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Biomedical subjects

W Adachi

Publications and source records attributed to W Adachi.

At least 55 records · Page 3Linked to original sources
PubMed1999

Hepatic resection of giant cavernous hemangioma of the liver.

Surgical treatment of giant hemangioma of the liver is still controversial. The aim of this study is to examine the efficacy of hepatic resection for giant hemangioma of the liver. Twenty patients with giant cavernous hemangioma of the liver were treated by hepatic resection. The mean diameter of the hemangiomas was 13.9 cm (range, 6.5-30 cm). The surgical outcome was reviewed retrospectively. Major hepatectomy was performed in 14 patients and minor hepatectomy in 6 patients. Complications occurred in 7 of the 20 patients treated by hepatic resection. At a mean follow-up of 79 months (range, 12-173 months), 18 patients were symptom free whereas 2 patients had died--one died of pneumonia at 2 years and the other died of gastric cancer 6 years after surgery. Mean intraoperative hemorrhage and blood transfusion in all patients was 4,343 mL (range, 270-24,000 mL) and 1,860 mL (range, 0-8,800 mL) respectively. In the seven patients with preoperative high levels of fibrin degradation products (FDP), mean intraoperative hemorrhage and blood transfusion were markedly higher (9,371 mL and 3,714 mL respectively) than in the 13 patients without abnormal FDP (1,603 mL and 900 mL respectively). Preoperative hematologic status returned to normal after operation in all patients. Hepatic resection is a useful treatment for giant cavernous hemangioma of the liver. More careful management to reduce intraoperative hemorrhage is recommended to increase the safety of surgery, particularly in patients with preoperative abnormal FDP.

Adult↗
PubMed1999

Alpha-fetoprotein-producing gastric cancer: histochemical analysis of cell proliferation, apoptosis, and angiogenesis.

OBJECTIVE: Alpha-fetoprotein (AFP)-producing gastric cancer has been associated with a poor prognosis. In the present study, the cell proliferation, apoptosis, and angiogenesis of this cancer were studied histochemically to determine its malignant potential. METHODS: Tissue samples were taken from four patients with AFP-producing gastric cancer and 26 patients with AFP-negative gastric cancer. Cell proliferation was evaluated by Ki-67 immunostaining, and the Ki-67 labeling index (LI) was determined. Apoptosis was studied by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling method, and the apoptotic index was determined. Angiogenesis was evaluated by measuring the microvessel density using factor VIII immunostaining, and immunostainings for vascular endothelial growth factor and thymidine phosphorylase were performed. RESULTS: The Ki-67 LI of the AFP-producing gastric cancers was significantly higher than that of the AFP-negative gastric cancers (p < 0.01). The apoptotic index of the AFP-producing gastric cancers was significantly lower than that of the AFP-negative gastric cancers (p < 0.01). The microvessel density of the AFP-producing gastric cancers was significantly higher than that of the AFP-negative gastric cancers (p < 0.01). Vascular endothelial growth factor expression was observed in all four of the AFP-producing gastric cancers, whereas thymidine phosphorylase was not expressed in any of the AFP-producing gastric cancers. CONCLUSIONS: These results suggest that AFP-producing gastric cancers have high malignant potential (high proliferative activity, weak apoptosis, and rich neovascularization) compared with that of AFP-negative gastric cancers. These biological characteristics of AFP-producing gastric cancer reflect the aggressive behavior and the poor prognosis of patients with this type of cancer.

Aged↗
PubMed1999

Detection of herpes simplex virus DNA in atypical epithelial keratitis using polymerase chain reaction.

AIM: To study herpes simplex virus (HSV) DNA in tears from patients with atypical epithelial keratitis of unknown aetiology. METHODS: Tear samples were collected from 17 affected eyes of 17 consecutive patients suffering from epithelial keratitis in whom HSV keratitis was suspected but whose diagnosis was difficult on the basis of clinical manifestations alone. Using reduced sensitivity polymerase chain reaction (PCR), tear samples were tested for HSV DNA. Tears from the unaffected eyes of the 17 patients were also examined, along with 38 tear samples from 19 normal volunteers. Southern blot analysis was performed to confirm that amplified DNA bands were specific for HSV. Clinical correlation with photographs of corneal lesions was also investigated. RESULTS: HSV DNA was detected in tears from the affected eyes of eight of the 17 patients with suspected HSV keratitis. Tears from the affected eyes of the other patients were PCR negative, as were tears from the unaffected eyes of all 17 patients, and from the 38 normal eyes. There was no correlation between PCR results and clinical manifestation of keratitis. CONCLUSIONS: Based on the sensitivity of the PCR system, eight of 17 suspected HSV keratitis patients were confirmed as suffering from HSV keratitis. HSV keratitis should therefore be considered as a possible diagnosis in atypical epithelial keratitis.

