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Biomedical subjects

H Teramoto

Publications and source records attributed to H Teramoto.

At least 19 recordsLinked to original sources
PubMed2006

Gene expression changes in a patient presenting nonleukaemic nasal granulocytic sarcoma to acute myelogenous leukaemia using 40 K cDNA microarray.

This is a case report of granulocytic sarcoma occurring as a nasal lesion prior to the onset of acute myelogenous leukaemia (AML). To understand this case in more detail, we used 40,000 human cDNA microarray to identify the gene expression patterns of nonleukaemic stage bone marrow (BM), AML stage BM and AML stage peripheral blood cells and subsequently define the molecular basis of this disease progression. Of significance, we have tracked the expression profile of BM samples during the course of nonleukaemic to leukaemic progression, and identified a number of genes that may account for the growth potential of leukaemia cells and indicate poor prognosis of this case.

Aged, 80 and over↗
PubMed2001

Gene expression of insulin-like growth factor-1 and epidermal growth factor is downregulated in the heart of rats with nitrofen-induced diaphragmatic hernia.

Newborns with congenital diaphragmatic hernia (CDH) still have high mortality. Recently, a possible role of cardiac maldevelopment has been suggested. Human and experimental studies have demonstrated that heart weight is significantly reduced in the presence of CDH. Recent studies have suggested an important role for insulin-like growth factor-I (IGF-I) in the regulation of cardiac growth, structure, and function. Administration of IGF-I to normal rats has been shown to cause cardiac hypertrophy. Epidermal growth factor (EGF) plays an important role in cardiac differentiation and development. The aim of this study was to determine the gene-level expression of IGF-I and EGF in the hearts of rats with nitrofen-induced CDH using the reverse-transcription polymerase chain reaction technique (RT-PCR). CDH was induced in pregnant rats following administration of 100 mg nitrofen on day 9.5 of gestation (term 22 days). In control animals, the same dose of olive oil was given without nitrofen. Cesarean section was performed on day 21 of gestation. The fetuses were divided into three groups: normal controls (n = 8), nitrofen without CDH (n = 8), and nitrofen-induced CDH (n = 8). Total RNA was extracted from the hearts in each group and measured. mRNA was extracted from total RNA. RT-PCR was performed to evaluate mRNA expressions of IGF-I and EGF. Levels of mRNA were expressed as a ratio of band density divided by that of beta-actin, a housekeeping gene known to be expressed at a constant level. IGF-I mRNA expression was significantly decreased in CDH hearts (0.177 +/- 0.109) compared to controls (0.393 +/- 0.138) (P < 0.01) and nitrofen hearts without CDH (0.321 +/- 0.088) (P < 0.05). EGF mRNA expression was significantly decreased in CDH hearts (0.218 +/- 0.118) compared to controls (0.534 +/- 0.196) (P < 0.01) and nitrofen hearts without CDH (0.383 +/- 0.136) (P < 0.05). Decreased cardiac gene expression of IGF-I and EGF in the hypoplastic heart suggests that cardiac hypoplasia in nitrofen-induced rat CDH may be due to reduced synthesis of IGF-I and EGF by myocytes in the developing heart.

Animals↗
PubMed2001

Stretch induces a growth factor in alveolar cells via protein kinase.

Positive-pressure mechanical ventilation can injure the lung, causing edema and alveolar inflammation in a complication termed ventilator-induced lung injury (VILI). Cytokines such as interleukin-8 (IL-8) reportedly are important in this inflammatory response. On the other hand, hepatocyte growth factor (HGF) promotes regeneration of the lung, and delays pulmonary fibrosis. We postulated that cyclic stretch upregulates production and release of both of mediators. Human alveolar epithelial cells (A549) cultured on a silicoelastic membrane were tested for mRNA expression and release of IL-8 and HGF after cyclic stretch in vitro. Stretch induced mRNA expression and release of these mediators. The signaling pathway from cyclic stretch to release of IL-8 and HGF appeared to involve protein kinase C in the signal transduction pathway.

Cells, Cultured↗
PubMed2001

Altered gene level expression of thyroid hormone receptors alpha-1 and beta-1 in the lung of nitrofen-induced diaphragmatic hernia.

