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Biomedical subjects

M Monden

Publications and source records attributed to M Monden.

At least 181 records · Page 10Linked to original sources
PubMed1998

Profiles of circulating inflammatory- and anti-inflammatory cytokines in patients with hemolytic uremic syndrome due to E. coli O157 infection.

The systemic inflammatory response to Escherichia coli O157 infection was studied from the profiles of circulating inflammatory and anti-inflammatory cytokines. Twelve patients transferred sequentially to our hospital for the intensive care with acute illness due to Escherichia coli O157 infection and the possible form of haemolytic uraemic syndrome were included in this study. Increased circulating concentrations of tumour necrosis factor, interleukin 6, interleukin 8, granulocyte colony-stimulating factor, and interleukin 10 were found in patients with various stages of this infection and haemolytic uraemic syndrome. Especially, the degree of the increase of circulating interleukin 10 in those who had a typical signs of haemolytic uraemic syndrome was higher than those of other inflammatory cytokines. Two groups of E. coli infection could be classified into one with a typical haemolytic uraemic syndrome and the other with atypically bacteremic state over haemolytic uraemic syndrome according to these cytokine levels.

Adult↗
PubMed1998

Successful resection of thoracic esophageal cancer associated with the right aortic arch.

A 52-year-old Japanese man with thoracic esophageal cancer associated with the right aortic arch was admitted to our hospital. Preoperative spiral computed tomography and three-dimensional image reconstruction also showed an associated aberrant left subclavian artery. After preoperative concurrent chemoradiation, the patient underwent a subtotal esophagectomy with regional lymphadenectomy via a left thoracotomy.

Aorta, Thoracic↗
PubMed1998

Protection of islet allografts transplanted together with Fas ligand expressing testicular allografts.

Fas ligand (FasL) is highly expressed in testicular tissues and thought to be responsible for protection from allograft rejection by inducing apoptosis of anti-graft activated T cells. FasL-expressing islets have been shown to induce a granulocyte-mediated inflammatory reaction. We investigated whether a graft can be protected from alloimmune responses by manipulating the Fas/FasL-system. We transplanted allogeneic islets under the kidney capsule of streptozotocin-induced diabetic mice together with testicular tissue. Significant prolongation of survival of C3H islet allograft was observed in C57BL/6 (B6) recipients transplanted with C3H testicular tissue, but not in those transplanted with C3H-gld testicular tissue expressing non-functional FasL. No significant prolongation was observed in B6-lpr recipients expressing non-functional Fas. Immunohistochemical staining of C3H testicular tissue in the composite graft showed a high expression of FasL, but not that of the C3H-gld testicular tissue. In situ terminal deoxynucleotidyl transferase-mediated dUDP-biotin catalysed DNA nick-end labelling (TUNEL) staining of a composite graft of C3H islet and testicular tissue in B6 recipients demonstrated extensive apoptosis of infiltrating mononuclear cells around the graft. The protective effect of C3H testicular tissue was abrogated when anti-FasL monoclonal antibody was administered i.p. postoperatively. Our results suggest that FasL-positive testicular allografts protect composite islet allografts and indicate that manipulation of Fas/FasL mediated apoptosis is a suitable strategy for controlling rejection of islet allografts.

Animals↗
PubMed1998

Localization of the gene responsible for Peutz-Jeghers syndrome within a 6-cM region of chromosome 19p13.3.

Patients with Peutz-Jeghers syndrome (PJS), an autosomal dominant disease characterized by hamartomatous polyposis of the gastrointestinal tract, are thought to be predisposed to malignancies of the digestive tract, genital tract, and other organs. Using microsatellite markers on chromosome 19p, we have closely defined the region containing the gene responsible for this disorder through linkage analysis in seven affected families. The lack of obligate recombinants at two of these loci, D19S883 and D19S878, with maximum LOD scores of 2.88 and 3.75, confirmed the localization of the PJS locus to chromosome 19. Furthermore, haplotype analysis placed the PJS locus within a 6-cM telomeric region of chromosome 19p, between D19S886 and D19S565.

