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Tsuyoshi Konishi

Publications and source records attributed to Tsuyoshi Konishi.

At least 19 recordsLinked to original sources
PubMed2007

Prognosis and risk factors of metastasis in colorectal carcinoids: results of a nationwide registry over 15 years.

BACKGROUND: Colorectal carcinoids are often described as low-grade malignant. However, no study has compared the survival between patients with colorectal carcinoids and those with carcinomas, in a large series. In addition, no global consensus has been established on the crucial determinants of metastasis in colorectal carcinoids. AIM: To determine the predictive factors for metastasis in colorectal carcinoids and clarify their prognosis compared with adenocarcinomas. METHODS: Data of all patients diagnosed as having colorectal carcinoids were extracted from a large nationwide database of colorectal tumours, the Multi-Institutional Registry of Large-Bowel Cancer in Japan, for the period from 1984 to 1998. Risk factors for lymph node (LN) metastases and distant metastases were analysed among those who were undergoing surgery, by univariate and multivariate analysis. Cancer-specific survival was also compared between patients with colorectal carcinoids and those with adenocarcinomas registered in the same period. RESULTS: Among the 90 057 cases of colorectal tumours that were diagnosed, a total of 345 cases of carcinoids were identified, including 247 colorectal carcinoids of those undergoing surgery. Risk factors for LN metastasis were tumour size >/=11 mm and lymphatic invasion, whereas those for distant metastasis were tumour size >/=21 mm and venous invasion. Colorectal carcinoids without these risk factors exhibited no LN metastasis or distant metastasis. Cancer-specific survival of patients with colorectal carcinoids without metastasis was better than that of those with adenocarcinomas. However, the survival was similar between carcinoids and adenocarcinomas if the tumours had LN metastasis or distant metastasis. CONCLUSIONS: The presence of metastasis in colorectal carcinoids could lead to survival that is as poor as in adenocarcinomas. Tumours </=10 mm and without lymphatic invasion could be curatively treated by local resection, but others would need radical LN dissection.

Adenocarcinoma↗
PubMed2006

Prospective surveillance effectively reduced rates of surgical site infection associated with elective colorectal surgery at a university hospital in Japan.

At a university hospital in Japan, the introduction of prospective surveillance and subsequent interventions was effective in reducing the rate of surgical site infection associated with elective colorectal surgery from 27.5% to 17.8% of surgeries. Japan should both recognize the importance of broader surveillance for surgical site infection and establish its own nationwide surveillance database.

Colorectal Surgery↗
PubMed2006

Reduced wavelength-dependent quarter-wave plate fabricated by a multilayered subwavelength structure.

We developed a novel fabrication method of a reduced wavelength-dependent quarter-wave plate (QWP) based on form birefringence of a multilayered subwavelength structure. The multilayered structure was constructed by depositing a high-refractive-index thin film on a subwavelength-structured substrate with a low refractive index. The surface structure of the substrate was shallow enough to be formed by a mass replication technology. A high-refractive-index subwavelength grating was formed on ridges of the substrate by sputtering Zn2SnO4 (refractive index of 2.03 at a wavelength of 633 nm). Moreover, since the grooves of the high-refractive-index grating were very deep and narrow, the dispersion of form birefringence suppressed the dependency of phase retardance on the wavelength of light in a limited spectral region. The phase retardance of the fabricated QWP was 89 degrees at a 633 nm wavelength and 79 degrees at a 785 nm wavelength.

Journal Article↗
PubMed2006

Risk factors for anastomotic leakage after surgery for colorectal cancer: results of prospective surveillance.

BACKGROUND: Anastomotic leakage in operations for colorectal cancer not only results in morbidity and mortality, but also increases the risk of local recurrence and worsens prognosis. So a better understanding of risk factors for developing anastomotic leakage in colorectal cancer surgery is important to surgeons. The aim of this study was to determine the incidence and risk factors for clinical anastomotic leakage after elective surgery for colorectal cancer. STUDY DESIGN: We conducted prospective surveillance of all elective colorectal resections performed by a single surgeon in a single university hospital from November 2000 to July 2004. The outcomes of interest was clinical anastomotic leakage. Eighteen independent clinical variables were examined by univariate and multivariate analyses. RESULTS: A total of 391 patients undergoing elective operations for colorectal cancer were admitted to the program. Clinical anastomotic leakage was identified in 11(2.8%) patients. Univariate and multivariate analyses showed that preoperative steroid use (odds ratio=8.7), longer duration of operation (odds ratio=9.9), and wound contamination (odds ratio=7.8) were independently predictive of clinical anastomotic leakage. Although there were no statistical differences in leakage rates between patients with and without covering stoma, all four patients requiring reoperation for leakage were without covering stoma. CONCLUSIONS: Preoperative steroid use, longer duration of operation, and contamination of the operative field were independent risk factors for developing clinical anastomotic leakage after elective resection for colorectal cancer. Surgeons should be aware of such high-risk patients, which would help them to decide whether to create a diversion stoma during surgery.

