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Biomedical subjects

N Iida

Publications and source records attributed to N Iida.

At least 73 records · Page 4Linked to original sources
PubMed1997

Nodular regenerative hyperplasia of the liver in systemic lupus erythematosus. The relationship with anticardiolipin antibody and lupus anticoagulant.

Recent reports have indicated that nodular regenerative hyperplasia (NRH) associated with systemic lupus erythematosus (SLE) is related to anticardiolipin antibodies (aCL) and/or lupus anticoagulant (LA). We describe a patient with SLE complicated by NRH, who did not show neither aCL nor LA activity. This case suggests that the pathogenesis of NRH in patients with autoimmune diseases is heterogeneous and not confined to aCL and LA.

Adult↗
PubMed1997

[Indication for percutaneous transluminal coronary angioplasty based on quality of life of patients with angina pectoris].

The changes in quality of life (QOL) before and after percutaneous transluminal coronary angioplasty (PTCA) were investigated to establish criteria for determining whether patients with angina pectoris should undergo PTCA. The QOL was surveyed twice by self-completed questionnaire for QOL by Iida and Kohashi (QUIK) before and about 4 months after PTCA in 84 patients (mean age 62.8 +/- 10.1 years) with angina pectoris. High QUIK score reflects a poor QOL, of which the internal consistency was 0.86, demonstrating high reliability. The subjects were classified into three groups according to the changes of total QUIK score before and after PTCA (I: QOL improved 31.0%, II: QOL unchanged 48.8%, III: QOL worsened 20.2%). Age, gender, total QUIK score prior to PTCA, presence of anginal pain, complications extent and degree of coronary artery stenosis, and left ventricular ejection fraction were compared between the three groups. The total QUIK score prior to PTCA in the improved QOL group was higher than that in the worsened QOL group (11.6 vs 5.1, p < 0.01). Most patients showing a poor QOL prior to PTCA demonstrated an improvement in their QOL after PTCA. The number of patients with anginal pain prior to PTCA was high in the improved QOL group (35.8%, p < 0.05). Percutaneous transluminal coronary angioplasty might not aggravate QOL (12.1%, p = 0.1) in patients with single-vessel disease. In patients with multivessel disease, PTCA might not improve (35.3%) but also might aggravate QOL (25.5%). Multivariate analysis showed that PTCA improved QOL in male or sixty-ager patients and in patients with a total QUIK score of 10 or more prior to PTCA (p < 0.01). The total QUIK score, presence of anginal pain and extent of coronary artery stenosis prior to PTCA, gender and age are factors predicting QOL after PTCA. The adaptation of PTCA for those patients should be prudently and inclusively taken into consideration to extend their QOL.

Adult↗
PubMed1996

The cell adhesion molecule, GP116, is a new CD44 variant (ex14/v10) involved in hyaluronic acid binding and endothelial cell proliferation.

In this study we have found that endothelial cells from different origins all contain a CD44-related transmembrane glycoprotein, named GP116. Using a bovine aortic endothelial cell line and a standard pulse-chase protocol, we show that GP116 is synthesized as a 52-kDa nascent polypeptide precursor (p52) which is processed to GP116 as follows, p52 --> p63/65 --> p82 --> p100 --> GP116. GP116 contains approximately 8 N- and approximately 11 O-linked oligosaccharide chains (but lacks glycosaminoglycans) and interacts directly with the cytoskeletal protein, ankyrin, both in vitro (Kd approximately 1.2 nM) and in vivo. The results of GP116 amino acid composition, reverse transcriptase-polymerase chain reaction, Southern blot, Northern blot, cloning, and sequence analyses indicate that endothelial cells express this new CD44 variant that contains an exon having significant homology with human CD44 exon 14 (ex14/v10). GP116, designated as CD44 (ex14/v10), has been shown to be a major hyaluronic acid (HA) receptor (Kd approximately 0.5-0.8 nM) responsible for cell adhesion. Most importantly, we have found that the interaction between CD44(ex14/v10) and HA or a small fragment of HA (10-15 disaccharide units) induces a mitogenic response in endothelial cells. These findings suggest that this CD44 variant plays an important role in regulating endothelial cell proliferation.

