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Biomedical subjects

Hitoshi Ikeda

Publications and source records attributed to Hitoshi Ikeda.

At least 37 records · Page 2Linked to original sources
PubMed2005

Diffuse xanthogranulomatous pyelonephritis in a patient with myotonic dystrophy and cerebral palsy.

Xanthogranulomatous pyelonephritis (XGP), a morphological and clinical variant of chronic pyelonephritis, is an uncommon disease in children. It is characterized by the destruction of the renal parenchyma and replacement by granulomatous tissue containing foamy lipid-laden macrophages and is classified into diffuse and focal XGP. We present a case of diffuse XGP in a child with myotonic dystrophy complicated by cerebral palsy and discuss the importance of correct diagnosis and preoperative management to reduce inflammation and improve malnutrition associated with the disease.

Adolescent↗
PubMed2005

[A case of lymphocytic hypophysitis mimicking pituitary macroadenoma].

Lymphocytic hypophysitis is a rare autoimmune disease of the pituitary gland mimicking pituitary macroadenoma on magnetic resonance imaging (MRI). We encountered a 32-year-old female who presented with a typical pituitary macroadenoma causing sudden on-set of visual disturbance during her second pregnancy. She underwent an endonasal-transsphenoidal resection of the mass diagnosed as a non-secreting pituitary macroadenoma after a cesarean operation. Intraoperatively, the lesion was found to be extremely tough and mucinous, and apparently differed from pituitary adenoma. The frozen section revealed hypophysitis and we performed only a biopsy of the mass. Histopathological examination showed diffuse infiltrate of non-specific lymphocytes. Postoperatively, prednisolone was given for two weeks, her visual disturbance improved with radiologically marked shrinking of the lesion. This case illustrates the difficulty of differentiation of lymphocytic hypophysitis from pituitary macroadenoma, and we discuss the clinical features and the management of this disease.

Adenoma↗
PubMed2005

[Participation of medical technologists in the nutrition support team (NST)].

In the nutrition support team (NST), medical technologists take a very important role in carrying out nutrition screening, nutrition assessment and nutrition monitoring. Medical technologists can look at the laboratory data of patients earlier than other NST staff. Using this advantage, the medical technologists can contribute to the NST. In addition, medical technologists join ward rounds together with other NST staff on a weekly basis. After discussion with all NST staff, medical technologists make a report on the nutrition assessment of patients and then sign their names to the report. The NST is a representative of medical treatment teams. All NST members should have equal levels of understanding of nutrition therapy. Therefore, medical technologists should not only look at the laboratory data of the patients, but also manage the patients through nutrition assessment and nutrition monitoring.

Humans↗
PubMed2004

Administration of ANG II induces iron deposition and upregulation of TGF-beta1 mRNA in the rat liver.

We previously found that ANG II infusion into rats causes iron deposition in the kidney and heart, which may have a role in the regulation of profibrotic gene expression and tissue fibrosis. In the present study, we have investigated whether ANG II can also induce iron accumulation in the liver. Prussian blue staining detected frequent iron deposition in the interstitium of the liver of rats treated with pressor dose ANG II for 7 days, whereas iron deposition was absent in the livers of control rats. Immunohistochemical and histological analyses showed that some iron-positive nonparenchymal cells were positive for ferritin and heme oxygenase-1 (HO-1) protein and TGF-beta1 mRNA and were judged to be monocytes/macrophages. It was shown that ANG II infusion caused about a fourfold increase in ferritin and HO-1 protein expression by Western blot analysis and about a twofold increase in TGF-beta1 mRNA expression by Northern blot analysis, which were both suppressed by treating ANG II-infused rats with losartan and deferoxamine. In addition, mild interstitial fibrosis was observed in the liver of rats that had been treated with pressor dose ANG II for 7 days or with nonpressor dose ANG II for 30 days, the latter of which also caused loss of hepatocytes and intrahepatic hemorrhage in the liver. Taken together, our data suggest that ANG II infusion induces aberrant iron homeostasis in the liver, which may have a role in the ANG II-induced upregulation of profibrotic gene expression in the liver.