PURPOSE: Thyroid receptor alpha-1 (TR-alpha1) and thyroid receptor beta-1 (TR-beta1) are thought to be essential for the fetal and postnatal development of the lung. The authors investigated gene level expression of TR-alpha1 and TR-beta1 in the lung of nitrofen-induced congenital diaphragmatic hernia (CDH) using reverse transcription polymerase chain reaction (RT-PCR). METHODS: CDH was induced in pregnant rats after administration of 100 mg nitrofen on day 9.5 of gestation. Cesarean section was performed on day 21 of gestation. The fetuses were divided into 3 groups: normal controls (n = 16), nitrofen-induced CDH (n = 16), and nitrofen-treated without CDH (n = 16). mRNA was extracted from the left lung in each group. RT-PCR was performed to evaluate mRNA expressions of TR-alpha1 and TR-beta1. Levels of mRNA were expressed as a ratio of the band density divided by that of beta-actin, a house-keeping gene. RESULTS: TR-alpha1 mRNA expression was decreased significantly in CDH lung (1.618 +/- 0.148) compared with controls (2.658 +/- 0.251; P <.01) and nitrofen-treated without CDH lung (2.232 +/- 0.193; (P <.05). TR-beta1 mRNA expression also was significantly decreased in CDH lung (2.223 +/- 0.270) compared with controls (3.569 +/- 0.262; P <.01) and nitrofen-treated without CDH lung (3.235 +/- 0.299; P <.05). CONCLUSION: These data suggest that the downregulation of thyroid hormone signaling pathway through altered expression of TR-alpha1 and TR-beta1 during lung morphogenesis may be a contributory factor in the pathogenesis of pulmonary hypoplasia in nitrofen-induced CDH.

Animals↗
PubMed2001

Identification of Lhcb gene family encoding the light-harvesting chlorophyll-a/b proteins of photosystem II in Chlamydomonas reinhardtii.

The Lhcb gene family in green plants encodes several light-harvesting Chl a/b-binding (LHC) proteins that collect and transfer light energy to the reaction centers of PSII. We comprehensively characterized the Lhcb gene family in the unicellular green alga, Chlamydomonas reinhardtii, using the expressed sequence tag (EST) databases. A total of 699 among over 15,000 ESTs related to the Lhcb genes were assigned to eight, including four new, genes that we isolated and sequenced here. A sequence comparison revealed that six of the Lhcb genes from C. reinhardtii correspond to the major LHC (LHCII) proteins from higher plants, and that the other two genes (Lhcb4 and Lhcb5) correspond to the minor LHC proteins (CP29 and CP26). No ESTs corresponding to another minor LHC protein (CP24) were found. The six LHCII proteins in C. reinhardtii cannot be assigned to any of the three types proposed for higher plants (Lhcb1-Lhcb3), but were classified as follows: Type I is encoded by LhcII-1.1, LhcII-1.2 and LhcII-1.3, and Types II, III and IV are encoded by LhcII-2, LhcII-3 and LhcII-4, respectively. These findings suggest that the ancestral LHC protein diverged into LHCII, CP29 and CP26 before, and that LHCII diverged into multiple types after the phylogenetic separation of green algae and higher plants.

Algal Proteins↗
PubMed2001

Presence of antibodies against retinoblastoma tumor suppressor protein in patients with lung cancer.

Retinoblastoma (RB) protein and antibody against RB protein in sera from 45 lung cancer patients and 30 healthy volunteers were examined using bacterially synthesized glutathione S-transferase (GST) RB fusion protein and immunoblot analysis. RB protein was not detected in sera from any individuals with lung cancer or in any healthy volunteers. Sera from 6 patients, including 4 with non-small cell carcinoma and 2 with small cell carcinoma, reacted to a GST-RB fusion protein but not with a GST protein. Sera from 30 normal volunteers reacted to neither GST-RB fusion protein nor GST protein. The backgrounds such as age, gender, performance status, histology, stage, smoking history, and prior treatment were not significantly different between the patients with and without anti-RB antibodies. This is the first report describing the presence of anti-RB antibody in patients with malignant tumors. Further studies are needed to establish clinical significance for anti-RB antibody.

