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Gallbladder perforation (GBP) represents a rare, but potentially life-threatening, complication of acute cholecystitis. GBP is subdivided into three categories whereas the development of biloma is extremely rare. The present case study reports on a 40-year-old man with a 10-year history of calculus cholecystitis, who was referred to The First Affiliated Hospital of Nanjing Medical University (Nanjing, China) for the surgical treatment of an emerging massive hepatic entity with insidious symptoms and normal laboratory tests. A preoperative imaging study demonstrated the collection with internal septations and mural nodules, but no visible communication with the biliary system. Given the suspected biliary cystic tumor, a laparotomy was performed and the lumen was scattered with papillae. An intraoperative frozen section examination illustrated a simple hepatic cyst. Biochemical analysis of the collection and histopathology of the gallbladder and capsule substantiated the diagnosis of biloma formation due to GBP. The purpose of the present case report was to demonstrate how a pinhole-sized perforation with extravasation of unconcentrated bile from the gallbladder may result in insidious clinical presentation and an undetected leak site. According to the clinicopathological characteristics and composition, formation of biloma should be classified as type IV GBP. To differentiate bilomas with intracystic septations and mural nodules from BCTs is difficult via a preoperative examination, and the definitive diagnosis should be based on a histological examination. Laparotomy with frozen section examination may be the optimal approach in such a case. [ABSTRACT FROM AUTHOR]

Sorbitol dehydrogenase (SDH), a key enzyme of the polyol pathway, has recently been demonstrated to have an important role in mediating tissue ischemia/reperfusion (I/R) injury. The present study investigated how this enzyme may affect the ischemic liver and the mechanism underlying its effect. Firstly, C57BL/6 mice were subjected to oral administration of CP-470,711 (5 mg/kg body weight/day for five days) and 70% hepatic I/R. Next the present study further investigated the changes in liver function, histology, inflammation, apoptosis and necrosis; the cytosolic adenosine triphosphate (ATP) and nictotinamide adenine dinucleotide [NAD(H)] contents and the protein level of caspase 3 and sirtuin 1 (SIRT1). The data demonstrated that sorbitol dehydrogenase inhibitor (SDI)-administration significantly alleviated I/R-induced liver injury, palliated histological changes and lowered the level of hepatocyte apoptosis and necrosis. In addition, SDI-pretreatment in ischemic liver markedly maintained the cytosolic ATP and NAD(H) proportion, enhanced SIRT1 and suppressed the activation of caspase 3 at the protein level. The findings in the present study revealed that the flux through SDH may render the liver more vulnerable to I/R-induced injury and interventions targeting this enzyme may provide a novel adjunctive approach to protect from severe tissue injury following liver ischemia. [ABSTRACT FROM AUTHOR]

Never in mitosis gene A-related kinase (Nek) 6 is a recently identified Nek that is required for mitotic cell cycle progression; however, the role and mechanism of Nek6 activity during hepatocarcinogenesis is not well known. The aim of this study was to investigate the potential roles and internal mechanism of Nek6 in hepatocellular carcinoma (HCC) development. In the present study, Nek6 was found to be overexpressed in HCC samples and cell lines by florescent real-time quantitative polymerase chain reaction, immunohistochemistry and western blot analysis. Furthermore, it was evidenced to contribute to oncogenesis and progression. The ectopic overexpression of Nek6 promoted cell proliferation and colony formation, whereas gene silencing of Nek6 inhibited these phenotypes, as documented in Huh7, PLC/PRF/5, Hep3B and HepG2 HCC cell lines. Mechanistic analyses indicated that Nek6 regulates the transcription of cyclin B through cdc2 activation, and promotes the accumulation of G0/G1-phase cells. In conclusion, the findings of the current study suggested that Nek6 contributes to the oncogenic potential of HCC, and may present as a potential therapeutic target in this disease. [ABSTRACT FROM AUTHOR]