Angiotensin II↗
PubMed2004

Treatment with leucine stimulates the production of hepatocyte growth factor in vivo.

Hepatocyte growth factor (HGF) has pleiotropic effects. Up-regulation of HGF activity in vivo may be beneficial. Branched-chain amino acids (BCAAs) are known to modulate various cellular functions. When starved rats received intraperitoneal injections of valine, leucine or isoleucine, only leucine treatment increased both hepatic and circulating levels of HGF in a dose-dependent manner, up to 1.5 and 2.3 times higher, respectively, than in controls. When young growing rats with free access to food were injected with leucine once a day for a week, HGF levels and liver weights were significantly higher than those of control rats. Furthermore, 1 week of leucine treatment of adult rats resulted in elevated serum albumin levels with an increase in HGF levels. Taken together with our previous report showing that leucine stimulates HGF production by hepatic stellate cells in culture, leucine, among BCAAs, may induce an increase in HGF production by the liver in vivo.

Animals↗
PubMed2004

Sphingosine 1-phosphate enhances portal pressure in isolated perfused liver via S1P2 with Rho activation.

Although structural changes are most important to determine vascular resistance in portal hypertension, vasoactive mediators also contribute to its regulation. Hepatic stellate cells (HSCs) are assumed to play a role in modulating intrahepatic vascular resistance based on their residence in the space of Disse and capacity to contract. Because sphingosine 1-phosphate (S1P) has been shown to stimulate HSC contractility, we wondered if S1P could regulate portal pressure. S1P at 0.5-5 microM increased portal pressure in isolated rat perfused liver. This effect was abrogated in the presence of a binding antagonist for S1P2, JTE-013. Perfusion of isolated rat liver with 5 microM S1P increased Rho activity in the liver, and co-perfusion with JTE-013 cancelled S1P-induced Rho activation. Because S1P is present in human plasma at approximately 0.2 microM, S1P might readily regulate portal vascular tone in physiological and pathological status. The antagonist for S1P2 merits consideration for treatment of portal hypertension.

Animals↗
PubMed2004

Umbilicoplasty for large protruding umbilicus accompanying umbilical hernia: a simple and effective technique.

A large umbilical protrusion with redundant skin accompanying an umbilical hernia sometimes needs umbilicoplasty. Although several different techniques for making umbilical depression have been used, the results of the plastic surgery are sometimes unsatisfactory due to postoperative flattening or disappearance of the umbilical depression. To make a permanent umbilical depression that is cosmetically acceptable, we have modified the techniques. Umbilicoplasty was performed in 14 children whose ages ranged from 6 months-6 years and 3 months (median, 1 year and 10 months) and who had umbilical hernia with a large umbilical protrusion. After the fascial defect was closed, the diameter of the umbilicus was reduced to half that before surgery by removing fan-shaped skin flaps and approximating skin edges, and then inverting the umbilicus and fixing it caudally to the fascia and skin. There were no postoperative complications, and no flattening or disappearance of umbilical depression was observed during the follow-up of 10-19 months. The authors' technique of umbilicoplasty for a large protruding umbilicus accompanying umbilical hernia is a simple method that produces acceptable cosmetic results.

Child↗
PubMed2004

D-lactic acidosis in short-bowel syndrome managed with antibiotics and probiotics.

D-lactic acidosis sometimes occurs in malabsorbed patients with short-bowel syndrome and is characterized by recurrent episodes of encephalopathy and metabolic acidosis. The characteristic neurologic abnormalities and the presence of metabolic acidosis raises a diagnostic suspicion, and the diagnosis is made when the serum level of D-lactic acid is greater than 3 mmol/L. Standard treatment consists of restricting oral carbohydrates or fasting, correction of metabolic acidosis, and a long-term suppression of pathogenic floras with antibiotics. The authors present a case of D-lactic acidosis in a 22-year-old patient with short-bowel syndrome, to whom intestinal bacterial agents (probiotics) were given in addition to oral kanamycin. Recolonization of the intestine with nonpathogenic floras should be a long-term treatment for D-lactic acidosis.

Acidosis, Lactic↗
PubMed2004

Infantile intestinal leiomyosarcoma is prognostically favorable despite histologic aggressiveness: case report and literature review.

