Human middle latency auditory evoked magnetic fields

Summary The magnetic equivalents of SN10, Po, Na, Pa, Nb and Pb (SN10m, Pom, Nam, Pam, Nbm and Pbm) in short and middle latency auditory evoked potentials were measured with a 7-channel DC superconducting quantum interference device (SQUID). The sources of Pom, Nam, Pam, Nbm and Pbm responses were estimated to be located in the auditory cortex, while the source of SN10m was considered to be in a deeper part of the brain. In addition, the source of Pam was estimated to be in the vicinity of the moving N100m source. The source of Pbm was considered to be in a separate area, anterior to the source of Pam and N100m, which suggested that the source of Pam was located in the primary auditory cortex, while the source of Pbm was located in the secondary auditory cortex. The source of N100m was considered to spread from the primary auditory cortex to the secondary auditory cortex.     

Decreased interleukin 1 production in aplastic anaemia

Interleukin 1 (IL-1) is an important regulator of immune system function. IL 1 also affects haematopoiesis in vitro: it causes release of colony stimulating factors from fibroblasts and endothelial cells and can directly act on primitive haematopoietic stem cells. We investigated IL 1 production in vitro by stimulated peripheral blood mononuclear cells of patients with aplastic anaemia (N = 17), patients with other haematologic diseases (N = 27), and normal individuals (N = 22) using a bioassay for IL 1 activity. Ten aplastic patients showed markedly decreased IL 1 production. IL 1 production by fibronectin-affinity purified monocytes was decreased in six of seven of these patients; in three other cases, in which IL 1 mononuclear cell production was undetectable, sufficient monocytes could not be isolated. IL 1 alpha and IL 1 beta precursor molecules were also absent or much decreased when mononuclear cell lysates from these patients were analysed by immunoblot using specific polyclonal sera. Aplastic patients with low IL 1 production were distinguished by the severity of their disease and the degree of neutropenia. Patients with myelodysplasia with comparable degrees of pancytopenia had normal IL 1 production. This is the first example of deficient haematopoietic growth factor production in a bone marrow failure syndrome. Decreased IL 1 production may contribute to the pathogenesis of some cases of aplastic anaemia and to susceptibility to infection.     

Laparoscopy-assisted distal gastrectomy with laparoscopic sentinel lymph node biopsy after endoscopic mucosal resection for early gastric cancer

Background There has been a trend toward minimally invasive treatment of early gastric cancer. We report the preliminary results of laparoscopy-assisted distal gastrectomy with laparoscopic sentinel lymph node biopsy after endoscopic mucosal resection. Methods Six patients underwent laparoscopy-assisted distal gastrectomy after endoscopic mucosal resection between February 2002 and October 2005 at Mie University Hospital. These patients first underwent laparoscopic sentinel lymph node biopsy and then laparoscopy-assisted distal gastrectomy with lymphadenectomy. Results No patient underwent conversion to open surgery during the operation. None of the patients had any postoperative complications. The mean length of postoperative hospital stay was 11.3 days. Sentinel lymph nodes were identified laparoscopically in five patients. There were 20 sentinel and 85 nonsentinel lymph nodes in the six patients. Postoperatively, tissue sections showed that none of the lymph nodes were metastasized. Immunohistochemistry with D2-40 antibody showed that there were normal lymphatics in the submucosal layer with mucosal defects at the endoscopic mucosal resection site. No patients had any tumor recurrence during followup. Conclusions Laparoscopy-assisted distal gastrectomy after endoscopic mucosal resection was a safe and curative procedure. Endoscopic mucosal resection before sentinel lymph node biopsy was acceptable for early gastric cancer.     

Novel vaginoplasty technique involving the use of peritoneal flaps during laparoscopic radical hysterectomy for early-stage cervical cancer

