Two-surgeon technique using saline-linked electric cautery and ultrasonic surgical aspirator in living donor hepatectomy: its safety and efficacy

Background

Saline-linked electric cautery (SLC) is introduced as an effective device to reduce blood loss in liver surgery. The aim of the current study was to evaluate the safety and efficacy of a 2-surgeon technique using SLC and the Cavitron Ultrasonic Surgical Aspirator (CUSA; Valleylab, Boulder, CO) in living donor hepatectomy.

Methods

Forty-three living donor right hepatectomy cases were enrolled in this study. The first 28 cases underwent liver transection with CUSA alone (CUSA group), while additional SLC was applied in the current 15 cases (2-surgeon technique, TS group).

Results

Blood loss was significantly reduced by the 2-surgeon technique (1,115.2 ± 652.9 g in CUSA group vs 732.3 ± 363.6 g in TS group, P < .05). In the TS group, there was no bile leakage from the cut surface. The early graft function and postoperative recipient survival were not significantly different between the groups.

Conclusions

According to our single-center experience, blood loss and donor complications in living donor hepatectomies were significantly reduced using a 2-surgeon technique using CUSA and SLC, while maintaining the graft viability.     

Sema4D deficiency results in an increase in the number of oligodendrocytes in healthy and injured mouse brains

Semaphorins, a family of secreted and membrane‐bound proteins, are known to function as repulsive axon guidance molecules. Sema4D, a class 4 transmembrane‐type semaphorin, is expressed by oligodendrocytes in the central nervous system, but its role is unknown. In this study, the effects of Sema4D deficiency on oligodendrocytes were studied in intact and ischemic brains of adult mice. As observed in previous studies, Sema4D marked by β‐galactosidase in Sema4D mutant mice was localized exclusively on myelin‐associated glycoprotein (MAG)‐positive oligodendrocytes but not on NG2‐positive oligodendrocyte progenitor cells (OPCs). Although there was no difference in the number of the latter cells between Sema4D‐deficient and wild‐type mice, the number of MAG‐positive cells was significantly increased in the cerebral cortex of both nonischemic and postischemic brains of Sema4D‐deficient mice. Cell proliferation, observed by using bromodeoxyuridine incorporation, was evident in the MAG‐positive cells that developed after cerebral ischemia. These data indicate that Sema4D is involved in oligodendrogenesis during development and during recovery from ischemic injury. © 2009 Wiley‐Liss, Inc.     

Multifocal metanephric adenoma in childhood

Metanephric adenoma is the most commonly occurring member of the metanephric tumor family, which also includes metanephric adenofibroma and metanephric stromal tumor. According to the World Health Organization classification, however, it is not commonly multifocal. Reported herein is the case of a 9-year-old boy with multifocal metanephric adenoma. Histologically, surgical sections showed multifocal proliferation of small rounded and uniform cells with smooth nuclear contours, scant pale-staining cytoplasm, dark-staining nuclei, and inconspicuous nucleoli: the cells were arranged in sheets and acinal, ductal, glomeruloid, and papillary structures. On immunohistochemistry the tumor cells were positive for vimentin, cytokeratins (CAM5.2, AE1/AE3, and CK18), and WT1, but negative for cytokeratin 7 (CK7) and epithelial membrane antigen (EMA). The Ki-67 labeling index was <1%. In addition, cytogenetic analysis indicated a normal karyotype (46XY). Other histologically similar tumors are papillary renal cell carcinoma and nephroblastoma, and it is necessary to distinguish metanephric adenoma from those tumors because of malignancy. In contrast to those tumors, metanephric adenoma has inconspicuous nucleoli, loss of CK7 and EMA expression, and no mitotic figures. Thus, the histological and immunohistochemical features of the present case were compatible with metanephric adenoma.     

Detection of M2 macrophages and colony-stimulating factor 1 expression in serous and mucinous ovarian epithelial tumors

Tumor-associated macrophages (TAM) are known to possess the immunosuppressive M2 macrophage phenotype. They contribute to tumor growth, invasion, and metastasis by producing various mediators. Macrophages, especially M2 polarized macrophages, preferentially express CD163 and CD204, but few studies have investigated macrophage phenotypes in human ovarian tumors. The purpose of the present study was therefore to present results on macrophage differentiation in human ovarian serous and mucinous epithelial tumors. The method focused on immunostaining of paraffin-embedded tumor samples. Almost all macrophages infiltrating tumor tissues expressed CD163 and CD204, indicating the phenotypic shift toward M2 macrophage. The numbers of CD68-positive macrophages as well as of CD163- and CD204-positive macrophages in borderline and malignant tumors were significantly higher than in benign tumors. They correlated well with histological gradient of malignancy. Macrophage colony-stimulating factor (also known as colony-stimulating factor; CSF-1), which is one of the cytokines considered to induce TAM to polarize toward an M2 phenotype, was then evaluated. CSF-1 expression in malignant tumor cells was significantly higher than that in benign tumor cells and correlated with histological malignancy. These results suggest that CSF-1 derived from tumor tissues induces macrophages to shift toward the M2 phenotype, which is considered to promote tumor growth.     

