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Fumio Endo

Publications and source records attributed to Fumio Endo.

At least 19 recordsLinked to original sources
PubMed2006

Hypermetabolism of fat in V1a vasopressin receptor knockout mice.

[Arg8]Vasopressin (AVP) has an antilipolytic action on adipocytes, but little is known about the mechanisms involved. Here, we examined the involvement of the V1a receptor in the antilipolytic effect of AVP using V1a receptor-deficient (V1aR-/-) mice. The levels of blood glycerol were increased in V1aR-/- mice. The levels of ketone bodies, such as acetoacetic acid and 3-hydroxybutyric acid, the products of the lipid metabolism, were increased in V1aR-/- mice under a fasting condition. Triacylglyceride and free fatty acid levels in blood were decreased in V1aR-/- mice. Furthermore, measurements with tandem mass spectrometry determined that carnitine and acylcarnitines in serum, the products of beta-oxidation, were increased in V1aR-/- mice. Most acylcarnitines were increased in V1aR-/- mice, especially in the case of 2-carbon (C2), C10:1, C10, C14:1, C16, C18:1, and hydroxy-18:1-carbon (OH-C18:1)-acylcarnitines under feeding rather than under fasting conditions. The analysis of tissue C2-acylcarnitine level showed that beta-oxidation was promoted in muscle under the feeding condition and in liver under the fasting condition. An in vitro assay using brown adipocytes showed that the cells of V1aR-/- mice were more sensitive to isoproterenol for lipolysis. These results suggest that the lipid metabolism is enhanced in V1aR-/- mice. The cAMP level was enhanced in V1aR-/- mice in response to isoproterenol. The phosphorylation of Akt by insulin stimulation was reduced in V1aR-/- mice. These results suggest that insulin signaling is suppressed in V1aR-/- mice. In addition, the total bile acid, taurine, and cholesterol levels in blood were increased, and an enlargement of the cholecyst was observed in V1aR-/- mice. These results indicated that the production of bile acid was enhanced by the increased level of cholesterol and taurine. Therefore, these results indicated that AVP could modulate the lipid metabolism by the antilipolytic action and the synthesis of bile acid via the V1a receptor.

3-Hydroxybutyric Acid↗
PubMed2006

Gene expression profiles of homogentisate-treated Fah-/- Hpd-/-mice using DNA microarrays.

Hereditary tyrosinemia I (HT I) is a genetic disorder of tyrosine metabolism caused by abnormalities of fumarylacetoacetate hydrolase. Disturbances in tyrosine metabolism lead to increased levels of succinylacetone and succinylacetoacetate. However, the mechanisms causing liver failure, cirrhosis, renal tubular dysfunction, and hepatocarcinoma are still unknown. Alterations in gene expression found in the livers of patients with HT I are responsible for the pathogenesis of this disease, for example acute liver failure. Therefore, gene expression analysis allows us to better understand its pathogenesis. We analyzed gene expressions in tyrosinemia type I model mice with liver failure using microarrays. The results were confirmed by quantitative PCR to evaluate the pathogenesis of tyrosinemia type I. We found that numerous genes, including amino acid metabolism and apoptosis related genes, were up- or down-regulated at the onset of liver failure. These findings are useful in understanding the pathogenesis of hereditary tyrosinemia.

Animals↗
PubMed2006

Newborn hearing screening in a single private Japanese obstetric hospital.

BACKGROUND: Hearing loss is one of the most common abnormalities present at birth. The authors examined the frequency of newborn hearing disturbance at a single obstetric hospital to exclude technical varieties or varieties of subjects which are inevitable in multiple institutional cooperative studies. METHODS: The newborns were examined with an automated auditory brainstem response screener, the ALGO 2e, on day 4 post-partum. This Screener uses 35 dB near hearing level click stimuli and provides a PASS/REFER result that requires no interpretation. The PASS result is accepted as adequate evidence of hearing and REFER result as required further diagnostic testing to determine hearing status. Screenings of REFER outcomes were repeated at 1 month of age. Comparisons were made of the results and the Japanese multiple institutional trials by Mann-Whitney U-test. RESULTS: The authors screened 8979 out of 13 494 neonates born from July 1999 to October 2004. The neonates with unilateral or bilateral REFER outcomes were 37 cases (0.41% of the total examined) on day 4, and 31 cases (0.35%) at 1 month of age. Five of the 31 neonates had PASS outcomes at 6 months of age. Among the 31 REFER neonates, eight (25.8%) had otolaryngeal complications. CONCLUSION: In the present study, screening results at 1 month of age resembled the final diagnosis obtained at 6 months of age; out of 31 REFER cases, 26 cases were diagnosed with hearing loss. In contrast, in the multiple institutional study, both unilateral and bilateral REFER rates were much higher than the rates of final hearing loss. Concerning the final diagnoses of bilateral hearing loss, the authors' results (0.10%) and the multiple institutional studies' results (0.05% in low-risk and 2.19% in high-risk neonates) were comparable to the results reported in the USA. To expand the newborn hearing screening program, it is crucial that authority and institutions concerned promote the development of a national or prefecture-based early hearing loss identification and intervention network.

