Hiroshi Shiroma

Single-incision laparoscopic adrenalectomy for primary aldosteronism: Report of a case

We herein report the first case of a single-incision laparoscopic access (SILA) adrenalectomy in Japan. A 74-year-old woman who was a hepatitis B virus carrier was referred to our hospital because of an abnormal screening result during a routine health checkup. Abdominal computed tomography and an endocrinologic workup revealed a 2-cm left adrenal tumor with primary aldosteronism. We prioritized the safety of the SILA adrenalectomy by choosing a left lower abdominal approach. A SILS port was inserted through a 2.5-cm incision. An ultrasonic coagulator was the main tool used during the surgical procedure. The duration of the surgery was 105 min and the blood loss was 1 ml. This result was comparable to that of a conventional laparoscopic adrenalectomy. Based on our experience, an SILA adrenalectomy is thus considered to be feasible and safe, with better cosmetic results and a greater overall patient satisfaction than that of a conventional laparoscopic adrenalectomy. However, further studies will be necessary before the universal adoption of this new technique can be considered.

Microscopic and immunohistological studies on intimal hyperplasia of the arterially implanted autovein graft and its anastomosis in dogs

The fate of intimal hyperplasia of arterially implanted autovein bypass grafts and their distal end-to-side ananstomoses in dogs was studied microscopically and immunohistologically. The bypass grafting was done under conditions of abnormal blood flow and high peripheral resistance. Intimal hyperplasia of the graft first became evident 7 days after implantation and the thickness increased to about 500 μm 3 months or more after the implantation. The intimal hyperplasia was related to an active proliferation of smooth muscle cells which proved positive for alpha-smooth muscle actin staining. Moreover, it was more dominant at the toe and heel of the anastomosis and moderately apparent on the floor of the host artery. The constituent elements of the hyperplastic intima at the anastomosis were fibroblast-like cells and extracellular collagen fibers which were negative for alpha smooth muscle actin staining. This study revealed that the features of intimal hyperplasia at the distal anastomosis in autovein bypass grafting differed from those of the implanted autovein graft itself; the former being related to excessive proliferation of fibroblasts and collagen fibers while the latter displayed an active proliferation of smooth muscle cells.

Clinical studies on the vasodilating and anti-platelet effects of OP-41483, a prostacyclin derivative

The vasodilating and anti-platelet actions of OP-41483 was studied to determine the effective dose of this drug for the treatment of ischemic lower limbs. The compound was given to 11 patients intravenously at rates of 2.5, 5.0 and 10.0 ng/kg/min. Infusion at a rate of 10 ng/kg/min increased the mean flow rate of the tibial arteries from 3.15±1.77 ml/min before the infusion, to 7.89±2.51 ml/min (p<0.001) and to 6.38±3.19 ml/min (p<0.001), at the time of, and 60 minutes after the cessation of the infusion, respectively. The peripheral flow resistance of the tibial arteries was reduced from 2.1±1.12×105 dyne·sec/cm5 before the infusion to 0.9 ±0.33×105 dyne·sec/cm5 (p<0.001) and to 1.2±0.78×105 dyne·sec/cm5 (p<0.05), at the time of, and 60 minutes after the cessation of the infusion. ADP-induced platelet aggregation was reduced from 73.3±17.6% before the infusion to 50.7±24.5% (p<0.01) and to 64.0±23.5% (p<0.05), at the time of, and 60 minutes after the cessation of the infusion, respectively. Collageninduced platelet aggregation was also reduced from 71.4±24.0% to 66.6±21.5% before and after the infusion (p<0.05).

Colonic metastasis from breast carcinoma: a case report

BackgroundColonic metastasis from breast carcinoma is very rare. Here, we report a case of colonic metastasis from breast carcinoma.Case presentationThe patient was a 51-year-old woman. She had upper abdominal pain, vomiting, and diarrhea, repeatedly. We performed abdominal contrast-enhanced computed tomography (CT) to investigate these symptoms. The CT scan revealed a tumor in the ascending colon with contrast enhancement and showed an expanded small intestine. For further investigation of this tumor, we performed whole positron emission tomography-computed tomography (PET-CT). The PET-CT scan revealed fluorodeoxyglucose uptake in the ascending colon, mesentery, left breast, and left axillary region. Analysis of biopsy samples obtained during colonoscopy revealed signet ring cell-like carcinoma. Moreover, biopsy of the breast tumor revealed invasive lobular carcinoma. Therefore, the preoperative diagnosis was colonic metastasis from breast carcinoma. Open ileocecal resection was performed. The final diagnosis was multiple metastatic breast carcinomas, and the TNM classification was T2N1M1 Stage IV.ConclusionsWe presented a rare case of colonic metastasis from breast carcinoma. PET-CT may be useful in the diagnosis of metastatic breast cancer. When analysis of biopsy samples obtained during colonoscopy reveals signet ring cell-like carcinoma, the possibility of breast cancer as the primary tumor should be considered.

