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Biomedical subjects

F Ito

Publications and source records attributed to F Ito.

At least 37 records · Page 2Linked to original sources
PubMed2000

Characterization of a mutant E-cadherin protein encoded by a mutant gene frequently seen in diffuse-type human gastric carcinoma.

The cell-cell adhesion molecule E-cadherin plays an essential role in the maintenance and function of epithelial tissues. Altered expression of E-cadherin has been implicated in tumor invasion. Analysis of mutations of the human E-cadherin gene in gastric carcinoma of the diffuse type has revealed that deletion of exon 8 or 9 in its cDNA appears to be predominant. In this study, we carried out structural and functional analyses of a mutant form of E-cadherin in a cell line, HSC45-M2, established from a human signet ring-cell carcinoma. Although immunohistochemical analysis showed that the mutant cadherin was localized at cell-cell contact sites as usually seen with the wild type, these cells did not form compact colonies. HSC45-M2 cells expressed aberrant E-cadherin with an m.w. larger than that of the wild type. In these cells, we found deletion of the exon 9-intron 9 boundary including the splicing donor site in E-cadherin genomic DNA. RT-PCR indicated 2 transcripts, which appeared to be caused by the splicing defect. Northern blotting, however, showed that the transcript lacking exon 9 was predominantly detected in these cells. The electrophoretic mobilities on SDS-PAGE of the mutant E-cadherin protein in HSC45-M2 cells and the protein expressed from cDNA lacking exon 9 appeared identical. Analysis of the amino-terminal region of the mutant E-cadherin protein revealed that the cadherin was capable of becoming a mature form by removal of its amino-terminal peptide. However, the mutant E-cadherin was susceptible to trypsinization in the presence of Ca(2+), which is not the case for wild-type E-cadherin, suggesting that the mutant E-cadherin frequently found in diffuse-type gastric carcinoma may have lost its Ca(2+)-binding ability, leading to disruption of the tight cell-cell association.

Animals↗
PubMed2000

Cloning and expression of mouse deafness dystonia peptide 1 cDNA.

Complementary DNA of mouse deafness dystonia peptide 1 (DDP1) was isolated from adipocyte cDNA library and expressed in mammalian cells. The sequence shares homology of 92 and 97% on the nucleic acid and the amino acid levels with human DDP1. In comparison to mouse Bruton's tyrosine kinase (Btk) locus, the coding region spans 2 exons and the splice point is the same as human DDP1. Northern blot analysis suggests that mouse DDP1 expresses ubiquitously. In vitro transcription/translation study showed that the cDNA of mouse DDP1 codes about 11 kDa peptide. DDP1 tagged with FLAG localized in mitochondria and cytoplasm of COS7 cells. P19 embryonal carcinoma cells transfected with anti sense DDP1 cDNA were frequently dead after subculture and all the survivals expressed endogenous DDP1 mRNA. Therefore, mouse DDP1 may play an important role to survive in contrast to Tim8p, a yeast homologue, which was unnecessary in yeast.

Amino Acid Sequence↗
PubMed2000

Queens and major workers of Acanthomyrmex ferox redistribute nutrients with trophic eggs.

In Acanthomyrmex ferox, two distinct egg-types are produced: reproductive eggs that give rise to offspring and trophic eggs that serve to distribute nutrients. Queens lay both reproductive and trophic eggs, while major and minor workers lay only trophic eggs in the presence of the queen. The queen lays on average 17% of the trophic eggs in a colony, while majors and minors produce 42% and 41%, respectively. The large proportion of trophic egg production by the queen and soldiers is quite remarkable, since ant queens are expected to focus entirely on reproduction and majors, which have a defensive function in many species, to be sterile.

Animals↗
PubMed2000

Expression of APG-2 protein, a member of the heat shock protein 110 family, in developing rat brain.