Evoked Potentials, Auditory, Brain Stem↗
PubMed2006

[Fall prevention strategy for elderly women wishing to attend community fall prevention programs].

AIM: Fall prevention programs for community-dwelling elderly people are carried out as part of disability-postponing programs in Japanese municipalities. This study examined how to design a fall prevention program for community health fair based on the characteristics of fall prevention strategies adopted by community-dwelling elderly women before attending community fall prevention programs. METHODS: One hundred and four community-dwelling elderly women (71.7 +/- 6.3 years old) who were attending community fall prevention programs for the first time were asked about their strategies for fall prevention. Age, regular attendance at outpatient programs, the Tokyo Metropolitan Institute of Gerontology Index, and Timed Up&Go were determined as factors related to whether or not the women had strategies for fall prevention. RESULTS: Sixty-four participants had their own strategies for fall prevention. Multiple logistic regression analysis showed that age (OR = 1.10, 95% CI:1.00-1.21) and regular attendance at outpatient programs (OR = 4.77, 95% CI:1.75-12.98) were significantly related to having fall prevention strategies. Timed Up&Go (OR = 1.42, 95% CI: 0.95-2.13) had a weak relationship to having such strategies (P = 0.085). The most common strategy was behavior such as lifting the toe when walking (n=38, 59.4%), followed by doing regular exercise (n=16, 25.0%). Few of the participants modified their environment (n=2, 3.1%). CONCLUSION: Community fall prevention programs for community-dwelling elderly women can motivate participants to develop interdisciplinary and comprehensive practices for fall prevention.

Accidental Falls↗
PubMed2005

Evaluation of small hypothalamic hamartomas with 3D constructive interference in steady state (CISS) sequence.

Hypothalamic hamartomas are relatively rare, non-neoplastic congenital malformations. With conventional MR images alone, small hypothalamic hamartomas may be difficult to diagnose because of artifacts from cerebrospinal fluid. We present the usefulness of three-dimensional constructive interference in steady state sequence for evaluating small hypothalamic hamartomas in three pediatric patients.

Child, Preschool↗
PubMed2005

Analysis of gene expression patterns in the developing chick liver.

The chick embryo has been used widely for studying liver development. However, in the past 30 years, the usage has decreased markedly due to lack of appropriate marker genes for differentiation in the developing chick liver. To use the chick embryo for analyzing the molecular mechanism of liver development, we surveyed marker genes in the developing chick liver by examining the expression pattern of genes that are well-characterized in the developing mammalian liver. By whole-mount in situ hybridization, Fibrinogen-gamma (FIB) expression was first detected at stage 12, specifically in the anterior intestinal portal, and its liver-specific expression persisted in the later stages. Albumin (ALB) expression was first detected at stage 30, when the liver starts maturing. Cytokeratin 19 (CK19) was first detected at stage 37 in the ductal plate of the liver, and its expression continued in the intrahepatic bile ducts derived from the ductal plate. Hex, a transcription factor, is an additional marker of bile duct differentiation. Hence, FIB, ALB, and CK19 expression can be used to trace hepatic induction, maturation, and bile duct differentiation, respectively.

Animals↗
PubMed2005

Markers associated with inborn errors of metabolism of branched-chain amino acids and their relevance to upper levels of intake in healthy people: an implication from clinical and molecular investigations on maple syrup urine disease.

Maple syrup urine disease (MSUD) is caused by a deficiency in the branched-chain alpha-ketoacid dehydrogenase complex. Accumulations of branched-chain amino acids (BCAAs) and branched-chain alpha-ketoacids (BCKAs) in patients with MSUD induce ketoacidosis, neurological disorders, and developmental disturbance. BCAAs and BCKAs influence on the nervous system can be estimated by analyzing these patients. According to clinical investigations on MSUD patients, leucine levels over 400 micromol/L apparently can cause any clinical problem derived from impaired function of the central nervous system. Damage to neuronal cells found in MSUD patients are presumably because of higher concentrations of both blood BCAAs or BCKAs, especially alpha-ketoisocapronic acids. These clinical data from MSUD patients provide a valuable basis on understanding leucine toxicity in the normal subject.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed2005

Apical membrane and junctional complex formation during simple epithelial cell differentiation of F9 cells.