Expression of sphingosine kinase 2 in synovial fibroblasts of rheumatoid arthritis contributing to apoptosis by a sphingosine analogue, FTY720

Gene expression profiles in synovial tissues from rheumatoid arthritis (RA) patients have yielded useful information on the pathogenetic process of the synovitis. In one group of them, sphingosine kinase 2 (SPHK2), a nuclear protein regulating cell proliferation, seemed to be highly expressed, undergoing a different pathogenetic process of synovitis. In the present study it was clarified that SPHK2 was expressed in the synovial fibroblasts of the synovial tissues obtained from the knee joints of the RA patients. In the cultured synovial fibroblasts from these patients, SPHK2 was more highly expressed than that in the human macrophage cell line, THP-1 and human dermal fibroblasts. SPHK2 was expressed in and around the nucleus and transferred to the cytoplasm and cell surface by the administration of epidermal growth factor, associated with the increased expression of sphingosine-1-phosphate. A sphingosine analogue, FTY720, which is activated by phosphorylation specifically by SPHK2, mediated apoptotic signaling of the cultured synovial fibroblasts. These findings suggest that SPHK2 may regulate the autonomous proliferation of synovial fibroblasts as one of the predisposing genes to RA and could be a target for a novel therapeutic strategy for RA.     

Evaluation of Early and Midterm Results of Offpump Coronary Artery Bypass in Patients with Left Main Disease

Abstract   Purpose : This study evaluated the early and midterm results of offpump coronary artery bypass (OPCAB) for left main coronary artery (LMCA) stenosis. Methods : Patients treated between November 2001 and December 2006, during which isolated coronary artery bypass grafting (CABG) was performed without cardiopulmonary bypass in principle, were included. Isolated CABG was performed in 206 patients, of whom 62 (30.1%) had LMCA stenosis >50 % . Results : The in-hospital mortality rate (LMCA stenosis > 50%, 1.6%; LMCA stenosis ≦50%, 0.7%, p = 0.512), the incidence of postoperative complications, and the midterm survival rate (LMCA stenosis≻50%, 86.7 ± 5.2%/5 years, LMCA stenosis ≦ 50%, 89.6 ± 3.8%/5 years, p = 0.21) did not significantly differ between the two groups. Conversion was significantly frequent in patients with LMCA stenosis >75% and severe stenosis >90% in the right coronary artery (RCA) trunk. Conclusions : Patients with LMCA stenosis can undergo OPCAB safely and the midterm results are good. As conversion was significantly frequent in patients with severe LMCA and RCA trunk stenosis, adequate preparation for pump application is necessary.     

Effects of intratumoral injection of CCL2 on monocyte-endothelial cell interactions in mouse pancreatic cancer

OBJECTIVE: Although monocyte infiltration is an important aspect of the host response to tumor growth, the mechanisms of recruitment and their impact on tumor growth are still unknown. The authors studied monocyte-endothelial interaction and the effect of chemokine CCL2 in orthotopic mouse pancreatic cancer. METHODS: The rolling and adhesion of labeled monocytes in peritumoral and intratumoral areas were assessed by using an intravital microscope. Further, the effects of intratumoral injection or superfusion of CCL2 on in situ recruitment of monocytes and other immune cells and adhesion molecules were investigated. RESULTS: More monocytes were recruited in the peritumoral area than in the intratumoral area with increased vascular interaction, and the effect was more apparent by intratumoral CCL2 injection than superfusion. In both CCL2-treated groups infiltration of CD11b(+), CD68(+), and CD4(+) cells were increased, but the magnitude of increase was larger in intratumoral injection. Quantitative RT-PCR for the tumor tissue revealed that ICAM-1 expression was increased by the injection of CCL2. CONCLUSION: These results show intratumoral injection of CCL2 induces effective interaction between monocytes and endothelial cells in the peritumoral area of pancreatic cancer accompanied by the upregulation of ICAM-1 and may possibly become a tool for immunotherapy by promoting the infiltration of immune cells in cancers.     

Anti-oxidative effect of Klotho on endothelial cells through cAMP activation

Klotho, a regulatory factor implicated in countering the aging process, has been reported to ameliorate endothelial dysfunction in vivo. To clarify whether Klotho protein directly affects endothelial cell function, we studied the effects of membrane-form Klotho on manganese superoxide dismutase (Mn-SOD) expression and nitric oxide production in human umbilical vein endothelial cells (HUVEC). We incubated HUVEC with conditioned medium from COS-1 cells transfected with expression vector, pCAGGS-klotho (Klotho-CM) or a recombinant, purified 6His-tagged Klotho protein. Both Klotho-CM and 6His-tagged Klotho protein enhanced Mn-SOD expression by approximately two-fold, partially via activation of the cAMP signaling pathway. Furthermore, Klotho-CM increased nitric oxide production, which also contributed to the up-regulation of Mn-SOD. Using the oxidation-sensitive dye dihydroethidium, we found that Klotho inhibited angiotensin II-induced reactive oxygen species production in HUVEC. These findings provide new insights into the mechanisms of Klotho action and support the therapeutic potential of membrane-form Klotho to regulate endothelial function. Hiromi Rakugi and Naomichi Matsukawa contributed equally to this work.