Abstract 1562: Efficient antigen presentation and induction of anti-tumor immunity by dendritic cells loaded with antigens by electroporation

For successful dendritic cell (DC) therapy of cancer, it is important to choose the optimal method to load DCs with antigens to induce higher anti-tumor immunity, particularly tumor-specific CTL responses. The co-incubation (Co) method is conventionally used to load DCs with tumor antigens in DC therapy. Although DCs could uptake tumor antigens by endocytosis in this method, they are thought to be processed in lysosome and presented mainly on MHC class II, but not efficiently on MHC class I. Electroporation (Ep) is one of the promising antigen-loading method because it is reported that DCs could uptake much larger amount of FITC-dextran by Ep in comparison with Co method. In this study, we performed side-by-side comparisons of these two antigen loading methods using murine bone marrow derived DCs. First, we compared antigen presentation using purified ovalbumin (OVA) and OVA-specific OT-I CD8 and OT-II CD4 T cells. To this end, DCs were loaded with OVA by either Co or Ep, and subsequently cultured with T cells. Two or three days later, T cell expansion and cytokine production were evaluated. As expected, OVA-Co-DCs induced moderate expansion and cytokine production of OT-II T cells, but had little effect on OT-I T cells. In contrast, OVA-Ep-DCs potently stimulated both OT-I and OT-II T cells to expand and produce cytokines, such as IL-2 and IFN-γ. Using monoclonal antibody specific for MHC class I/OVA peptide complex, we confirmed efficient presentation of the OVA peptide on MHC class I by OVA-Ep-DCs. Furthermore, when we used the lysate of EG7 tumor cell line (OVA gene-transfected) as antigen instead of purified OVA, Ep-DCs induced expansion of both OT-I and OT-II T cells efficiently compared with Co-DCs. In the case of Alexa488-OVA, unexpectedly, similar amounts of uptake were seen in Ep-DCs and Co-DCs by FCM analysis. By using confocal microscopy, however, there was a critical difference of intracellular localization of Alexa488-OVA. Although Alexa488-OVA was localized in intracellular vesicles of both DCs, the cytosolic localization was observed only in Ep-DCs, suggesting that antigen loaded by Ep entered cytosol of DCs and would be processed by proteasome and presented on MHC class I efficiently. Finally, to determine the ability of these DCs to induce anti-tumor immunity in vivo, mice were subcutaneously immunized twice at 7 days intervals with 3-5 x 10 5 cells of either OVA-Ep-DCs or OVA-Co-DCs and then challenged with 3 x 10 6 of EG7 cells at 7 days after the 2 nd immunization. When OVA-Co-DCs were used for immunization, tumor formations were partially prevented. On the contrary, mice immunized with OVA-Ep-DCs were almost completely protected from tumor formations. These results demonstrate that DCs loaded with tumor antigens by Ep have greater antigen presentation capacity, especially through MHC class I pathway, and could induce stronger anti-tumor immunity in vivo than those loaded by Co. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1562. doi:1538-7445.AM2012-1562

Pathophysiological features of intimal hyperplasia of the arterially implanted autovein graft and its anastomosis in dogs

We investigated pathophysiological features of intimal hyperplasia of arterially implanted autovein graft and its distal end-to-side anastomosis under conditions of poor distal runoff. Intimal hyperplasia of the graft was significantly evident, became 70.5±38.5 µm thick at 14 days with infiltration of myofibroblasts, and increased to 420±199.7 µm at 6 months. The proliferated neointima was strongly positive for alpha-smooth muscle (A-sm) actin staining. Cells in the entire layer of the graft were diffusely labeled with BrdU at 14 days. At 3–6 months after grafting, cells in the superficial layer of the neointima were scarcely labeled with BrdU, however, cells in the deeper layer were strongly labeled. At the distal end-to-side anastomosis, mural thrombi deposited on the suture line were replaced by fibrous tissues with infiltration of fibroblast-like cells within 14 days, and proliferated considerably at 3–6 months. The neointima at the toe portion was thickened to 82.5±50.7 µm at 14 days and increased to 370.6±40.0 µm at 6 months. The superficial layer of the proliferated neointima consisted of mature smooth muscle cells positive for A-sm actin staining and scarcely labeled with BrdU. However, the deeper layer was negative for A-sm actin staining and strongly labeled with BrdU. In conclusion, intimal hyperplasia is caused by infiltration of myofibroblasts in the graft and of fibroblast-like cells at the anastomosis. Proliferation of these cells is progressive at the deeper layer of the neointima, even at 6 months after grafting.