Epithelium formation is a common event in animal morphogenesis. It has been reported that F9 cells differentiate into visceral endoderm-like epithelial cells when cell aggregates are cultured in the presence of retinoic acid. The present investigation set out to determine whether this in vitro model could be used under monolayer culture conditions, which is suitable for a detailed analysis of epithelial differentiation. We performed comparative gene expression analyses of F9 cells grown under aggregate and monolayer culture conditions prior to and following treatment with retinoic acid. Under these conditions, induction in the expression of differentiation marker genes was confirmed, even in monolayer cultures. Junctional complex and apical membrane formation, both of which are characteristic of epithelial cells, were also observed under monolayer culture conditions. Because of the merit of monolayer culture condition, we found that apical membrane and junctional complex formation are strictly regulated during epithelial differentiation. It was also revealed that F9 cells differentiated into epithelial cells predominantly on the fourth and fifth day following retinoic acid induction. These results showed that a monolayer culture of F9 cells represents a viable in vitro model that can be employed to elucidate mechanisms pertaining to epithelium formation.

Animals↗
PubMed2005

Apoptosis under hypercytokinemia is a possible pathogenesis in influenza-associated encephalopathy.

BACKGROUND: Influenza-associated encephalopathy is reported to be frequent in Japan and East Asia. No evaluating markers except interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha and no likely pathological mechanism for the disease have yet been elucidated. METHODS: In this study, influenza-associated encephalopathy was defined by clinical symptoms, and the use of an anti-influenza antibody test and/or influenza antigen detection kits, as well as computed tomography and/or magnetic resonance imaging. The levels of proinflammatory cytokines, acute phase proteins, endothelial markers and cytochrome c were compared in sera from 11 patients with and 42 without encephalopathy. RESULTS: Cytochrome c concentration in sera from patients with encephalopathy was markedly increased compared with that from patients without encephalopathy and normal controls. Although levels of several other proinflammatory cytokines and acute phase proteins such as TNF-alpha and IL-8 were also elevated in patients with influenza virus infection, the difference between those with and without encephalopathy, though significant, was less dramatic. The mean serum concentration of cytochrome c in 11 patients with encephalopathy, consisting of four deceased, four with and three without residual central nervous system sequelae, was 26.7 +/- 19.5 ng/mL on admission. In contrast, cytochrome c levels in 42 patients without encephalopathy were 0.3 +/- 0.7 ng/mL. CONCLUSION: The present results indicate that cytochrome c is a useful marker to follow patients with influenza-associated encephalopathy and suggest that an apoptosis of cells in several organs including the cerebrum and liver under the influence of hypercytokinemia is a possible mechanism of the disease.

Apoptosis↗
PubMed2004

Evaluation of systemic inflammatory responses in neonates with herpes simplex virus infection.

Neonatal herpes simplex virus (HSV) infection is a severe disease with high mortality and morbidity. To investigate the pathogenesis of neonatal HSV infection, we examined inflammatory responses and markers of apoptosis in patients with neonatal HSV infection. Concentrations of inflammatory cytokines and markers of apoptosis were significantly higher in patients with disseminated HSV infection and were correlated with HSV load. It appears that the immunopathological damage that results from host responses to viral infection leads to organ dysfunction in patients with neonatal HSV infection.

Apoptosis↗
PubMed2004

Flow cytometric isolation of endodermal progenitors from mouse salivary gland differentiate into hepatic and pancreatic lineages.

Experimental injury is useful to induce tissue stem cells, which may exist in small numbers under normal conditions. The salivary glands originate from the endoderm and consist of acinar and ductal epithelial cells, which have exocrine function. After salivary gland duct ligation, acinar cells disappear as a result of apoptosis, and duct epithelium subsequently proliferates. In this study, we analyzed the tissue stem cells induced by salivary gland duct ligation in mice using immunohistochemistry and flow cytometry. We sorted the Sca-1(+)/c-Kit(+) fraction from adult mice salivary glands by way of fluorescence-activated cell sorting. The sorted cells were apparently homogeneous and were designated mouse salivary gland-derived progenitors (mSGPs). mSGP cells differentiated into a hepatic lineage when cultured in matrigel. In spherical culture in the presence of glucagon-like peptide-1 (GLP-1), these cells differentiated into a pancreatic endocrine lineage. When spheroidal bodies of mSGP, 20 to 30 microm in diameter, were transplanted into liver via the portal vein, the cells integrated into hepatic cords and expressed albumin and alpha1-antitrypsin, suggesting that they had differentiated into hepatic-type cells. Moreover, ductlike structures formed by mSGP cells also appeared, epithelial cells of which were positive for cytokeratin 19. In conclusion, fluorescence-activated cell sorting (FACS) based on histologic evidence is efficient in isolating adult tissue stem cells of the salivary gland. Tissue stem cells of endodermal origin (e.g., hepatic oval cells, pancreatic epithelial progenitor cells, and salivary gland progenitor cells) have similarities in their molecular markers and tissue location. Our findings suggest the existence of common tissue stem cells in endoderm-derived organs.