APG-2 protein is a member of the heat shock protein 110 family, and it is thought to play an important role in the maintenance of neuronal functions under physiological and stress conditions. However, neither the tissue-distribution of APG-2 protein nor developmental change of its expression has been studied at the protein level. Therefore, we generated an antiserum against APG-2 protein and studied expression of this protein in rat brain and other tissues by use of the Western blot method. The results showed a high expression of APG-2 protein in various regions of the central nervous system (cerebral cortex, hippocampus, striatum, midbrain, hypothalamus, cerebellum, medulla pons, and spinal cord) throughout the entire postnatal stage. Similarly, a high level of APG-2 protein was detected in the whole brain of rat embryos and in adult rat tissues such as liver, lung, spleen, and kidney. In contrast, its expression in heart was high at postnatal days 1 and 3, but thereafter drastically decreased to a low level. Furthermore, APG-2 protein was detected in neuronal primary cultures prepared from rat cerebral cortex, and its level did not change notably during neuronal differentiation. These results show that APG-2 protein is constitutively expressed in various tissues and also in neuronal cells throughout the entire embryonic and postnatal period. suggesting that it might play an important role in these tissues under non-stress conditions.

Aging↗
PubMed2000

Cytokines accumulated in acquired renal cysts in long-term hemodialysis patients.

BACKGROUND: Cytokines play a pivotal role in growth, differentiation, and apoptosis. In this study, we measured cytokine content in the renal cyst fluid of patients with acquired cystic disease of the kidney (ACDK) in order to elucidate the possibility that cytokines are related to the development of ACDK. PATIENTS AND METHODS: All or some of 15 cytokines, IL-1a, -1b, -2, -4, -5, -6, -8, -10, IFN-alpha, -gamma, G-, M-, GM-CSF, TNF-alpha, and vascular endothelial growth factor (VEGF) were analyzed in cyst fluid and serum of 12 patients on hemodialysis (HD) including 8 with ACDK and 8 with normally functioning kidneys by sandwich enzyme-linked immunosorbent assay. RESULTS: Out of these cytokines, only IL-6, -8, M-CSF, and VEGF were detected in the cyst fluid of patients with ACDK. Moreover, IL-6, -8, and VEGF showed significantly higher concentrations in the cyst fluid than in the blood (194.9 +/- 90.9 vs. 0.0 +/- 0.0 pg/ml, 2,377. 5 +/- 602.9 vs. 0.0 +/- 0.0 pg/ml, 5,167.8 +/- 1,316.9 vs. 41.1 +/- 14.7 pg/ml, respectively), while M-CSF showed comparable concentrations in the cyst fluid with those in the blood (3,519.4 +/- 730.0 vs. 3,250.3 +/- 319.1 pg/ml, p = 0.69). Additionally, IL-6, -8, and VEGF accumulated more abundantly in the cyst fluid of patients with ACDK than in that of patients with other cystic nephropathies including ADPKD patients on HD (194.9 +/- 90.0 vs. 4.6 +/- 3.2 pg/ml, 2,377.5 +/- 602.9 vs. 76.8 +/- 46.5 pg/ml, 5,167.8 +/- 1,316.9 vs. 131.1 +/- 63.1 pg/ml, respectively). However, there was no significant correlation between the intracystic concentrations of these cytokines and the corresponding cyst diameters. CONCLUSION: These results showed that in ACDK patients a local environment exists in which production or accumulation of certain cytokines is selectively enhanced compared with patients with other cystic nephropathies. They imply that these cytokines are closely related to pathogenesis particular to ACDK.

Adult↗
PubMed1999

High-level expression of the Mnb/Dyrk1A gene in brain and heart during rat early development.