Adult↗
PubMed2001

K-ras and rho A mutations in malignant pleural effusion.

Mutations of the Kristen ras (K-ras) gene have been implicated in the pathogenesis of human lung cancer, especially adenocarcinoma, and have been proposed to be a prognostic factor. The K-ras mutation in codon 12 is detectable even in cell-free fluids by using the enriched polymerase chain reaction (PCR) technique. On the other hand, based on experimental results, the rho A mutation in codon 14 is also proposed to be oncogenic as observed in the K-ras mutation. Malignant pleural effusion is a common complication of lung cancer. We studied the point mutation of K-ras codon 12 and rho A codon 14 using enriched PCR in specimens of pleural effusion. Forty patients with pleural effusion were enrolled in this study. The causes of pleural effusion were non-small cell lung cancer (18 cases), small cell lung cancer (6 cases), malignant mesothelioma (2 cases), metastatic lung tumor (5 cases), thymoma (1 case), malignant lymphoma (1 case), and pleuritis tuberculosa (7 cases). The K-ras mutation was detected in 4 of 14 cases with adenocarcinoma, 1 of 3 cases with squamous cell carcinoma, 1 of 1 case with large cell carcinoma, and 1 of 5 cases with metastatic lung tumor, respectively. The rho A mutation was not detected in any pleural effusion examined in this study. Our study demonstrates the usefullness of pleural effusion as a clinical specimen for a search of point mutation of oncogenes. The K-ras codon 12 mutation is readily detected in pleural effusion, and the demonstration of this mutation has potentially important implications for the diagnosis of malignant pleural effusion.

Adult↗
PubMed2000

The Rho family GTPase Cdc42 regulates the activation of Ras/MAP kinase by the exchange factor Ras-GRF.

The Ras guanine-nucleotide exchange factor Ras-GRF/Cdc25(Mn) harbors a complex array of structural motifs that include a Dbl-homology (DH) domain, usually found in proteins that interact functionally with the Rho family GTPases, and the role of which is not yet fully understood. Here, we present evidence that Ras-GRF requires its DH domain to translocate to the membrane, to stimulate exchange on Ras, and to activate mitogen-activated protein kinase (MAPK). In an unprecedented fashion, we have found that these processes are regulated by the Rho family GTPase Cdc42. We show that GDP- but not GTP-bound Cdc42 prevents Ras-GRF recruitment to the membrane and activation of Ras/MAPK, although no direct association of Ras-GRF with Cdc42 was detected. We also demonstrate that catalyzing GDP/GTP exchange on Cdc42 facilitates Ras-GRF-induced MAPK activation. Moreover, we show that the potentiating effect of ionomycin on Ras-GRF-mediated MAPK stimulation is also regulated by Cdc42. These results provide the first evidence for the involvement of a Rho family G protein in the control of the activity of a Ras exchange factor.

3T3 Cells↗
PubMed2000

Tensin can induce JNK and p38 activation.

Cells organize diverse types of specialized adhesion sites upon attachment to extracellular matrix (ECM) components. One of the physiological roles of such cell-ECM interactions is to initiate and regulate adhesion-mediated signal transduction responses. The association of cells with fibronectin fibrils has been shown to regulate the JNK and p38 signaling pathways. We tested whether tensin, a cytoskeletal component localized to both focal contacts and fibronectin-associated fibrillar adhesions, can induce these signaling pathways. We found that tensin overexpression resulted in activation of both the c-Jun amino-terminal kinase (JNK) and p38 pathways. Tensin-mediated JNK activation was independent of the activities of the small GTP binding proteins Rac and Cdc42, but did depend on SEK, a kinase involved in the JNK pathway. We suggest that tensin may directly activate the JNK and p38 pathways, acting downstream or independent of the activities of the small GTP binding proteins Rac and Cdc42.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1999

[A case of acute disseminated encephalomyelitis accompanying Mycoplasma pneumoniae infection].