Centromere↗
PubMed1998

Nine novel germline mutations of STK11 in ten families with Peutz-Jeghers syndrome.

Peutz-Jeghers Syndrome (PJS) is an autosomal dominant hereditary disease characterized by hamartomatous polyposis involving the entire bowel. Recently STK11, a gene bearing a mutation responsible for PJS, was isolated. We investigated the entire coding region of STK11 in 15 unrelated PJS families by the PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) method and PCR-direct sequence analysis, and found nine different, novel mutations among ten of those families. One nonsense mutation and five different frameshift mutations (two families carried the same mutation), all of which would cause truncation of the gene product, were found in seven families; mutations found in five families were clustered within exon 6. Among these five mutations, three occurred at the mononucleotide-repeat region (CCCCCC) of codons 279-281, suggesting that this region is likely to be a mutational hotspot of this gene. One of the remaining three families carried a 3-bp in-frame deletion that would eliminate an asparagine residue within a kinase domain of the product; the other two carried intronic mutations at or adjacent to the consensus dinucleotide sequences of splice-acceptor or -donor sites, which were likely to lead to aberrant splicing.

AMP-Activated Protein Kinase Kinases↗
PubMed1998

New retraction technique to allow better visualization of Calot's triangle during laparoscopic cholecystectomy.

BACKGROUND: Bile duct injuries during laparoscopic cholecystectomy (LC) are thought to occur because surgeons tend to confuse the common bile duct (CBD) with the cystic duct. Among reasons for this misidentification, the difference in the way the operating field is exposed in LC compared to open cholecystectomy should be noticed. Using Dr. Reddick's technique, which is commonly practiced, the upward and the lateral traction of the gallbladder results in a narrower Calot's triangle and angulation of the CBD. These anatomical distortions are thought to contribute to ductal injuries during LC. METHODS: We propose a new method to expose Calot's triangle during LC. The principle of this technique is to expose the hepatic hilus by retracting the caudal surfaces of the quadrate and lateral lobes of the liver using an atraumatic curved instrument. RESULTS: The advantages of this technique are that one gains wide exposure of the hepatic hilus, leaves Calot's triangle undistorted, and avoids tenting the CBD. CONCLUSIONS: This new technique may make LC safer and decrease the number of bile duct injuries associated with the misidentification of the anatomy.

Cholecystectomy, Laparoscopic↗
PubMed1998

Primary malignant melanoma of the esophagus associated with adenocarcinoma of the lung.

We herein report an extremely rare case of a 55-year-old Japanese woman with a primary malignant melanoma of the esophagus associated with adenocarcinoma of the lung. The patient was admitted to our hospital with a malignant melanoma of the lower esophagus. The chest X-ray and computed tomography (CT) findings revealed an incidental abnormal shadow in the left lung, which was diagnosed to be adenocarcinoma of the lung by means of a CT-guided needle biopsy. After administering systemic chemotherapy with dacarbazine (DTIC), vincristine sulfate (VCR), and nimustine hydrochloride (ACNU) plus interferon-beta, the esophageal tumor markedly decreased in size. Subsequently, the patient underwent a radical resection of both the malignant melanoma of the esophagus and lung cancer via a left thoracotomy and laparotomy.

Adenocarcinoma↗
PubMed1998

Identification of pathologic parathyroid glands in patients with primary hyperparathyroidism.