Radical hysterectomy is often performed to treat early-stage cervical cancer in women of reproductive age, and sexual dysfunction due to postoperative vaginal shortening is a major concern [^1,2]. Vaginoplasty using various techniques is commonly performed in patients with congenital vaginal agenesis [³]. However, there are few reports of vaginoplasty being performed for vaginal shortening after radical hysterectomy in a patient with cervical cancer [^4,5]. We demonstrate a novel vaginoplasty technique in which peritoneal flaps are used during laparoscopic radical hysterectomy to prevent postoperative vaginal shortening and consequent sexual dysfunction in patients with early-stage cervical cancer. A 37-year-old woman with early-stage cervical cancer who wished to perform sexual activity postoperatively underwent laparoscopic radical hysterectomy and vaginoplasty. After radical hysterectomy, the residual vaginal length was 4 cm. The dissected peritoneum of pouch of Douglas (posterior peritoneal flap) was sutured to the posterior vaginal stump. The supravesical peritoneum was dissected from the ventral to the dorsal side to create an anterior peritoneal flap, which was inverted, pulled down, and sutured to the anterior vaginal stump. The anterior peritoneal flap and suprarectal peritoneum were sutured to create a 10-cm neovaginal vault. Subsequently, a methacrylic resin mold was inserted into the neovagina to prevent postoperative neovaginal stenosis. The patient had sexual intercourse 3 months postoperatively. She was satisfied with the sexual activity and experienced no vaginal shortening or stenosis. Our novel vaginoplasty technique is feasible and effective for preventing sexual dysfunction by lengthening the vagina during laparoscopic radical hysterectomy for early-stage cervical cancer.Trial RegistrationJapan Registry of Clinical Trials Identifier: jRCT1030210227     

Expression of the bric-a-brac tramtrack broad complex protein NAC-1 in cervical carcinomas seems to correlate with poorer prognosis.

PURPOSE: Recent studies have suggested a novel oncogenic role of a bric-a-brac tramtrack broad complex (also known as POZ) domain gene, NAC-1, in ovarian carcinomas. The aim of this study was to clarify the functional role of NAC-1 in human cervical carcinomas. EXPERIMENTAL DESIGN: NAC-1 expression in cervical cancer was assessed by immunohistochemistry, and data on clinical variables were collected by retrospective chart review. NAC-1 gene knockdown using small interfering RNA and a NAC-1 gene transfection system were used to asses NAC-1 function in cervical cancer in vivo. RESULTS: Immunohistochemical and gene expression analysis revealed that NAC-1 is significantly overexpressed in cervical adenocarcinomas and adenosquamous carcinomas compared with squamous cell carcinomas. Patients with squamous cell carcinomas positive for NAC-1 expression who received radiotherapy had significantly shorter overall survival than peers whose tumors did not express NAC-1, and multivariate analysis showed that NAC-1 expression was an independent prognostic factor for overall survival after radiotherapy. Overexpressions of the NAC-1 gene stimulated cell proliferation in cervical carcinoma cells of the TCS, CaSki, and HeLa P3 lines, which do not have endogenous NAC-1 expression. NAC-1 gene knockdown inhibited cell growth and induced apoptosis in HeLa, HeLa TG, and ME180 cells, all of which overexpressed NAC-1. CONCLUSIONS: Our findings suggest that NAC-1 may play an important role in cervical carcinomas; moreover, these findings provide a rationale for future development of NAC-1-based therapy for cervical carcinomas that overexpress this candidate oncogene.     

Establishment of an ovarian metastasis model and possible involvement of E‐cadherin down‐regulation in the metastasis

Clinical observations of cases of ovarian metastasis suggest that there may be a unique mechanism underlying ovarian‐specific metastasis. This study was undertaken to establish an in vivo model of metastasis to the ovary, and to investigate the mechanism of ovarian‐specific metastasis. We examined the capacity for ovarian metastasis in eight different human carcinoma cell lines by implantation in female NOD/SCID mice transvenously and intraperitoneally. By transvenous inoculation, only RERF‐LC‐AI, a poorly differentiated carcinoma cell line, frequently demonstrated ovarian metastasis. By intraperitoneal inoculation, four of the eight cell lines (HGC27, MKN‐45, KATO‐III, and RERF‐LC‐AI) metastasized to the ovary. We compared E‐cadherin expression among ovarian metastatic cell lines and others. All of these four ovarian metastatic cell lines and HSKTC, a Krukenberg tumor cell line, showed E‐cadherin down‐regulation and others did not. E‐cadherin was then forcibly expressed in RERF‐LC‐AI, and inhibited ovarian metastasis completely. The capacity for metastasizing to the other organs was not affected by E‐cadherin expression. We also performed histological investigation of clinical ovarian‐metastatic tumor cases. About half of all ovarian‐metastatic tumor cases showed loss or reduction of E‐cadherin expression. These data suggest that E‐cadherin down‐regulation may be involved in ovarian‐specific metastasis. (Cancer Sci 2008; 99: 1933–1939)