Adult↗
PubMed2006

Elective colon and rectal surgery differ in risk factors for wound infection: results of prospective surveillance.

OBJECTIVE: The objective of this study was to clarify the incidence and risk factors for developing incisional surgical site infection (SSI) in both elective colon and rectal surgery. SUMMARY BACKGROUND DATA: SSI is a frequent complication after elective colorectal resection. The National Nosocomial Infection Surveillance system surveys all colorectal surgeries together, without differentiating the type of colorectal surgery performed. However, rectal surgery may have a higher risk for SSI, and identifying risk factors that are more specific to each procedure would be more predictive. METHODS: We conducted prospective SSI surveillance of all elective colorectal resections performed by a single surgeon in a single institution from November 2000 to July 2004. The data for colon and rectal surgeries were collected separately. The outcome of interest was incisional SSI. Univariate and multivariate analyses were performed to determine the predictive significance of variables in each type of surgery. RESULTS: A total of 556 colorectal resections, consisting of 339 colon and 217 rectal surgeries, were admitted to the program. The incisional SSI rates in colon and rectal surgeries were 9.4% and 18.0%, respectively (P = 0.0033). Risk factors for developing incisional SSI in colon surgery were ostomy closure (OR = 7.3) and lack of oral antibiotics (OR = 3.3), while in rectal surgery, risk factors were preoperative steroids (OR = 3.7), preoperative radiation (OR = 2.8), and ostomy creation (OR = 4.9). CONCLUSIONS: Colon and rectal surgeries differ with regard to incidence and risk factors for developing incisional SSI. SSI surveillance for such surgeries should be performed separately, as this should lead to more efficient identification of risk factors and a reduction in SSI.

Adolescent↗
PubMed2006

hRFI overexpressed in HCT116 cells modulates Bcl-2 family proteins when treated with 5-fluorouracil.

Exogenous overexpression of hRFI, originally isolated in our laboratory, inhibits not only death receptor-mediated apoptosis but also the mitochondrial apoptosis induced by several chemotherapeutic agents including 5-fluorouracil (5-FU). Recently, it has become clear that hRFI targets and degradates caspase-8 and -10 in death receptor-mediated apoptosis by E3 ubiquitin activity in a ring finger domain homologous to that of X-chromosome-linked inhibitor of apoptosis protein (XIAP). However, the cellular mechanism of the inhibition of mitochondrial apoptosis by hRFI has not been fully elucidated. We prepared HCT116 overexpressing hRFI (HCT116/hRFI) cells and comprehensively analyzed the expression changes of 51 apoptosis-related genes with or without 5-FU treatment between HCT116/hRFI and mock cells using microfluidic low-density arrays. As a result, we identified four genes (Bcl-2, Bcl-XL, cIAP2, and CFLAR) whose expression was four or more times higher in HCT116/ hRFI cells than in HCT116/LacZ cells, and found that Bcl-2 and the ratio of Bcl-2/Bax or Bcl-2/Bak were upregulated when HCT116/hRFI cells were treated with 5-FU. Furthermore, we also validated the up-regulation of Bcl-2 and Bcl-XL in HCT116/hRFI cells treated with 5-FU by Western blot analysis. Such evidence suggests that the modulation of Bcl-2 family proteins seen in 5-FU treatment plays an important role in the anti-apoptotic function of HCT116/hRFI cells.

Antimetabolites, Antineoplastic↗
PubMed2005

Overexpression of hRFI (human ring finger homologous to inhibitor of apoptosis protein type) inhibits death receptor-mediated apoptosis in colorectal cancer cells.

The acquisition of antiapoptotic properties is one of the essential mechanistic steps in colorectal carcinogenesis and is closely correlated with a loss of chemosensitivity and radiosensitivity. Human ring finger homologous to inhibitor of apoptosis protein type (hRFI) is a newly discovered gene encoding a ring finger domain highly homologous to that of X chromosome-linked inhibitor of apoptosis protein. Immunohistochemistry has revealed that the expression of hRFI increased in transition from normal colorectal mucosas to adenomas and from adenomas to carcinomas, suggesting an essential role in the early stage of colorectal carcinogenesis. However, the function role of hRFI in colorectal carcinoma has not been elucidated. To determine whether hRFI possesses an antiapoptotic function in colorectal cancer cells, HCT116 colorectal cancer cells stably overexpressing hRFI were established. The hRFI transfectant exhibited significant resistance to apoptosis induced by tumor necrosis factor-alpha or tumor necrosis factor-related apoptosis-inducing ligand compared with control. This antiapoptotic response was associated with decreased activity of caspase-3, -8, and -9. We also established an antisense down-regulation of hRFI, which effectively reversed the antiapoptotic activity of the hRFI transfectant. This confirmed that the antiapoptotic property of the hRFI transfectant was not due to the clonal effect but in fact dependent on hRFI function. In conclusion, hRFI possesses an antiapoptotic function in HCT116 colorectal cancer cells. Considering the progressive increase of hRFI expression in the advance of the colorectal adenoma-carcinoma sequence, hRFI is one of the important players in colorectal carcinogenesis through its effect on apoptosis regulation.