Adult↗
PubMed1999

Laparoscopic resection of a retroperitoneal schwannoma.

Although laparoscopic surgery for retroperitoneal diseases has been widely performed, there are few reports of laparoscopic resection for retroperitoneal tumors. We present the case of a 5-cm retroperitoneal tumor compressing the right common iliac vein and inferior vena cava that was successfully resected using a laparoscopic technique. Dissection between the tumor and the large vessels was performed safely using a harmonic scalpel and an ultrasonic surgical aspirator. Histopathology of the resected tumor showed a benign schwannoma. Laparoscopic surgical techniques should be considered for treatment of selected retroperitoneal tumors.

Adult↗
PubMed1998

p73, a gene related to p53, is not mutated in esophageal carcinomas.

A novel gene, termed p73, encodes a protein with a significant homology to p53 and has been mapped at chromosome 1p36.3, which is a locus of multiple suppressor genes for tumors including neuroblastoma and other cancers. Since the 1p36 locus is reported to be deleted and p53 is frequently mutated in esophageal carcinomas, we examined loss of heterozygosity (LOH) and mutation of the p73 gene in 48 untreated esophageal tumors, as well as mRNA expression in 8 tumors. We screened the P1 genomic library to obtain a P1 clone containing the p73 gene and found a polymorphic short tandem CT repeat site at intron 9. Intragenic sequences for 14 PCR primer sets and a primer pair flanking the repeat were also determined for the analysis of PCR single-strand conformation polymorphism (SSCP) and LOH studies, respectively. Expression of p73 mRNA was detectable but at low levels in all 8 tumor tissues by reverse transcriptase PCR. We did not find any type of mutation other than polymorphisms in the 48 esophageal carcinomas, though aberration of the p53 gene on the PCR-SSCP gels was observed in 15 of 38 (39%) tumors of the same set. In addition, LOH for p73 was found in only 2 of 25 (8%) tumors. These results suggest that, at least in esophageal carcinomas, allelic loss or mutation of p73 may not be a main genetic event for the tumorigenesis as it is with p53.

Adenocarcinoma↗
PubMed1998

Involvement of vascular endothelial growth factor and urokinase-type plasminogen activator receptor in microvessel invasion in human colorectal cancers.

To evaluate the association among known angiogenic growth factors or factors related to the plasminogen activation system and clinicopathological factors in patients with colorectal cancer, we examined the expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), transforming growth factor-alpha (TGF-alpha), urokinase-type plasminogen activator (u-PA), u-PA receptor (u-PA-R) and plasminogen activator inhibitor-1 (PAI-1) in clinical specimens of colorectal cancers by Northern blot analysis. In comparison with the expression of these angiogenesis-related genes in 7 paired samples of colorectal cancers and the adjacent normal mucosa, VEGF mRNA level was significantly higher in the cancer tissues than in the adjacent normal mucosa (p < 0.05). We analyzed expression of these genes in 44 cases of primary colorectal cancers. Among the 3 angiogenic growth factors we examined, VEGF mRNA expression was significantly higher in the cancer tissues with blood vessel invasion or with lymphatic vessel invasion than in those without, respectively (p < 0.05). On the other hand, u-PA-R mRNA expression was significantly higher in the cancers with blood vessel invasion than in those without (p < 0.05). In addition, there was a correlation between the expression levels of VEGF and u-PA-R mRNA in the cancer tissues we have examined. Using immunohistochemistry, strong staining of VEGF or u-PA-R was observed in the cancer cells invading the microvessels. Our findings suggest that malignant transformation might accompany the upregulation of VEGF expression in colorectal cancers and that VEGF and u-PA-R might contribute cooperatively to increase angiogenesis around the tumor as well as the metastasis via microvessels.

Adult↗
PubMed1998

Multiple carcinoids of the duodenum accompanied by type I familial multiple endocrine neoplasia.