Intestinal leiomyosarcomas in children are extremely rare. The authors present a case of infantile intestinal leiomyosarcoma of the colon that was resected and was classified histologically as grade 2 because of abundant mitoses. The tumor cells infiltrated the submucosa and the serosal surface. Immunohistochemically, these cells were positive for alpha-smooth muscle actin but not for CD34 or CD117, by which the tumor was differentiated from gastrointestinal stromal tumor (GIST). The patient underwent follow-up without adjuvant therapy and is now doing well with no evidence of the disease for 42 months. Based on the current case and a review of 18 reported cases, it is concluded that infantile intestinal leiomyosarcoma, which is differentiated from GIST, has a favorable prognosis even when the histologic appearance is suggestive of aggressive biological characteristics. Adjuvant therapy is unnecessary when tumors are completely resected.

Actins↗
PubMed2004

Laparoscopic versus open appendectomy in children with uncomplicated and complicated appendicitis.

PURPOSE: To address whether laparoscopic appendectomy could be an alternative to conventional open appendectomy in children with complicated appendicitis as well as uncomplicated appendicitis, a retrospective study comparing laparoscopic and open appendectomies was performed. METHODS: One hundred patients who were treated by immediate appendectomy, either laparoscopically or by the open method, between May 2000 and August 2003 were included in the study. There were 53 patients in the laparoscopic appendectomy group and 47 patients in the open appendectomy group. RESULTS: The operating time was significantly longer for laparoscopic appendectomy than for open appendectomy (P < .001). The length of hospital stay was significantly shorter in laparoscopic appendectomy in patients with uncomplicated appendicitis (P = .001). Thirteen of the 100 patients (13.0%) had 15 postoperative complications including wound infection (n = 8), intraabdominal abscess (n = 4), stitch abscess (n = 2), and small bowel obstruction (n = 1). In both uncomplicated and complicated appendicitis, there was no significant difference between laparoscopic and open appendectomies in the complication rates, and the incidences of each complication did not differ between the procedures. Among the 14 patients with generalized peritonitis, postoperative complications were seen in 5 patients (35.7%). Although the presence of generalized peritonitis was associated significantly with postoperative complications (P = .017), there was no significant association between the procedure and complications. Overall treatment costs were increased by 26.0% in laparoscopic appendectomy. CONCLUSIONS: Laparoscopic appendectomy should remain an option in children with uncomplicated and complicated appendicitis, and when laparoscopy is selected, consideration of the advantages and disadvantages of the procedure is essential.

Adolescent↗
PubMed2004

Differential modulation of gene expression among rat tissues with warm ischemia.

The aim of this study is to determine if warm ischemia after surgical extirpation impacts gene expression in tissue samples which will be used for cDNA array analysis. We investigated effects of warm ischemia on gene expression in lung, liver, kidney, and spleen of rats, chronologically, using an original cDNA array, real-time quantitative RT-PCR and immunohistochemistry. Although no visible alteration was found in RNA quality, cDNA array showed that expression of many genes was modulated by warm ischemia within 60 min in these tissues, 19.1% of the tested genes in lung, 11.0% in liver, 5.1% in kidney, and 16.2% in spleen. Quantitative RT-PCR revealed that warm ischemia significantly induced up-regulation of immediate early genes, c-fos, Egr-1, and c-jun, in lung, but not in liver. These findings suggest that genes may show tissue-dependent differential transcriptional response against warm ischemia. Tissue samples obtained from patients during surgery cannot completely escape effects of ischemia. In case of examination by cDNA array analysis, biologists should keep in mind that tissue samples come equipped with particular footprints.

Animals↗
PubMed2004

Hematopoietic progenitor cells as possible origins of epithelial thymoma in a human T lymphocyte virus type I pX gene transgenic rat model.