We previously isolated human MNB/DYRK1A cDNA from "the Down syndrome critical region" of human chromosome 21 (Shindoh et al., 1996, Biochem. Biophys. Res. Commun. 225: 92-99). As described herein, we prepared a polyclonal anti-MNB/DYRK1A antibody and used it in a Western blot assay to assess the expression of the MNB/DYRK1A protein during rat development. The MNB/DYRK1A protein was expressed strongly not only in the brain but also in other tissues from embryonic rats. At the early postnatal stage, expression of the protein was high in the central nervous system and heart, but low in liver, lung, spleen, and kidney. The level of MNB/DYRK1A protein in all tissues studied gradually decreased with postnatal growth. Similarly, Northern blot analysis revealed that a major 6.0-kb transcript of the Mnb/Dyrk1A gene was expressed at a high level in the brain during the early postnatal period but that its level was low in the adult. The finding that the MNB/DYRK1A protein is expressed strongly in the central nervous system and heart may indicate a significant role for this protein in the development of these organs.

Amino Acid Sequence↗
PubMed1999

Dipole Moment Function of LiF and LiCl Obtained from the Herman-Wallis Analysis: A Comparative Study with the MBER Data.

FTIR absorption spectra of the fundamental bands of LiF and LiCl were measured with an apodized resolution of 0.01 cm-1. The Herman-Wallis analysis of these spectra led to the determination of the ratio of the dipole derivative to the permanent dipole moment, [µe/(dµ/dr)ere], for each molecule. The vibrational dependence of the dipole moment for each molecule has been already reported and these data were reanalyzed to determine the dipole moment function independently. The results from the Herman-Wallis analysis were compared with these results, and good agreement was found. This demonstrates that the Herman-Wallis analysis can produce reliable relative values of dipole moment functions. Copyright 1999 Academic Press.

Journal Article↗
PubMed1999

Handlebar hernia with intra-abdominal extraluminal air presenting as a novel form of traumatic abdominal wall hernia: report of a case.

An 18-year-old male was admitted to our Emergency Department with a traumatic abdominal wall hernia (TAWH) of the left lower quadrant (LLQ) after suffering hypogastric blunt injury and urogenital lacerations in a motorcycle accident. Upright chest X-ray showed a small amount of right infradiaphragmatic free air, and a computed tomographic (CT) scan demonstrated an abdominal wall hernia. At surgery, no impairment was found in the digestive tract, and an abdominal herniorrhaphy was performed. It is suggested that the free air had passed through a connection between the scrotal laceration and the contralateral abdominal defect via the subcutaneous space and was palpated as emphysema. This is a new type of TAWH, which suggests that blunt abdominal trauma may result in negative pressure in the subcutaneous and peritoneal cavity, and this could reflect the pathophysiology of TAWH.

Abdominal Muscles↗
PubMed1999

An accessory lobe of the liver disturbing closure of the umbilical ring.

The authors report a small omphalocele involving an accessory lobe of the liver (ALL) embedded in a cranial portion of the amniotic sac. The pedicle of liver tissue was markedly elongated. In this case, it was reasonable to assume that the ALL was formed during development of the embryonic body-wall folds and disturbed complete closure of the umbilical ring. Surgical resection of the ALL was performed to avoid its postoperative torsion. The pertinent literature is also reviewed.

Biopsy↗
PubMed1999

Glucocorticoids inhibit proliferation and adhesion of the IL-3-dependent mast cell line, MC/9, to NIH/3T3 fibroblasts, with an accompanying decrease in IL-3 receptor expression.

We investigated the effects of glucocorticoids on IL-3-dependent proliferation and c-kit expression of cells of the mouse mast cell line, MC/9. Glucocorticoids (dexamethasone, prednisolone, and hydrocortisone) inhibited IL-3-dependent MC/9 cell proliferation, whereas sex steroids (progesterone, beta-estradiol, and testosterone) had no effect. Flow cytometric analysis revealed that glucocorticoids reduced the expression of the IL-3 receptor on MC/9 cells. Immunoblot and Northern blot analyses indicated that glucocorticoids also reduced the expression of both c-kit protein and c-kit mRNA transcript. Furthermore, the adhesion of MC/9 cells to stem cell factor-expressing NIH/3T3 cells was reduced following glucocorticoid treatment. Our results indicate that glucocorticoids inhibit IL-3-dependent MC/9 mast cell proliferation, with an accompanying decrease in IL-3 receptor expression. Glucocorticoids also reduced c-kit expression on MC/9 cells resulting in a decreased adhesion to NIH/3T3 fibroblasts.