Localization of the parathyroid glands is not necessarily easy before surgery and can also be troublesome during surgery. This study focuses on the identification of pathologic parathyroid glands. The records of 32 patients who underwent parathyroidectomy at our institution in the past 14 years for primary hyperparathyroidism were reviewed. Twenty-three patients had a single lesion while 9 had multiple-gland involvement. Localization studies identified 17 of 23 patients with a single lesion. All patients with multiple lesions were diagnosed with an enlargement of the parathyroids, but not all glands were identified in each patient preoperatively. At surgery, 8 of 32 patients were explored unilaterally. Solitary enlarged glands were resected, and a subtotal parathyroidectomy was performed for multiple-gland involvement. The intraoperative serum intact parathyroid hormone (PTH) level dropped after resection of the largest gland. The serum PTH level correlated with the gland size (r = 0.861, intact PTH assay). Eight of 9 patients with multiple-gland involvement had an elevated serum PTH (>2000 pg/ml in midportion and >200 pg/ml in intact PTH assays, respectively). No patient developed persistent or recurrent hyperparathyroidism. The serum PTH level was normalized by a resection of relatively enlarged glands in our cases. It is usual to explore all glands during surgery, and in cases with a high serum PTH level, multiple-gland involvement should also be considered.

Adult↗
PubMed1998

Increased urinary excretion of bilirubin metabolites in association with hyperbilirubinemia after esophagectomy.

This study was conducted to investigate the rationale for postoperative hyperbilirubinemia after major surgery. The serum bilirubin values and urinary excretion of bilirubin metabolites (BM) were monitored in 11 patients who underwent esophagectomy via right thoracotomy for esophageal cancer. Both the serum bilirubin values and the urinary excretion of BM increased postoperatively in all patients. The maximum serum bilirubin level in four patients with septic complications, two of whom developed pneumonia and two, anastomotic leakage (group A), was significantly higher at 5.25+/-4.16 mg/dl than in the remaining patients without septic complications (group B), at 2.11+/-0.07 mg/dl. The peak value of urinary BM was 99.5+/-88.2 micromol/day in group A and 23.5 +/-26.7 micromol/day in group B. The correlation between the level of serum bilirubin and urinary BM excretion was found to be significant. Thus, the metabolism of bilirubin was increased by extensive surgical stress and septic insult.

Aged↗
PubMed1998

A unique method of closure for an aortocaval fistula in association with a ruptured abdominal aortic aneurysm: report of a case.

We report herein the case of a 78-year-old man in whom an aortocaval fistula caused by spontaneous rupture of an abdominal aortic aneurysm (AAA) was successfully treated by a unique surgical technique. The aortocaval fistula had been revealed by an aortography after the patient presented with high-output heart failure. During the operation, massive bleeding from the fistula was evident. The fistula measured 2 cm in diameter, and was located between the right posterior wall of the AAA and the inferior vena cava (IVC). Direct suturing of the defect in the IVC failed to close the fistula because the tissue around it would not hold together due to degeneration. However, the bleeding was finally able to be controlled by plugging the fistula with isolated and properly trimmed omentum packed within the excluded aneurysmal sac. Unfortunately, the patient died due to respiratory failure on the 201st postoperative day. A pathological autopsy revealed that the aortocaval fistula had been closed by fibrous tissue and that the IVC was patent. Although such a drastic operative measure to repair an aortocaval fistula has never before been reported, it could be an alternative when direct closure proves unsuccessful.

Aged↗
PubMed1998

Novel germline mutations of hMSH2 in a patient with hereditary nonpolyposis colorectal cancer (HNPCC) and in a patient with six primary cancers.

We screened for germline mutations of mismatch repair genes, hMLH1 and hMSH2, in five Japanese families carrying hereditary nonpolyposis colorectal cancer (HNPCC) and in a patient with multiple primary cancers. Screening the entire coding regions of both genes using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis, we found two novel germline mutations in hMSH2. One was a 1-bp insertion in exon 12, detected in a patient who had undergone surgery six times for independent tumors (four primary colorectal carcinomas, a small intestinal carcinoma, and an endometrial cancer). The other, in a second patient, was a missense mutation from CTT to TTT at codon 390 in exon 7 that resulted in substitution of phenylalanine for leucine. This conservative alteration was not found in any of 50 normal controls, but we cannot exclude the possibility that it may represent a rare polymorphism rather than a factor in the disease.

