion was ECS with a vertical positive margin (T1b stage), indicating that we made a misdiagnosis and achieved a noncurative resection. Due to the potential tumor residue, additional open surgery was performed at the patient's request. In the postoperative pathological study, no tumor remnants or metastases were discovered. The patient was followed for 1 year and had no recurrence. CONCLUSION: ECS can be misdiagnosed at the initial endoscopy. EUS can help to identify the tumor stage. Patients with T1b stage ECS cannot be routinely referred to ESD treatment due to the high risk of metastasis and recurrence rate.

Technetium-99m-labeled macroaggregated albumin lung perfusion scan for diagnosis of hepatopulmonary syndrome: A prospective study comparing brain uptake and whole-body uptake.

BACKGROUND: Hepatopulmonary syndrome (HPS) is an arterial oxygenation defect induced by intrapulmonary vascular dilatation (IPVD) in the setting of liver disease and/or portal hypertension. This syndrome occurs most often in cirrhotic patients (4%-32%) and has been shown to be detrimental to functional status, quality of life, and survival. The diagnosis of HPS in the setting of liver disease and/or portal hypertension requires the demonstration of IPVD (i.e., diffuse or localized abnormally dilated pulmonary capillaries and pulmonary and pleural arteriovenous communications) and arterial oxygenation defects, preferably by contrast-enhanced echocardiography and measurement of the alveolar-arterial oxygen gradient, respectively. AIM: To compare brain and whole-body uptake of technetium for diagnosing HPS. METHODS: Sixty-nine patients with chronic liver disease and/or portal hypertension were prospectively included. Brain uptake and whole-body uptake were calculated using the geometric mean of technetium counts in the brain and lungs and in the entire body and lungs, respectively. RESULTS: Thirty-two (46%) patients had IPVD as detected by contrast-enhanced echocardiography. The demographics and clinical characteristics of the patients with and without IPVD were not significantly different with the exception of the creatinine level (0.71 ± 0.18 mg/dL vs 0.83 ± 0.23 mg/dL; P = 0.041), alveolar-arterial oxygen gradient (23.2 ± 13.3 mmHg vs 16.4 ± 14.1 mmHg; P = 0.043), and arterial partial pressure of oxygen (81.0 ± 12.1 mmHg vs 90.1 ± 12.8 mmHg; P = 0.004). Whole-body uptake was significantly higher in patients with IPVD than in patients without IPVD (48.0% ± 6.1% vs 40.1% ± 8.1%; P = 0.001). The area under the curve of whole-body uptake for detecting IPVD was significantly higher than that of brain uptake (0.75 vs 0.54; P = 0.025). The optimal cut-off values of brain uptake and whole-body uptake for detecting IPVD were 5.7% and 42.5%, respectively, based on Youden's index. The sensitivity, specificity, and accuracy of brain uptake > 5.7% and whole-body uptake > 42.5% for detecting IPVD were 23%, 89%, and 59% and 100%, 52%, and 74%, respectively. CONCLUSION: Whole-body uptake is superior to brain uptake for diagnosing HPS.