Alternative Splicing↗
PubMed1996

A new process of cancer prevention mediated through inhibition of tumor necrosis factor alpha expression.

Mechanisms of cancer prevention were studied using structurally different cancer-preventive agents, sarcophytol A, canventol, (-)-epigallo-catechin gallate, and tamoxifen, based on our evidence that tumor necrosis factor alpha (TNF-alpha) acts as an endogenous tumor promoter relevant to human carcinogenesis. Pretreatment with the four preventive agents commonly inhibited TNF-alpha mRNA expression and TNF-alpha release in BALB/3T3 cells induced by a tumor promoter, okadaic acid, whereas the expression of early response genes (c-jun, junB, c-fos, and fosB) was enhanced. These results strongly suggest that inhibition of TNF-alpha mRNA expression and its release is a new process of cancer prevention.

3T3 Cells↗
PubMed1996

Leukocyte-derived growth factor links the PDGF and CXC chemokine families of peptides.

Leukocytes produce many biological mediators that orchestrate the subsequent cellular events during wound healing. We have identified a novel cytokine, leukocyte-derived growth factor (LDGF), which is mitogenic for connective tissue cells. Sequence analysis of the LDGF peptide revealed that it is a precursor of other known peptides including platelet basic protein (PBP), connective tissue activating peptide III (CTAP-III), and neutrophil activating peptide 2 (NAP-2). None of these shorter peptides are active as mitogens for fibroblasts. LDGF appears to stimulate fibroblast growth by stimulation of tyrosine kinase activity of the PDGF receptors. One of the truncated products of LDGF, NAP-2, is a potent neutrophil chemoattractant. Peptides larger than NAP-2, such as PBP and CTAP-III, are not active as neutrophil chemoattractants. Collectively, these findings demonstrate that the LDGF peptide must remain intact in order to retain its fibroblast mitogenic activity. If the LDGF peptide is processed to release the carboxyl terminal half to generate NAP-2, a peptide with proinflammatory activity is generated. These results indicate that the multiple peptides produced from the LDGF-PBP gene posses divergent biological activities that could regulate different phases of the repair process.

Amino Acid Sequence↗
PubMed1995

New CD44 splice variants associated with human breast cancers.

Changes in the CD44 variant (CD44v) isoforms on the cell surface have been correlated with tumor metastasis. In this study we have examined the expression of CD44 variant isoforms in human breast carcinoma samples by a variety of techniques including immunohistochemistry, reverse transcriptase-polymerase chain reaction (RT-PCR), and nucleotide sequencing. Using RT-PCR, we have determined that normal human breast tissue contains primarily the CD44 epithelial (CD44E) form and very little CD44 standard (CD44s) form. However, metastatic breast carcinomas appear to overexpress both the CD44E and CD44s forms and also display multiple new species of CD44 variant isoforms. Histocytochemical staining using anti-CD44 antibody (recognizing a common determinant of the CD44 class of glycoproteins) confirms that the CD44 molecules are overexpressed and preferentially located in metastatic breast cancer tissues. Nucleotide sequencing analyses indicate that at least four new CD44 variant isoforms (i.e., displaying unique splicing via the insertion or the deletion of exons 7, 10, 11, and 14) may be closely associated with human metastatic breast cancers. These newly described CD44 variant isoforms may be useful for monitoring the progression of human breast cancer metastasis.

Base Sequence↗
PubMed1995

Involvement of CD44 and its variant isoforms in membrane-cytoskeleton interaction, cell adhesion and tumor metastasis.