Adult↗
PubMed1998

Regulation of albumin mRNA and its promoter-binding nuclear factors under different perioperative nutritional methods in hepatectomized rats.

BACKGROUND: Regulation of perioperative albumin synthesis under parenteral (PN) and enteral (EN) nutrition was investigated. METHODS: Rats were divided into PN and EN groups. Both groups received the same regimen of artificial nutrition for 7 days and then underwent 70% hepatectomy. Serum albumin and mRNA levels of albumin and its promoter-binding nuclear factors (C/EBPalpha, beta, and DBP) were measured. RESULTS: Serum albumin and albumin mRNA in the PN group were significantly lower than those in the EN group at 72 hours after hepatectomy. Preoperative and postoperative DBP and C/EBPalpha mRNA levels in the EN group were significantly higher than those in the PN group. CONCLUSION: Serum albumin was well maintained by EN after hepatectomy owing to an early recovery of albumin mRNA level and its nuclear factor mRNA levels (C/EBPalpha and DBP). Compared with PN, EN is a more advantageous from of perioperative nutrition as pertains to albumin synthesis.

Animals↗
PubMed1998

Expression of platelet-activating factor receptor transcript-2 is induced by shear stress in HUVEC.

Platelet-activating factor (PAF) is an important lipid involved in inflammation reaction and circulation regulation. The receptor for human PAF is synthesized from two spliced transcripts of the same gene. Our observation in the present study shows that HUVEC express transcript-1 only in the static condition. Shear stress induces the expression of transcript-2 in these cells but not transcript-1, resulting in increased PAF receptor expression as measured by FACS analysis. These results suggest that shear stress may increase the susceptibility of endothelial cells to PAF by inducing transcript-2 expression.

Alternative Splicing↗
PubMed1998

A role for local calcium gradients upon hypoxic injury in human umbilical vein endothelial cells (HUVEC).

Upon hypoxic injury, bleb formation is an early event of cell damage observed in a variety of cell types. Although a rise in cytosolic free Ca2+ ([Ca2+]i) has been considered to be involved in this process, the exact relationship between these phenomena remains ill-defined. In order to examine the relationship between bleb formation, and [Ca2+]i or nuclear free Ca2+ ([Ca2+]n), we analyzed [Ca2+]i and [Ca2+]n in HUVEC during hypoxic injury using confocal laser scanning microscopy. [Ca2+]i and [Ca2+]n were measured using Fluo-3, and cell viability and mitochondrial membrane potential were assessed by the exclusion of propidium iodide (PI) and rhodamine 123, respectively. After the initiation of hypoxia, [Ca2+]i and [Ca2+]n rose gradually up to 15 min reaching peak values of 447 +/- 62 and 516 +/- 105 nM, respectively, which was accompanied by a decrease in rhodamine 123 fluorescence and an increase in PI-stained cells. Bleb formation was observed after [Ca2+]i and [Ca2+]n had reached their peak values and the number of blebs increased thereafter. Confocal z-sectioning images revealed a localized increase in [Ca2+]i at the bleb forming site and this localized elevation in [Ca2+]i was observed before bleb formation in the corresponding area. In conclusion, bleb formation induced by hypoxic stress appears to involve Ca(2+)-dependent reactions that are linked to a regional elevation of [Ca2+]i.

Analog-Digital Conversion↗
PubMed1998

Down-regulation of focal adhesion kinase, pp125FAK, in endothelial cell retraction during tumor cell invasion.