We report a 30-year-old man with acute disseminated encephalomyelitis (ADEM) accompanying Mycoplasma pneumoniae (M. pneumoniae) infection. He was admitted to our hospital because of headache, disturbed behavior, and unconsciousness following an upper respiratory tract infection on December 19, 1996. On admission, he was febrile (37.3 degrees C) and showed hypersomnia and neck stiffness. There were scattered rhonchi in both lungs. Cerebrospinal fluid (CSF) contained 19 white cells; the protein was 20 mg/dl and glucose 71 mg/dl (blood glucose 170 mg/dl); no organisms were seen or cultured. Cranial MRI showed multiple T 2-weighted hyperintense in the periventricular region of the cerebral white matter. M. pneumoniae antibody titer in serum was remarkably elevated. ADEM related to M. pneumoniae was suspected. Although intravenous methylprednisolone, piperacillin and clindamycin were administered, there was no subsequent improvement in the symptoms. Further MRI scan revealed extension of the inflammatory lesion. He had both pneumonia and he required mechanical ventilation. Since the end of the critical period, he has been in an akinetic mutism. We conclude that M. pneumoniae has to be considered as a possible cause of ADEM with severe respiratory symptoms.

Adult↗
PubMed1998

Effector domain mutants of Rho dissociate cytoskeletal changes from nuclear signaling and cellular transformation.

The small GTP-binding Rho proteins control a variety of biological activities, including organization of the actin cytoskeleton, regulation of gene expression and cellular transformation. In contrast, Ras proteins do not induce actin stress fibers, but potently transform cells which exhibit a morphology clearly distinct from that caused by activated forms of Rho. To investigate whether nuclear signaling and oncogenic potential of Rho are a consequence of its profound effect on cytoskeletal organization, we replaced each amino acid in the Rho effector loop with those of Ras, or replaced conserved residues with others known to result in differential signaling capability when introduced into Ras and Rac1. These Rho mutants did not gain the ability to induce the MAPK, JNK or p38 pathways but, surprisingly, all Rho effector loop mutants still continued to induce actin stress fiber formation. However, three of these Rho mutants, with substitutions of leucine-39, glutamic acid-39, or cysteine-42, lost the ability to stimulate gene transcription via the serum response factor (SRF) and failed to induce neoplastic transformation. Thus, these results indicate that cytoskeletal changes are not sufficient to induce the transformed phenotype, and that Rho-effector molecules regulating the actin cytostructure are distinct from those signaling to the nucleus and subverting normal growth control.

3T3 Cells↗
PubMed1998

[A survival case of fulminant pneumococcal meningitis as overwhelming postsplenectomy infection (OPSI) syndrome].

A 39-year-old female, who had splenectomy for idiopathic thrombocytopenic purpura (ITP) in 1988, was admitted to our hospital with high fever, headache, and loss of consciousness on November 29,1997. Neck stiffness and Kernig's sign were present. Examination of cerebrospinal fluid showed pleocytosis up to 506 cells/mm3 with 89% of polymorphonuclear cells and elevated protein to 1,135 mg/dl, and absence of glucose, Streptococcus pneumoniae phagocytosis was detected in the fluid. We diagnosed her as having pneumococcal meningitis as overwhelming postsplenectomy infection (OPSI) syndrome. After administration of dexamethasone (8 mg/day), cefotaxime (4 g/day), and ampicillin (6 g/day), she survived without any complications. Splenectomized patients have been recognized as immunocompromized hosts, and carry high morbidity and mortality risk from fulminant bacterial infections. Therefore, emergency treatment is important to reduce high mortality in such infections. We present an adult case of OPSI syndrome which occurred as pneumococcal meningitis, and we would like to emphasize the importance of prompt use of corticosteroids and high dose of sensitive antibiotics before DIC may occur during the course of illness.

Adult↗
PubMed1998

[A case of intracranial tuberculoma followed by MRI].

A 62-year-old woman with pulmonary tuberculosis was admitted to our hospital. She was completely neurologically free at admission and her CSF was normal. Brain MRI with Gd-DTPA enhancement demonstrated two mass lesions with ring-enhancement in the left temporal lobe and the right frontal lobe. The left temporal lesion had a bright central core with hypointense periphery on T2 weighted image. Extended hyperintense area was observed around this lesions, which represented brain edema. On T1 weighted image, the central core was demonstrated hypointense and its periphery was isointense. After starting antituberculous therapy, MRI revealed paradoxical expansion of left temporal lesion and neurological symptoms worsened temporarily, but, eventually the intracranial lesions diminished in size and disappeared, and the symptoms improved. So we diagnosed her as having intracranial tuberculoma. By long-term following up with MRI, we observed that the central core of the left temporal tuberculoma had changed gradually to hypointense on T2 weighted image and hyperintense on T1 weighted image respectively. We thought that the change of the central core on MRI represented organization of caseated necrosis.