CD44s (standard form of CD44) is a transmembrane glycoprotein whose external domain displays extracellular matrix adhesion properties by binding both hyaluronic acid (HA) and collagen. The cytoplasmic domain of CD44s interacts with the cytoskeleton by binding directly to ankyrin. It has been shown that post-translational modifications, such as phosphorylation (by protein kinase C), acylation (by acyl-transferase) and GTP-binding enhanced CD44's interaction with cytoskeletal proteins. Most importantly, the interaction between CD44s and the cytoskeletal protein, ankyrin, is required for the modulation of CD44s cell surface expression and its adhesion function. Recently, a number of tumor cells and tissues have been shown to express CD44 variant (CD44v) isoforms. Using RT-PCR and DNA sequence analyses, we have found that unique CD44 splice variant isoforms are expressed in both prostate and breast cancer cell lines and carcinomas. Most importantly intracellular ankyrin is preferentially accumulated underneath the patched/capped structures of CD44 variant isoform in both breast and prostate cancer cells attached to HA-coated plates. We propose that selective expression of CD44v isoforms unique for certain metastatic carcinomas and their interaction with the cytoskeleton may play a pivotal role in regulating tumor cell behavior during tumor development and metastasis.

Animals↗
PubMed1995

Ear reconstruction with chondrocutaneous postauricular island flap.

Skin and cartilage defects from the conchal cavity to the external auditory canal were reconstructed with the use of a chondrocutaneous postauricular island flap. Although based on the experience of only one case, the authors believe that this island flap is extremely useful in the repair of skin and cartilage defects of the conchal cavity and the external auditory canal.

Adolescent↗
PubMed1995

Activation of protein kinase C by mycobacterial cord factor, trehalose 6-monomycolate, resulting in tumor necrosis factor-alpha release in mouse lung tissues.

Cord factors are mycoloyl glycolipids in cell walls of bacteria belonging to Actinomycetales, such as Mycobacterium, Nocardia and Rhodococcus. They induce granuloma formation in the lung and interstitial pneumonitis, associated with production of macrophage-derived cytokines. We studied how cord factors induce biological activities in the cells. Cord factors isolated from M. tuberculosis, trehalose 6-monomycolate (mTMM) and trehalose 6,6'-dimycolate (mTDM), enhanced protein kinase C (PKC) activation in the presence of phosphatidylserine (PtdSer), diacylglycerol and Ca2+, and mTMM activated PKC alpha more strongly than PKC beta or gamma under the same assay conditions. Kinetic studies of mTMM in response to PKC activation revealed that mTMM increased the apparent affinity of PKC to Ca2+ in the presence of both PtdSer and diolein. Although this is similar to observations with unsaturated fatty acids, such as arachidonic acid, mTMM was synergistic with PtdSer for PKC activation, but arachidonic acid was not. mTMM was also different as regards PKC activation, as phorbol ester was. A single i.p. administration of mTMM to mouse induced tumor necrosis factor-alpha (TNF-alpha) in serum and in the lung, which is a unique target tissue of cord factors. Based on our recent finding that TNF-alpha is an endogenous tumor promoter, the correlation between lung cancer and pulmonary tuberculosis is discussed.

Animals↗
PubMed1995

Different flow regulation mechanisms between celiac and mesenteric vascular beds in conscious rats.

The aims of this study were to elucidate the vasoconstrictor mechanism that mediates the changes in celiac and mesenteric vascular resistances during vasoconstriction and hypertension induced by ganglionic blockade and to explore the preferential mechanism that contributes to the elevation of arterial pressure in conscious spontaneously hypertensive rats (SHR). In conscious SHR and normotensive control rats, blood flow and arterial pressure were measured with an implanted electromagnetic flow probe and an indwelling arterial catheter. Peripheral vascular resistance was calculated as arterial pressure divided by regional flow. Celiac contribution to the hypertension in SHR was below average for the entire body and was smaller than that from the superior mesenteric bed. The increase of mesenteric resistance with arterial pressure elevation after ganglionic blockade suggests that mesenteric blood flow is regulated by a stretch-dependent myogenic mechanism, whereas celiac blood flow is regulated preferentially by the sympathetic neural mechanism. It is speculated that the flow superregulation in the mesenteric bed in SHR is due to the enhanced myogenic response and contributes to the early stage of hypertension.