A case of multiple carcinoid tumors of the duodenum accompanied by familial multiple endocrine neoplasia is reported. A 46-year-old man with duodenal polyps discovered during a mass screening was followed up for 5 years. In August 1994, a histological examination revealed carcinoid tumors, and he was thus referred to our hospital for surgery. He underwent a parathyroidectomy and cholecystectomy for primary hyperparathyroidism and cholecystolithiasis, respectively. The patient's sister had also undergone a parathyroidectomy and distal pancreatectomy for primary hyperparathyroidism and insulinoma of the pancreas. In addition, his two children were also followed up for hypercalcemia. A serum examination of the patient revealed high levels of somatostatin and pancreatic polypeptide, but normal levels of gastrin and serotonin. In November 1994, a pancreaticoduodenectomy with a D2 lymph node dissection was performed. The macroscopic findings of the resected specimen showed multiple polypoid lesions with delles on the top, measuring 3 to 15 mm in size throughout the duodenum. A microscopic examination revealed the tumor to have infiltrated into the submucosa extensively, and an immunohistochemical analysis also demonstrated the tumor cells to be positive for somatostatin, but not for pancreatic polypeptide. After surgery, the serum level of somatostatin returned to normal but the pancreatic polypeptide remained high. The post-operative course was uneventful, and the patient remains in good health.

Carcinoid Tumor↗
PubMed1998

Gelatinous drop-like corneal dystrophy is not one of the beta ig-h3-mutated corneal amyloidoses.

PURPOSE: To discover if beta ig-h3 is mutated in gelatinous drop-like corneal dystrophy, as has been suggested. METHODS: Genomic DNA was isolated from unrelated individuals with lattice corneal dystrophy type I (n = 3), Avellino corneal dystrophy (n = 3), and gelatinous drop-like corneal dystrophy (n = 3) and used as a template for polymerase chain reaction to amplify all exons in beta ig-h3. The polymerase chain reaction product was then sequenced. RESULTS: Beta ig-h3 is mutated in lattice corneal dystrophy type I (Arg124Cys) and Avellino corneal dystrophy (Arg124His). In gelatinous drop-like corneal dystrophy, on the other hand, no mutation was detected in the entire coding region of beta ig-h3 (all 17 exons). CONCLUSION: Unlike the amyloidotic corneal dystrophies lattice type I and Avellino, gelatinous drop-like corneal dystrophy is not likely to be caused by a mutation in beta ig-h3.

Amyloidosis↗
PubMed1998

Synchronous gastric tumors associated with esophageal cancer: a retrospective study of twenty-four patients.

OBJECTIVES: Synchronous gastric tumors (including benign and secondary tumors) associated with esophageal cancer present diagnostic and therapeutic issues. We investigated this synchronous association, and retrospectively determined the frequency of the gastric tumors and the clinical characteristics. METHODS: In a series of 208 patients with esophageal cancer, we investigated the synchronous gastric tumors, as well as the frequency of association, clinicopathological characteristics, diagnosis, treatment, and the clinical outcome after surgery. RESULTS: Twenty-eight gastric tumors were found in 24 patients. Adenocarcinoma was most frequent. Most of these tumors were located at the upper or middle third of the stomach. Eight gastric tumors in six patients could not be detected preoperatively. Six of these tumors including a gastric remnant cancer were detected in the resected stomach, and two leiomyomas were detected during the operation. In one patient in which an endoscope could not pass through the esophagus, a leiomyoma was detected in the resected stomach. For the gastric cancers, total gastrectomy or proximal gastrectomy with lymph node dissections was performed. For the benign tumors, partial resection of the stomach was performed, and endoscopic resection was performed preoperatively for an adenoma. In both the postoperative hospital mortality rate and the survival rate after surgery, there were no significant differences between the patients with and without gastric tumors. CONCLUSIONS: Synchronous gastric tumors associated with esophageal cancer are not rare. When an endoscope cannot pass through the esophagus before surgery, other techniques must be performed to explore the stomach. For these patients, surgical treatment should be adapted positively.

Aged↗
PubMed1998

[Continuous intraportal chemotherapy for prevention of metachronous hepatic metastasis in colorectal cancer].