We earlier reported that Fischer 344/jcl strain (F344) rats carrying a unique pX gene of human T lymphocyte virus type I (HTLV-I) under control of a rat lymphocyte-specific protein tyrosine kinase (p56lck) type I promoter (lck-pX rats) spontaneously developed epithelial thymomas from the thymic medulla. To investigate the role of bone marrow cells carrying the HTLV-I pX gene in development of thymomas, the bone marrow of normal F344 rats after lethal irradiation was reconstituted by bone marrow mononuclear cells (BMMC) of lck-pX rats. Epithelial thymomas similar to the original thymoma of lck-pX rats frequently developed in the nontransgenic recipients within 5 months after the BMMC transplantation. The thymomas expressed the pX gene, thereby indicating the thymoma cells to be of donor BMMC origin. Since the thymoma also developed in nontransgenic recipients reconstituted by BMMC depleted of adherent cells, it is suggested that nonadherent BMMC of donor lck-pX rats may migrate to and lodge in the thymus of recipient nontransgenic rats then transform into thymoma cells with epithelial characteristics. The thymoma cells were shown to bind to Ulex europaeus Agglutinin-1 (UEA-1) lectin, which binds epithelial cells in the thymic medulla. It was also shown that the nonadherent BMMC fraction used for bone marrow reconstitution contained a number of UEA-1-positive cells. Taken together, UEA-1 positive BMMC may be progenitor cells of the epithelial thymoma. The epithelial thymoma in lck-pX rats sheds light on epithelial cell development in thymic medulla and for oncogenesis of epithelial thymoma in humans.

Animals↗
PubMed2004

Ischemic preconditioning protects hepatocytes via reactive oxygen species derived from Kupffer cells in rats.

BACKGROUND AND AIMS: Hepatic ischemic preconditioning decreases sinusoidal endothelial cell injury and Kupffer cell activation after cold ischemia/reperfusion, leading to improved survival of liver transplant recipients in rats. Ischemic preconditioning also protects livers against warm ischemia/reperfusion injury, in which hepatocyte injury is remarkable. We aimed to determine whether ischemic preconditioning directly protects hepatocytes and to elucidate its mechanisms. METHODS: Rats were injected with gadolinium chloride to deplete Kupffer cells or with N -acetyl- l -cysteine, superoxide dismutase, or catalase to scavenge reactive oxygen species. Livers were then preconditioned by 10 minutes of ischemia and 10 minutes of reperfusion. Subsequently, livers were subjected to 40 minutes of warm ischemia and 60 minutes of reperfusion in vivo or in a liver perfusion system. In other rats, livers were preconditioned by H(2)O(2) perfusion instead of ischemia. In the other experiments, livers were perfused with nitro blue tetrazolium to detect reactive oxygen species formation. RESULTS: Ischemic preconditioning decreased injury in hepatocytes, but not in sinusoidal endothelial cells. Kupffer cell depletion itself did not change hepatocyte injury after ischemia/reperfusion, indicating no contribution of Kupffer cells to ischemia/reperfusion injury. However, Kupffer cell depletion reversed hepatoprotection by ischemic preconditioning. Reactive oxygen species formation occurred in Kupffer cells after ischemic preconditioning. Scavenging of reactive oxygen species reversed the effect of ischemic preconditioning, and H(2)O(2) preconditioning mimicked ischemic preconditioning. CONCLUSIONS: Ischemic preconditioning directly protected hepatocytes after warm ischemia/reperfusion, which is not via suppression of changes in sinusoidal cells as in cold ischemia/reperfusion injury. This hepatocyte protection was mediated by reactive oxygen species produced by Kupffer cells.

Acetylcysteine↗
PubMed2004

Bone marrow cells carrying the env-pX transgene play a role in the severity but not prolongation of arthritis in human T-cell leukaemia virus type-I transgenic rats: a possible role of articular tissues carrying the transgene in the prolongation of arthritis.