Animals↗
PubMed1995

[The reliability and validity of a new self-completed questionnaire (QUIK)].

In order to evaluate the reliability and validity of a self-completed questionnaire (QUIK), devised to measured QOL, we examined the QUIK scores of elderly who visited the Kumamoto Health Administrative Center for a medical check-up in March 1994. The QUIK questionnaire, which is a close-ended and disease non-specific questionnaire, covered four domains such as physical functioning, emotional adjustment, interpersonal relationships, and attitudes toward life, interacting reciprocally. The mean and standard deviation on QUIK were much better in terms of total score (5.1 +/- 5.4), for each domain score in comparison with the patient group, and even in comparison with the non-patient group. The distribution of total scores on QUIK were as follows: excellent 15%, good 35%, fair 36%, poor 11%, very poor 2% and grossly impaired 0% according to a six-tiered rating scale. The internal consistency in terms of total score was alpha = 0.86. Very close correlation were seen among score, each domain score and satisfaction, being healthy and present state of feeling. If the cut-off points of total score were set between 9 and 10, the sensitivity were 0.65, specificity was 0.65 for the age index, sensitivity 1.00, validity 0.29 for the satisfaction index, while, sensitivity was 0.85 and validity 0.48, for the feeling index. There was a very close reciprocal correlation among the four domains, except for the relation between physical functioning and interpersonal relationship using multiple regression analysis. Further, significant correlations were obtained between the score in each domain and the score based on subtracting each domain score from the total score.

Aged↗
PubMed1994

Nodularin, a potent inhibitor of protein phosphatases 1 and 2A, is a new environmental carcinogen in male F344 rat liver.

Nodularin and microcystin-LR are cyanobacterial toxins and environmental hazards. Nodularin inhibits protein phosphatases 1 and 2A with the same potency as does microcystin-LR, which has recently been identified as a potent tumor promoter in rat liver. Our results suggested that nodularin is also a new tumor promoter in rat liver. A two-stage carcinogenesis experiment in rat liver initiated with diethylnitrosamine and without partial hepatectomy revealed that nodularin stimulated glutathione S-transferase placental form-positive foci in rat liver more effectively than did microcystin-LR, and that nodularin alone induced glutathione S-transferase placental form-positive foci as well as did diethylnitrosamine alone. Thus, nodularin itself is a new liver carcinogen, and microcystin-LR is a tumor promoter rather than a carcinogen. Nodularin induced hyperphosphorylation of cytokeratin peptides 8 and 18 in primary cultured rat hepatocytes 20% more effectively than did microcystin-LR, suggesting that nodularin penetrates more easily into the hepatocytes than does microcystin-LR. Nodularin up-regulated induction of c-jun, jun-B,jun-D,c-fos,fos-B, and fra-1 mRNA transcripts in rat liver after i.p. administration, and the accumulation of the mRNA transcripts was sustained for over 9 h after treatment. The environmental hazards of cyanobacterial toxins are discussed in relation to human primary liver cancer in Qidong county in the People's Republic of China. Our results support this hypothesis and indicate the need for prevention measures against cyanobacterial toxins.

Animals↗
PubMed1994

Mapping the fodrin binding domain in CD45, a leukocyte membrane-associated tyrosine phosphatase.

CD45 belongs to a family of high molecular mass leukocyte glycoproteins. It contains both an intrinsic protein tyrosine phosphatase (PTPase) activity and a cytoskeleton binding site in its cytoplasmic domain. Certain cytoskeletal proteins, such as fodrin (a spectrin-like molecule), are known to play an important role in the regulation of CD45's PTPase activity. In this study we mapped the fodrin binding domain of CD45 by deleting various portions of the cytoplasmic region, followed by the expression of these truncated cDNAs using an in vitro transcription/translation system. The results of these experiments indicate that the CD45 fodrin binding domain resides between amino acids 825 and 939. Construction of a fusion protein encoding the region between amino acids 825 and 939 shows that this particular sequence itself is sufficient for fodrin binding. Further analyses indicate that the sequence (930EENKKKNRN939S) in CD45 has good sequence homology with the spectrin binding domain found in the MSP1 glycoprotein of the malarial parasite. Biochemical studies, using binding competition assays, and a synthetic peptide containing the sequence 930EENKKKNRN939S, support the conclusion that the sequence between amino acids 930 and 939 is a critical part of CD45's fodrin binding domain. Further analyses indicate that this sequence is also involved in the fodrin-induced up-regulation of CD45 PTPase activity. Therefore, we suggest that fodrin binding to this domain is required for the onset of CD45-mediated signal transduction and leukocyte activation.