Antitubercular Agents↗
PubMed1997

A human suppressor of c-Jun N-terminal kinase 1 activation by tumor necrosis factor alpha.

Tumor necrosis factor alpha (TNFalpha) has pleiotropic effects on cellular metabolism. One of the signaling paths from the TNFalpha receptor induces a stress-activated protein kinase cascade. Components within this TNFalpha kinase cascade include mitogen-activated protein kinase/extracellular signal-regulated kinase kinase kinase 1 (MEKK1) and stress-activated protein kinase/extracellular signal-regulated kinase kinase (SEK), which regulate the activity of c-Jun N-terminal kinase 1 (JNK1). Currently, molecules upstream of MEKK1 that link TNFalpha receptor to downstream kinases are not well understood. Besides TNFalpha, many other stimuli including several oncoproteins can activate JNK1. In most cases, the signaling cascade(s) leading from oncoproteins to JNK1 is poorly elucidated. We report here that the human T-cell lymphotrophic virus, type I (HTLV-I) oncoprotein, Tax, can activate JNK1. We isolated a novel human cell factor, G-protein pathway suppressor 2 (GPS2), by its ability to bind the HTLV-I oncoprotein, and we show that this factor can potently suppress Tax activation of JNK1. In trying to understand the mechanism of GPS2 activity, we found that it also suppressed TNFalpha activation of JNK1 but not TNFalpha activation of p38 kinase nor phorbol activation of extracellular signal-regulated kinase 2. Because GPS2 has minimal effect on MEKK1- or SEK-regulated JNK1 activity, it could act at a point between the TNFalpha receptor and MEKK1 in the initial step(s) of this kinase cascade. Alternatively, it is not excluded that GPS2 could work in a parallel pathway that leads from TNFalpha to JNK1. GPS2 represents a new molecule that could contribute important insights toward how cytokine- and oncoprotein-mediated signal transduction might converge.

Amino Acid Sequence↗
PubMed1997

Signaling from G protein-coupled receptors to the c-jun promoter involves the MEF2 transcription factor. Evidence for a novel c-jun amino-terminal kinase-independent pathway.

The c-Jun amino-terminal kinases (JNKs) are a subfamily of mitogen-activated protein kinases that phosphorylate c-Jun and ATF2, and it has been postulated that phosphorylated c-Jun enhances its own expression through AP-1 sites on the c-jun promoter. In this study, we asked whether signals activating JNK regulate the c-jun promoter. Using NIH 3T3 cells expressing G protein-coupled m1 acetylcholine receptors as an experimental model, we have recently shown that the cholinergic agonist carbachol, but not platelet-derived growth factor, potently elevates JNK activity. Consistent with these findings, carbachol, but not platelet-derived growth factor, increased the activity of a c-jun promoter-driven reporter gene (for chloramphenicol acetyltransferase). However, coexpression of JNK kinase kinase (MEKK) effectively increased JNK activity, but resulted in surprisingly limited induction of the c-jun promoter. This raised the possibility that pathway(s) distinct from JNK control the c-jun promoter, and prompted us to explore which of its regulatory elements participate in transcriptional control. We observed that deletion of the 3' AP-1 site diminished chloramphenicol acetyltransferase activity in response to carbachol, but only to a limited extent. In contrast, deletion of a MEF2 site dramatically reduced expression, and deletion of both the MEF2 and 3' AP-1 sites abolished induction. Furthermore, cotransfection with MEF2C and MEF2D cDNAs potently enhanced the activity of the c-jun promoter in response to carbachol, and stimulation of m1 receptors, but not direct JNK activation, induced expression of a MEF2-responsive plasmid. Taken together, these data strongly suggest that MEF2 mediates c-jun promoter expression by G protein-coupled receptors through a yet to be identified pathway, distinct from that of JNK.

3T3 Cells↗