Transgenic rats carrying the env-pX gene of human T-cell leukaemia virus type-I (env-pX rats) were immunized with type II collagen (CII), and chronological alterations of arthritis were compared with findings of collagen-induced arthritis (CIA) in wildtype Wistar-King-Aptekman-Hokudai (WKAH) rats. Arthritis induced by CII in env-pX rats was more severe and persisted longer than CIA in WKAH rats. To determine whether the phenomenon is caused mainly by the transgene-carrying lymphocytes or articular tissues, we immunized lethally irradiated env-pX and WKAH rats with reciprocal bone marrow cell (BMC) transplantation. A severe but transient arthritis was induced by CII in WKAH rats reconstituted by env-pX BMC (w/tB/CII rats). On the other hand, in env-pX rats reconstituted by WKAH BMC, arthritis persisted longer than in w/tB/CII rats, although the degree was less at an early phase after CII immunization. These findings suggest that articular tissues rather than the BMCs carrying the env-pX transgene play a role in the prolongation of arthritis in env-pX rats, although BMCs carrying the transgene are associated with the severity of arthritis. When inflammatory cytokines in synovial cells isolated from env-pX rats before they developed arthritis were examined, interleukin-6 (IL-6) was detected at a higher level than in synovial cells from WKAH rats, thus suggesting the critical role of IL-6 in env-pX arthritis.

Animals↗
PubMed2004

Serological identification of endothelial antigens predominantly recognized in Kawasaki disease patients by recombinant expression cloning.

We showed IgG immune response against endothelial antigens in sera obtained from convalescent Kawasaki disease (KD) patients after recovery from the disease during the follow-up period using serological analysis of recombinant cDNA expression library (SEREX) methodology. We identified 46 antigens represented by 69 clones by immunoscreening of a cDNA expression library from tumor necrosis factor-alpha (TNFalpha) treated human umbilical vein endothelial cells (HUVEC) with sera from 4 KD patients. They included ubiquitin pathway proteins, transcriptional factors, signal transduction molecules, metabolic enzymes, cytoskeletal proteins, an adhesion molecule, and a cell cycle protein. By serological survey using phage plaque assay, sera from 5 non-KD patients were rarely reactive with the antigens. Among the antigens, tropomyosin was most frequently isolated (18 of 69 clones). Seventeen of the 18 clones were identified using KD3 serum. The second most frequently isolated antigen was also a cytoskeletal protein, called Tplastin (3 of 69 clones).

Antibodies↗
PubMed2004

Dexamethasone increased plasminogen activator inhibitor-1 expression on human umbilical vein endothelial cells: an additive effect to tumor necrosis factor-alpha.

OBJECTIVE: In patients with autoimmune diseases, blood vessels may be critically involved at the site of inflammation. For these patients, glucocorticoids (GC) are often used as therapeutics. The aim of this study is to determine the effects of GC on vascular endothelial cells which are under inflammatory conditions. METHODS: We examined the molecular expressions in human umbilical vein endothelial cells (HUVEC) induced by dexamethasone (Dex) and tumor necrosis factor (TNF)-alpha. Live cell number of HUVEC under exposure to Dex and TNF-alpha was also assayed. RESULTS: The cDNA array analysis showed that a number of genes were upregulated, but only a few were downregulated by Dex and TNF-alpha, respectively. Among them, thrombomodulin (TM) gene showed the least fold change when HUVEC were stimulated by TNF-alpha. Since TM inhibits blood coagulation, we took notice of molecules associated with coagulation and fibrinolysis. The quantitative real-time RT-PCR revealed that the expression of plasminogen activator inhibitor-1 (PAI-1) gene increased when HUVEC were exposed to Dex and TNF-alpha, respectively, and the corresponding augmentation of its protein expression was confirmed by immunohistochemistry. The expression of PAI-1 gene additively increased when Dex and TNF-alpha were added to stimulate HUVEC. Under our experimental conditions, TNF-alpha induced proliferation of HUVEC. On the other hand, Dex did not change the number of live cells regardless of stimulation by TNF-alpha. CONCLUSION: TNF-alpha can induce proliferation of vascular endothelial cells with downregulation of the anticoagulation molecule, TM, and upregulation of the anti-fibrinolysis molecule, PAI-1. Dex further increased the expression of PAI-1 gene in the cells stimulated by TNF-alpha, and did not reduce the effect on cell proliferation induced by TNF-alpha. These findings suggest that the balance of blood coagulation versus fibrinolysis may incline to coagulation when Dex and TNF-alpha cooperate on vascular endothelial cells.

Cell Proliferation↗