3T3 Cells↗
PubMed1999

FK506 and cyclosporin A inhibit stem cell factor-dependent cell proliferation/survival, while inducing upregulation of c-kit expression in cells of the mast cell line MC/9.

Murine mast cell proliferation and maturation are regulated by two distinct cytokines, interleukin-3 (IL-3) and the c-kit ligand, stem cell factor (SCF). In this study using cells of the mouse mast cell line, MC/9, the effects of two immunosuppressants, FK506 and cyclosporin A (CsA), were investigated. Withdrawal of IL-3 from the culture medium resulted in loss of viability of MC/9 cells. The addition of SCF in the absence of IL-3 maintained MC/9 cell survival but no cell proliferation was detected. The combined addition of IL-3 and SCF to the culture medium resulted in a more marked MC/9 cell proliferation than the addition of IL-3 alone. FK506 and CsA inhibited the SCF-dependent, but not the IL-3 dependent, stimulatory effects on MC/9 cell proliferation/survival. Apoptotic changes were analyzed using fluorescent staining with acridine orange and DNA electrophoresis. FK506 and CsA inhibited the SCF-dependent rescue effect from apoptosis. Flow cytometry showed that FK506 and CsA did not affect IL-3 receptor expression. However, immunoblot and reverse transcriptase-polymerase chain reaction (RT-PCR) analyses indicated that c-kit protein and c-kit mRNA transcripts were increased following the FK506 and CsA treatments in the presence of IL-3. In addition, MC/9 cells pretreated with FK506 or CsA showed an increased adhesiveness to NIH/3T3 cells that express membrane-bound SCF. Neither FK506 nor CsA affected c-kit tyrosine phosphorylation or MAP kinase nuclear translocation of MC/9 cells following SCF stimulation. These results indicate that FK506 and CsA, while inducing c-kit of MC/9 cells, selectively inhibit the SCF-dependent stimulatory effects on MC/9 cell proliferation/survival by a mechanism independent of, or at point(s) distal to, the c-kit-MAP kinase pathway.

3T3 Cells↗
PubMed1999

Embryogenesis of pancreaticobiliary maljunction inferred from development of duodenal atresia.

The embryogenesis of pancreaticobiliary maljunction is inferred from the embryogenesis of duodenal atresia. The epithelial cells of the duodenum begin to proliferate and completely plug the lumen, but a process of vacuolation recanalizes the duodenum. Recanalization of the common duct frequently appears with two lumina and openings into the duodenum with two orifices. These two major canals create a narrow segment of the duodenum and this narrow zone is the area in the duodenum that is most prone to faulty recanalization and atresia formation. A bifid biliary system inserts at blind upper and lower pouches of the duodenum, and the common bile duct inserts in a Y fashion. The common bile duct inserts at the stenotic segment, and the end result is a T-shaped formation in patients with duodenal stenosis. During the development of the bile duct, abnormal fusion may occur between the bile duct and branches of the right ventral pancreatic duct. The site in the bile duct where a branch of the pancreatic duct joins is likely to develop atresia due to disturbance of the recanalization process, as seen in duodenal atresia. Severe impairment of vacuolation causes divided atretic bile duct at the site where the pancreatic duct inserts in a Y-fashion into the upper and lower bile duct. Moderate impairment of vacuolation causes a stenosis at the site where the pancreatic duct inserts in a T-shape, with a moderate dilatation of the bile duct.