Amino Acid Sequence↗
PubMed1994

Identification of an IP3 receptor in endothelial cells.

In this study we have used saponin to permeabilize bovine endothelial cell membranes in order to directly test the involvement of IP3 in regulating internal Ca2+ release. Our results indicate that the release of internal Ca2+ occurs as early as 1-3 seconds after IP3 addition. This IP3-induced internal Ca2+ release can be inhibited by heparin (an IP3 receptor antagonist). Further binding of [3H]IP3 to saponin-permeabilized bovine endothelial cells reveals the presence of a single, high affinity class of IP3 receptor with a dissociation constant (Kd) of approximately 0.50 (+/- 0.03) nM. Using a panel of monoclonal and polyclonal antibodies against IP3 receptor, we have established that the bovine endothelial cell IP3 receptor (approximately 260 kDa) displays immunological cross-reactivity with the rat brain IP3 receptor. Immunofluorescence data indicates that the IP3 receptor is preferentially located at the perinuclear region of the cells. In addition, PCR analysis of first-strand cDNAs from both bovine endothelial cells and rat brain tissues reveals that the IP3 receptor transcript in bovine endothelial cells belongs to the short non-neuronal form and not the long neuronal form detected in rat brain tissue. These findings suggest that the IP3 receptor in endothelial cells is both structurally and functionally analogous to that reported in non-neuronal cell systems and probably plays an important role in agonist-induced endothelial cell activation.

Animals↗
PubMed1994

Against the re-definition of death.

The diagnosis of death by the use of brain death criteria is a familiar practice in modern Western medicine, especially in ICUs, where the function of the heart and lungs is artificially maintained. In other countries, notably Japan, brain death criteria are not accepted. In this article, which was presented in the Japanese Dept. at Monash University on April 11, 1993, Prof. Iida argues against the "brain-death" definition of death. His argument is based on the role of the immune system, and not just the nervous system, in keeping an organism functioning as an integrated individual. He concludes that those who are declared brain-dead in ICUs are not in fact dead.

Brain Death↗
PubMed1994

A new splice variant of the inositol-1,4,5-triphosphate (IP3) receptor.

In this study we have identified a new splice variant of the IP3 receptor (IP3R) transcript in a number of mouse cell lines (e.g. mouse T-lymphoma cells, mouse splenic lymphocytes and mouse NIH 3T3 fibroblast cell lines) using the reverse transcriptase-polymerase chain reaction. This variant IP3 receptor (designated as IP3RV-S2, approximately 453 bp) is larger than the non-neuronal form (402 bp) but smaller than the neuronal form (522 bp) of the IP3 receptors. Nucleotide sequencing data indicate that this new isoform (IP3RV-S2) contains a 51 nucleotide insertion within the non-neuronal form of IP3R at the S2 splice site. During mitogenic stimulation by Con A, the ratio between IP3R (non-neuronal form) and IP3RV-S2 (variant isoform) in mouse splenic T-lymphocytes increases approximately 1.5-fold. The change in relative amounts of these two IP3 receptor isoforms during mitogenic-stimulation suggests that T-lymphocytes may have different requirements for the IP3 isoforms in order to control intracellular calcium mobilization. The selective expression of these two IP3R isoforms (IP3RV-S2 and non-neuronal IP3R) may be critically important for the onset of signal transduction and cell activation.

Animals↗