Background Non-parasitic splenic cysts are associated with elevated serum carbohydrate antigen (CA) 19–9 levels. We report a case in which a 23-year-old female exhibited a large ruptured splenic cyst and an elevated serum CA19–9 level. Case presentation The patient, who experienced postprandial abdominal pain and vomiting, was transferred to our hospital and was found to have a large splenic cyst during an abdominal computed tomography (CT) scan. On physical examination, her vital signs were stable, and she demonstrated rebound tenderness in the epigastric region. An abdominal CT scan revealed abdominal fluid and a low-density region (12 × 12 × 8 cm) with enhanced margins in the spleen. The patient’s serum levels of CA19–9 and CA125 were elevated to 17,580 U/mL and 909 U/mL, respectively. A cytological examination of the ascitic fluid resulted in it being categorized as class II. Finally, we made a diagnosis of a ruptured splenic epidermoid cyst and performed laparoscopic splenic fenestration. The patient’s postoperative course was uneventful, and she was discharged on postoperative day 5. The cystic lesion was histopathologically diagnosed as a true cyst, and the epithelial cells were positive for CA19–9. Follow-up laboratory tests performed at 4 postoperative months showed normal CA19–9 (24.6 U/L) and CA125 (26.8 U/L) levels. No recurrence of the splenic cyst was detected during the 6 months after surgery. Conclusion Laparoscopic fenestration of a ruptured splenic cyst was performed to preserve the spleen, after the results of abdominal fluid cytology and MRI were negative for malignancy.

Patient: Female, 48 Final Diagnosis: Spinal schawnnoma Symptoms: Dysuria • leg pain Medication: — Clinical Procedure: — Specialty: Orthopedics and Traumatology Objective: Challenging differential diagnosis Background: Spinal schwannomas are benign tumors arising from Schwann cells. Although they have been well described, tumor movement in the spinal canal is an extremely rare finding, and entirely cystic spinal schwannomas have rarely been reported. This is the first report of a spinal schwannoma that simultaneously exhibited both these unusual features. Case Report: A 48-year-old female presented with dysuria and right leg pain. Initial magnetic resonance imaging (MRI) revealed a well-delineated intradural cystic lesion at the level of L4–S1 vertebrae that was isointense with cerebrospinal fluid on both T1- and T2-weighted images. A follow-up MRI 6 months later showed that the tumor had moved to the level of L2–L4; it also revealed tortuous configuration of nerve roots of the cauda equina. The tumor was resected, and a diagnosis of schwannoma with extensive cystic degeneration was pathologically confirmed. Conclusions: Various possible mechanisms have been suggested for the mobility of extramedullary tumors. In the present case, MRI findings indicated the cause of the tumor movement might be attributed to the laxity of nerve roots. Besides, it is highly atypical for a schwannoma to present an entirely cystic appearance, and the combination of the 2 extraordinary features made preoperative diagnosis difficult. However, 16 out of 22 (73%) of previously reported mobile spinal tumors were schwannomas, so the differential diagnosis for a mobile spinal tumor should include schwannoma, even when the lesion seems entirely cystic on MRI. To minimize the risk of complications and additional surgical dissection, physicians should acknowledge that spinal tumors can migrate.

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We expressed luciferase (RLuc) from Renilla reniformis in Escherichia coli RLuc was purified using a Ni-NTA column and subsequently characterized. It was unstable in acidic solutions and at 30°C. To increase the stability of RLuc, the Rluc gene was randomly mutated using error-prone polymerase chain reaction. E. coli harboring the mutated gene was screened by detecting luminescence on a plate containing the substrate coelenterazine at 34°C. Three mutants, i.e. N264SS287P, N178D and F116LI137V, were obtained. The solubilities and specific activities of these mutants were higher than those of the wild type. Furthermore, the N264SS287P mutant maintained stability at a temperature approximately 5°C higher than that of the wild type, while denaturation of the F116LI137V mutant started at a temperature that was 5°C lower than the wild type, and ended at a temperature that was 7°C higher. We examined the obtained mutations using thermal shift assays and a computer program Coot in this study.

Lipomembranous fat necrosis (LFN) is an uncommon but distinct form of fat necrosis, which is characterized by eosinophilic, crenulated and/or serpiginous membranes. LFN exhibits macrocystic, microcystic and/or crushed features. LFN is routinely detectable on hematoxylin and eosin (H&E)-stained sections, and is present both in the acute phase and in the later or fibrous stage of necrotic fatty lesions. Smaller crushed LFN embedded within fibrous tissues may be difficult to recognize on H&E-stained sections, but can be highlighted by some staining techniques, including Masson trichrome, periodic acid-Schiff, orcein, long Ziehl-Neelsen stain, silver impregnation, phosphotungstic acid-hematoxylin and luxol fast blue staining. LFN was initially considered a specific feature of Nasu-Hakola disease, but has since been identified in various subcutaneous or intraabdominal lesions related to ischemic conditions or venous insufficiency. In addition, LFN is detectable in intra-articular loose bodies and aortic valves with or without dysfunction, suggesting that LFN is also associated with ischemia-like hypoxic conditions or malnutrition. LFN is considered to be a histological hallmark of hidden ischemic or hypoxic/malnourished conditions in various diseases; however, the exact mechanisms of LFN remain poorly understood. The present review described the clinicopathological features of this interesting, but poorly characterized, condition.