Choledochal Cyst↗
PubMed1999

Gastric duplication communicating with the left hepatic duct: a rare case of recurrent hemobilia in a child.

Gastric duplication is a rare anomaly, usually manifested as an abdominal mass or gastric outlet obstruction mimicking congenital hypertrophic pyloric stenosis during the first year of life. Occasionally, it communicates with the pancreatic duct and causes pancreatitis. However, communication with the intrahepatic bile duct has not been described. The authors report a rare case of gastric duplication that communicated with the left hepatic duct and caused recurrent hemobilia in a 2-year-old girl. Left hepatectomy and excision of the duplication were curative.

Bile Ducts, Extrahepatic↗
PubMed1999

Morphological investigation of the enteric nervous system in Hirschsprung's disease and hypoganglionosis using whole-mount colon preparation.

BACKGROUND/PURPOSE: A suction rectal mucosal biopsy with positive staining for acetylcholinesterase is a useful test for diagnosis of Hirschsprung's disease (HD). However, hypoganglionosis has not been diagnosed by a rectal mucosal biopsy. The authors morphologically examined the enteric nervous systems in HD and hypoganglionosis patients using whole-mount preparations. METHODS: Six HD patients, two hypoganglionosis patients, and 10 with normally innervated colons were examined. Colonic specimens were incubated with the primary antibodies against protein gene product 9.5 (PGP 9.5) mixed with S-100b protein, tyrosine hydroxylase (TH), calcitonin gene-related peptide (CGRP), substance P (SP), and neurofilament protein 200 kDa (NFH). They were observed by histochemical technique using light-microscopy in whole-mount preparations. RESULTS: The aganglionic distal colon had thick nerve strands stained with PGP 9.5 mixed with S100 or NFH located in the layer between the longitudinal muscle and the circular one, and the submucosal layer. The nerve strands in the myenteric layer contained few CGRP- and SP-positive fibers and ran along the long axis of the intestine. Ganglion cells appeared along with those thick nerve strands in the transitional zone of HD. In hypoganglionosis, we found small myenteric ganglia with no thick nerve strands. CONCLUSIONS: The enteric nervous system in oligoganglionic segments of HD morphologically differed from the one in hypoganglionosis. A suction rectal mucosal biopsy would be of no use in the diagnosis of hypoganglionosis.

Child, Preschool↗
PubMed1999

Acute respiratory failure associated with intrathoracic masses in neonates.

BACKGROUND: Intrathoracic masses are uncommon in children. Occasionally, they present with acute respiratory failure in the neonatal period. Although emergency resection usually is the treatment of choice, other modalities are sometimes necessary to stabilize the patient. METHODS: Seven neonates with intrathoracic masses were treated. Five had congenital cystic adenomatoid malformations (CCAM), 1 had a mediastinal teratoma, and 1 had a pneumatocele. These cases were reviewed retrospectively. RESULTS: Four of the 7 infants had respiratory failure in the neonatal period. A patient with a large mediastinal teratoma and 1 with a CCAM that increased rapidly after presentation underwent emergency operation, relieving respiratory distress. The other 2 large CCAMs presented with severe respiratory distress immediately after birth because of pulmonary hypoplasia. One neonate with a Stocker-I CCAM died after emergency resection. One more recent patient with a Stocker-III CCAM survived after successful treatment with delayed resection, performed 3 days after birth. Nitric oxide (NO), and extracorporeal membrane oxygenation (ECMO) were instituted as supportive care because of profound persistent fetal circulation (PFC). CONCLUSIONS: Acute respiratory failure associated with intrathoracic masses in neonates may be managed in 1 of 2 ways. A small mass that increases rapidly should be resected soon after presentation. In neonates with large masses with associated PFC, surgery can be delayed until the patient is stable. ECMO, NO, and high-frequency oscillation (HFO) can be used aggressively for stabilizing such neonates.

Extracorporeal Membrane Oxygenation↗