Although endothelial cell retraction is required before tumor cell invasion, its molecular mechanism still remains obscure. We previously demonstrated that conditioned medium (CM) derived from a human pancreatic cancer cell line, PSN-1, induced endothelial cell retraction and facilitated tumor cell invasion. To investigate the molecular change of events in the transduction of extracellular signals during endothelial cell retraction, we examined the effect of the CM derived from PSN-1 cells on the tyrosine phosphorylation in endothelial cells. Immunoblot analyses revealed that the PSN-1 CM decreased tyrosine phosphorylation of a 120-130 kD protein, and induced the concomitant down-regulation of focal adhesion kinase, pp125FAK, during endothelial cell retraction in time- and dose-dependent fashions. These changes preceded endothelial cell retraction and were reversible after removal of the CM. Further quantitative densitometric analyses demonstrated that the extent of decrease in tyrosine phosphorylated 120-130 kD protein during the endothelial cell retraction was likely to be proportional to that of the down-regulation of pp125FAK. A tyrosine phosphorylated 120-130 kD protein immunoprecipitated by anti-phosphotyrosine antibody immunoreacted with anti-pp125FAK antibody. These results suggested that decreased amount of a tyrosine phosphorylated 120-130 kD protein probably due to the down-regulation of pp125FAK might be associated with the signal transduction pathway in the endothelial cells during their retraction. Furthermore, these findings were also observed in the CM from another four human cancer cell lines, suggesting the down-regulation of pp125FAK in endothelial cells during tumor cell invasion.

Animals↗
PubMed1998

Characterization of soluble E-cadherin as a disease marker in gastric cancer patients.

The soluble fragment of E-cadherin protein (S-ECD) is reported to be increased in the peripheral blood of cancer patients. In this study, we investigated the clinical significance of serum S-ECD in 81 patients with gastric cancer. The amount of serum S-ECD was significantly higher in the gastric cancer patients (4735 +/- 2310 ng ml(-1)) than in healthy volunteers (2515 +/- 744 ng ml(-1)). With the normal range cut-off at average +2 s.d., 67% patients showed abnormally high serum S-ECD levels. This frequency was significantly higher than that of other tumour markers, such as CEA (4.4%) or CA19-9 (13.3%). However, there was no significant correlation between the amount of S-ECD and clinicopathological factors. Serum S-ECD might be derived from cancer tissue, as removal of cancers by surgical treatment results in quick decline of the serum S-ECD and S-ECD can be detected by immunoblot in cancer tissues but not in normal epithelium. The serum S-ECD amount was compared with the E-cadherin expression in cancer tissues, which were classified into those showing preserved (+), partially reduced (+/-) or lost (-) expression. Interestingly, E-cadherin (+/-) tumours showed higher serum S-ECD levels than the other types, and a higher amount of S-ECD in the immunoblot analysis. Thus, the serum level of S-ECD may serve as an excellent tumour marker with high sensitivity. Furthermore, analysis of S-ECD in serum and cancer tissue can offer clues for elucidating the mechanism of reduction of E-cadherin expression in cancer cells.

Adult↗
PubMed1998

Aberrant expression and phosphorylation of beta-catenin in human colorectal cancer.

The cytoplasmic domain of cadherins is known to associate with the intracellular proteins, catenins, which link cadherins to the actin-based cytoskeleton. In this study, we immunohistochemically investigated the expression of beta-catenin as well as E-cadherin and alpha-catenin in 86 human colorectal cancers, and we analysed their coexpression pattern and relationship to clinicopathological factors. In cancerous tissues, the frequency of reduced expression of beta-catenin (28 of 86, 33%) was similar to that of E-cadherin (19 of 86, 22%), but less than that of alpha-catenin (47 of 86, 55%). All three molecules were expressed strongly, as was the normal epithelium, in 36 cases (42%), whereas the rest (50 cases, 58%) showed reduction in one of the molecules. The reduction of beta-catenin expression was significantly correlated with dedifferentiation, Duke's stage, lymph node metastasis and liver metastasis. Next, we examined tyrosine phosphorylation in the protein complex immunoprecipitated with E-cadherin, as E-cadherin function is down-regulated by receptor-type tyrosine kinase in vitro. It was of interest that up-regulation of tyrosine phosphorylation of beta-catenin was more frequently observed in cancerous tissues than in the matching normal mucosa. These results suggest that beta-catenin may have important regulatory roles within an E-cadherin-mediated adhesion system in human colorectal cancers.

Cadherins↗