Animals↗
PubMed2004

Serum cytochrome c level as a prognostic indicator in patients with systemic inflammatory response syndrome.

BACKGROUND: Apoptosis may play an important role in the development of systemic inflammatory response syndrome (SIRS) and progression to multiple organ dysfunction syndrome (MODS). To quantify the extent of apoptosis in these morbidities, we developed a sandwich ELISA system to measure serum cytochrome c (cyt-c) levels and we investigated the prognostic significance of cyt-c concentration in SIRS/MODS patients. METHODS: Cyt-c concentrations in patients with SIRS (n=53) with or at risk for MODS were measured and compared with those of control subjects (n=14). RESULTS: Cyt-c concentrations in SIRS/MODS patients increased (0.24-210 ng/ml), whereas those in control subjects were under detection limits (0.1 ng/ml). Cyt-c concentrations in non-survivors increased significantly compared with those in survivors both on the day of admission and on the fifth hospital day. A significant positive correlation was found between cyt-c concentration and two representative organ dysfunction scores, APACHE II and multi-organ failure (MOF) score. Cyt-c concentrations increased earlier than MOF score during the exacerbation phase and rapidly decreased during the convalescence phase in a survivor, but the level continued to be high in a non-survivor. CONCLUSIONS: Determination of serum cyt-c concentrations may be useful to assess the severity of organ dysfunction and to predict the prognosis of SIRS/MODS patients.

Adolescent↗
PubMed2004

Clinical manifestations of inborn errors of the urea cycle and related metabolic disorders during childhood.

Various disorders cause hyperammonemia during childhood. Among them are those caused by inherited defects in urea synthesis and related metabolic pathways. These disorders can be grouped into two types: disorders of the enzymes that comprise the urea cycle, and disorders of the transporters or metabolites of the amino acids related to the urea cycle. Principal clinical features of these disorders are caused by elevated levels of blood ammonium. Additional disease-specific symptoms are related to the particular metabolic defect. These specific clinical manifestations are often due to an excess or lack of specific amino acids. Treatment of urea cycle disorders and related metabolic diseases consists of nutritional restriction of proteins, administration of specific amino acids, and use of alternative pathways for discarding excess nitrogen. Although combinations of these treatments are extensively employed, the prognosis of severe cases remains unsatisfactory. Liver transplantation is one alternative for which a better prognosis is reported.

Child↗
PubMed2003

Complete absence of bile and pancreatic ducts in a newborn: a new entity of congenital anomaly in hepato-pancreatic development.

We examined a newborn who had no bile and pancreatic ducts. Hydrops was evident after 29 weeks of gestation and she died shortly after birth, weighing 1,368 g. One of her siblings had died of hydrops at about six months of gestation, and there were two more miscarriages of unknown cause. At autopsy on the newborn, the liver had an abnormally round shape and the pancreas was not in the normal position. There was an ectopic small pancreas with normally developed islets. Histological analysis revealed the complete absence of extra- and intra-hepatic bile and pancreatic ducts. Immunostaining of these tissues showed no positive bile duct marker staining using epithelial membrane antigen and cytokeratin 19 in the liver. Albumin and alpha-fetoprotein staining was positive in the liver, and insulin and glucagon staining was positive in the remaining islets. Thus, this case is characterized by complete absence of bile and pancreatic ducts. These findings suggest the existence of a gene linked to the development of bile and pancreatic ducts.

Abnormalities, Multiple↗
PubMed2003

In situ evaluation of podocin in normal and glomerular diseases.

BACKGROUND: Mutations of the NPHS2 gene are responsible for autosomal-recessive steroid-resistant nephrotic syndrome. Its product, podocin, faces the slit diaphragm area with its two ends in the cytoplasm of foot processes. METHODS: We generated rabbit polyclonal antibodies against conjugated peptides from human podocin N- and C-termini, and studied podocin and synaptopodin using kidney tissues of normal humans and those with glomerular diseases. RESULTS: Antipodocin antibodies detected the original 42 kD fragment and an extra smaller fragment by Western blot analysis using human isolated mature glomeruli. RNA analysis showed two bands, the original and the other of a decreased length. Immunohistochemically, podocin was detected in a linear pattern along the glomerular capillary loop. Antipodocin antibody (C-terminal) stained the smooth muscles of renal arterioles and aorta. Among 42 patients, podocin was normally expressed in glomeruli in purpura nephritis, IgA nephropathy (IgAN), and minimal-change disease (MCD), while it was either decreased or absent in most subjects with focal segmental glomerulosclerosis (FSGS). The expression of synaptopodin was similar to that of podocin, although some discrepancy existed. CONCLUSION: Although indirect, our data suggest the existence of a vascular isoform of podocin with a different molecular mass. We propose that examination of podocin expression may help differentiate MCD from FSGS.

Adolescent↗