Fifty-five colorectal cancer patients who had continuous intraportal chemotherapy between 1990 and 1993 (treated group) and 130 colorectal cancer patients who did not have portal chemotherapy between 1982 and 1993 (untreated group) were studied to clarify the effects of continuous intraportal chemotherapy on the prognosis. After a catheter was placed in the portal vein through the right gastroepiploic vein at the time of radical operation, 10 mg of MMC was continuously infused for 4 hours at operation and 500 mg/day of 5-FU was continuously infused for 7 days postoperatively. The toxicities of this therapy were not serious. The five-year survival rate was 65.3% in the treated group and 65.6% in the untreated group. The five-year disease-free survival rate was 69.8% in the treated group and 58.6% in the untreated group, with no significant difference. In stage II patients, however, the five-year disease-free survival rate in the treated group was slightly higher than in the untreated group (90.0% vs 70.3%, p = 0.073), and the rate of hepatic recurrence in the treated group was significantly lower than in the untreated group. These results suggest that continuous intraportal chemotherapy may prevent metachronous hepatic metastases in stage II colorectal cancer patients.

Aged↗
PubMed1998

Mutational analysis of the p73 gene localized at chromosome 1p36.3 in colorectal carcinomas.

Genetic alteration of p53, which monitors DNA damage and operates cellular checkpoints, is a major factor in the development of human colorectal carcinoma (CRC). Recently, p73, a novel family member of p53, has been identified and found, like p53, to activate p21Waf1/Cip1 and to induce apoptosis. The p73 gene was mapped at chromosome 1p36.3 which is a region frequently deleted in CRCs and other cancers including neuroblastoma. To assess whether or not p73 is a tumor suppressor gene of CRC, we performed mutational analysis of p73 in 82 colorectal tumor tissues paired with constitutional DNA. Using a microsatellite marker for p73, the loss of heterozygosity (LOH) study was performed and allelic loss of p73 was found in 17% of the CRCs. RT-PCR single strand conformation polymorphism analysis showed no mutation except three polymorphisms in the p73 coding region. In addition, p73 was expressed at higher levels in the CRC tissues than in the normal mucosa or neuroblastoma tissues, though the transcripts were detectable only by the RT-PCR method. Our results suggest that, in CRCs, p73 may not play a role as a tumor suppressor, at least not in a classic Knudson manner.

Adolescent↗
PubMed1998

Isolation and characterization of human cathepsin V: a major proteinase in corneal epithelium.

PURPOSE: To isolate and characterize a novel cathepsin gene, as part of the systematic isolation of genes uniquely active in corneal epithelium. METHODS: For the isolation of a full-length cDNA clone, a probe was selected from a set of expressed sequence tag clones classified as unique to corneal epithelium. Inserted cDNA was introduced into insect cells using a baculovirus expression system, and the secretion of recombinant protein was identified using antisera against a synthetic peptide. Proteolytic activity was determined using bovine serum albumin (BSA) as substrate. The expressions of the novel cathepsin in human cornea and other tissues were examined by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The full-length cDNA clone encoded a peptide of 334 amino acids with 82% identity with bovine cathepsin L and 77% identity with human cathepsin L when aligned. The recombinant protein produced in the baculovirus expression system cleaves BSA, and its activity was inhibited by the cysteine proteinase inhibitors E-64 and leupeptin, but not by pepstatin A, phenylmethylsulfonyl fluoride, and EDTA. By RT-PCR, a low level of expression was observed in some other epithelial tissues of ectodermal origin, but only in cornea was it higher than cathepsin L, which is known to be a general lysosomal cathepsin. Cathepsin V protein was detected in human corneal epithelium by western blot analysis, but not in tear fluid. CONCLUSIONS: The amino acid homology and proteolytic activity of the recombinant protein indicate that the novel gene is a new member of the cathepsins that have features of cysteine proteinase. Its uniquely high expression in corneal epithelium strongly implies an important role in corneal physiology.

Amino Acid Sequence↗
PubMed1997

Genotyping of the CYP1A1 and GSTM1 genes in esophageal carcinoma patients with special reference to smoking.