Apoptosis↗
PubMed2004

Dual mode regulation of migration by lysophosphatidic acid in human gastric cancer cells.

Lysophosphatidic acid (LPA), which interacts with at least three G protein-coupled receptors (GPCRs), LPA1/Edg-2, LPA2/Edg-4, and LPA3/Edg-7, is a lipid mediator with diverse effects on various cells. Here, we investigated the expression profiles of LPA receptors and patterns of LPA-induced migration in gastric cancer cells. Northern blot analysis revealed that various gastric cancer cells expressed variable levels of LPA1, LPA2, and LPA3 without a consistent pattern. Using a Boyden chamber assay, LPA markedly increased cell migration of LPA1-expressing cells, the effects of which were almost totally abrogated by Ki16425, an LPA antagonist against LPA1 and LPA3. In contrast, LPA by itself did not significantly induce migration in MKN28 and MKN74 cells, which exclusively expressed LPA2. However, when hepatocyte growth factor (HGF) was placed with LPA in the lower chamber, LPA induced migration of these cells in a dose-dependent manner. Immunoprecipitation analysis revealed that LPA induced transient tyrosine phosphorylation of c-Met in LPA2-expressing cells, which suggests that the transactivation of c-Met by LPA causes a cooperative migratory response with HGF to these cells. Our results indicate that LPA regulates the migration of gastric cancer cells in a receptor-specific manner and suggest that the expression pattern of LPA receptors may affect the metastatic behavior of gastric cancer.

Chemotaxis↗
PubMed2004

Successfully treated idiopathic rectosigmoid perforation 7 years after renal transplantation.

Colon perforation (CP) is still a critical complication after renal transplantation (RT), and idiopathic perforation is extremely rare. Here we describe a successfully treated case of idiopathic rectosigmoid perforation that occurred 7 years after RT. In our research this is the tenth reported case of idiopathic CP after RT and the second case that has occurred in the rectosigmoid. The patient was a 51-year-old Japanese male RT recipient still receiving immunosuppressive medication. He was admitted to the hospital for sudden onset of abdominal pain during defecation. Emergency laparotomy was performed 5 h after the onset, and a longitudinal 1.5 cm perforation with a clear margin was observed in the rectosigmoid, 8 cm above the peritoneal reflection. Hartmann's operation was performed. Macroscopic and histological examination did not reveal any specific findings that may have caused perforation, so the case was diagnosed as idiopathic rectosigmoid perforation.

Humans↗
PubMed2004

Aberrant expression of lysophosphatidic acid (LPA) receptors in human colorectal cancer.

Lysophosphatidic acid (LPA) is a simple bioactive phospholipid with diverse effects on various cells, that interacts with three G protein-coupled transmembrane receptors, LPA1, LPA2, and LPA3. The expression pattern and functions of these LPA receptors in various tumors have not been fully examined, except in ovarian cancer. To evaluate the LPA receptor expression profile in human colorectal cancer and in normal mucosa, we used real-time reverse transcription-polymerase chain reaction (RT-PCR) and measured the expression levels of LPA1, LPA2, and LPA3 messenger RNA (mRNA) in 26 colorectal cancers and 16 corresponding normal tissue samples. Normal epithelium expressed both LPA1 and LPA2 mRNA at similar levels. In comparison, colorectal cancers expressed LPA1 mRNA at a significantly lower level (0.3-fold; P<0.05), and LPA2 mRNA at a significantly higher level (three-fold; P<0.05), as compared with normal tissues. Thus, the ratio of LPA2/LPA1 increased markedly during malignant transformation (18-fold increase). LPA3 mRNA was expressed at only a low level in both normal and cancer tissues. We also assessed LPA2 expression immunohistochemically using a rat anti-LPA2 monoclonal antibody, and confirmed high expression of LPA2 in colorectal cancer at the protein level. As for LPA1, we examined Western blot analysis for 16 matched normal and cancer tissues. It revealed a significant decrease in the expression of LPA1 protein in cancer tissues compared to normal mucosa in nine of 16 cases, and in the remaining seven cases the expression levels was much the same. These results suggested that alteration of LPA receptor expression might be an important event in the development of colorectal cancer, and therefore, LPA and its receptors could be a chemopreventive target against colorectal cancer.

Adenocarcinoma↗