BACKGROUND: Aromatic hydrocarbons, including benzol[a]pyrene, in tobacco smoke first require metabolic activation by phase I enzymes, cytochrome P450s (CYP450s), and then are subjected to detoxification by phase II enzymes, the glutathione-S-transferases. A high risk lung carcinoma group has been reported to have specific polymorphisms of the cytochrome P450 (CYP1A1) gene and the glutathione-S-transferase (GSTM1) gene. In this study, the authors investigated whether such genotypes were also risk factors for esophageal carcinoma. METHODS: Subjects were comprised of 89 esophageal carcinoma patients and 137 noncancer controls. Forty-nine of the patients and 60 of the control subjects were smokers. Genotypic studies of both CYP1A1 and GSTM1 were performed in the cancer tissues of all 89 patients. Genotypes of peripheral blood leukocytes taken from the control subjects were also determined. Genotypes of the CYP1A1 and GSTM1 genes were determined by the polymerase chain reaction. RESULTS: Patients who were heavy smokers with the genotypes Val/Val (V/V) for CYPIAI and the combined genotype of V/V for CYP1A1 and GSTM1- were a statistically high risk group compared with control subjects (P < 0.01, chi-square = 10.6 vs. P < 0.01, chi-square = 11.0). The association of V/V for CYPIAI with a smoking index > or = 600 in esophageal carcinoma patients was estimated at 6.63 (95% confidence interval [CI], 1.86-23.7). The association of combined genotypes of V/V of CYP1A1 and GSTM1 with a smoking index > or = 600 in esophageal carcinoma patients was estimated at 12.7 (95% CI, 1.97-81.8) CONCLUSIONS: Specific genotypes of the CYP1A1 and GSTM1- genes are related to the incidence of esophageal carcinoma, especially in heavy smokers.

Adult↗
PubMed1997

Adverse effects of intraportal chemotherapy on natural killer cell activity in colorectal cancer patients.

BACKGROUND: Adjuvant intraportal chemotherapy has been used with a view to prevent the development of metachronous hepatic metastases following curative resection for colorectal cancer. To evaluate the effects of this therapy on systemic antitumor immunological activity, 35 colorectal cancer patients who underwent curative resection were investigated. METHOD: Among them. 19 had adjuvant intraportal chemotherapy with mitomycin C and 5-fluorouracil (treated group) and 16 had no chemotherapy (untreated group). Natural killer (NK) cell activity, lymphocyte subpopulations, and immunosuppressive acidic protein (IAP) in the peripheral blood were measured serially before and after operation, and the values were compared between the two groups. RESULTS: The NK cell activity and the percentages of CD16 positive and CD56 positive cells were markedly reduced in the treated group postoperatively. Significant difference was also observed between the two groups on the 4th postoperative day in regard to NK cell activity and CD56 positive cells. CONCLUSIONS: Intraportal chemotherapy in our study reduced the NK cell activity and its population in the peripheral blood.

Aged↗
PubMed1997

Immunohistochemical expression of bcl-2 protein in squamous cell carcinoma and basaloid carcinoma of the esophagus.

In the present study, the expression of bcl-2 protein in esophageal squamous cell carcinoma (SCC) and basaloid carcinoma (BC) was immunohistochemically examined, and its relation to tumor progression and postoperative survival was determined in SCC. A total of 42 SCC and 4 BC tumor samples were fixed with formalin, embedded in paraffin, and stained using monoclonal bcl-2 protein antibody, clone 124. Immunoreactivity was semiquantitatively scored, and the staining results were compared with the pathologic features and survival rates. The cytoplasm of basal cells from the normal esophageal epithelium was stained. In some well- and moderately differentiated SCCs, bcl-2 protein-positive reaction was observed in the peripheral part of the tumor cord, but in poorly differentiated SCC, the cells were weakly or hardly stained. However, in BC, the cells were strongly stained. The immunoreactivity was positive in 45.2% of the SCCs and all of the BCs. There were no significant differences in pathological features or patient survival between the bcl-2 protein-positive and protein-negative SCCs. In conclusion, the expression was not related to tumor progression and had no prognostic significance in SCC. Conversely, BC had strong immunohistochemical expression, probably associated with the differentiation of carcinoma cells simulating the basal cells of the esophagus.

Carcinoma, Squamous Cell↗
PubMed1997

Germline mutations of the APC gene in two Japanese adenomatous polyposis patients.

Germline mutations of the adenomatous polyposis coli (APC) gene have been reported in patients with familial adenomatous polyposis (FAP) and are believed to be an early event in colorectal carcinoma. We report the results of screening for germline mutations of the APC gene in 4 cases of 2 kindreds using non-radioactive PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) analysis. The mutation in kindred 1 was a 4 bp deletion at codon 849 in exon 15, resulting in a frameshift leading to truncation of the APC gene product. In kindred 2, a transversion of C to G at codon 2038 was observed, resulting in an amino acid change from leucine to valine. In this case, it is possible to screen presymptomatic diagnosis easily and quickly by digestion with restriction enzyme EcoNI.

Adenomatous Polyposis Coli↗