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Biomedical subjects

J Iida

Publications and source records attributed to J Iida.

18 recordsLinked to original sources
PubMed1992

Stimulation of host-defense mechanism with synthetic adjuvants and recombinant cytokines against viral infection in mice.

The efficacy of synthetic immunoadjuvants and recombinant cytokines for the potentiation of host-resistance against virus infection was investigated using mouse models infected with Sendai virus and herpes simplex type 1 virus (HSV). The synthetic MDP derivative, MDP-Lys(L18), and recombinant cytokines, IL-1 beta, IFN-gamma, G-CSF and GM-CSF were shown to be effective for the stimulation of nonspecific protection against Sendai virus infection in mice. Both MDP-Lys(L18) and GM-CSF were effective for the protection against HSV infection in cyclophosphamide (CY)-treated mice. B30-MDP was suggested to be useful as an immunoadjuvant for the potentiation of antigenicity of recombinant or component vaccines.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1992

Coordinate role for cell surface chondroitin sulfate proteoglycan and alpha 4 beta 1 integrin in mediating melanoma cell adhesion to fibronectin.

Cellular recognition and adhesion to the extracellular matrix (ECM) has a complex molecular basis, involving both integrins and cell surface proteoglycans (PG). The current studies have used specific inhibitors of chondroitin sulfate proteoglycan (CSPG) synthesis along with anti-alpha 4 integrin subunit monoclonal antibodies to demonstrate that human melanoma cell adhesion to an A-chain derived, 33-kD carboxyl-terminal heparin binding fragment of human plasma fibronectin (FN) involves both cell surface CSPG and alpha 4 beta 1 integrin. A direct role for cell surface CSPG in mediating melanoma cell adhesion to this FN fragment was demonstrated by the identification of a cationic synthetic peptide, termed FN-C/H-III, within the fragment. FN-C/H-III is located close to the amino terminal end of the fragment, representing residues #1721-1736 of intact FN. FN-C/H-III binds CSPG directly, can inhibit CSPG binding to the fragment, and promotes melanoma cell adhesion by a CSPG-dependent, alpha 4 beta 1 integrin-independent mechanism. A scrambled version of FN-C/H-III does not inhibit CSPG binding or cell adhesion to the fragment or to FN-C/H-III, indicating that the primary sequence of FN-C/H-III is important for its biological properties. Previous studies have identified three other synthetic peptides from within this 33-kD FN fragment that promote cell adhesion by an arginyl-glycyl-aspartic acid (RGD) independent mechanism. Two of these synthetic peptides (FN-C/H-I and FN-C/H-II) bind heparin and promote cell adhesion, implicating cell surface PG in mediating cellular recognition of these two peptides. Additionally, a third synthetic peptide, CS1, is located in close proximity to FN-C/H-I and FN-C/H-II and it promotes cell adhesion by an alpha 4 beta 1 integrin-dependent mechanism. In contrast to FN-C/H-III, cellular recognition of these three peptides involved contributions from both CSPG and alpha 4 integrin subunits. Of particular importance are observations demonstrating that CS1-mediated melanoma cell adhesion could be inhibited by interfering with CSPG synthesis or expression. Since CS1 does not bind CSPG, the results suggest that CSPG may modify the function and/or activity of alpha 4 beta 1 integrin on the surface of human melanoma cells. Together, these results support a model in which the PG and integrin binding sites within the 33-kD fragment may act in concert to focus these two cell adhesion receptors into close proximity on the cell surface, thereby influencing initial cellular recognition events that contribute to melanoma cell adhesion on this fragment.

Amino Acid Sequence↗
PubMed1992

Bulimia nervosa in a pair of male monozygotic twins.

This is a report of a pair of male monozygotic twins meeting the DSM-III-R criteria for bulimia nervosa. At the age of 15, both brothers began to diet and suffered from bulimia. They were admitted to psychiatric hospitals and separated. After admission, their clinical course dramatically changed. The differences in their clinical courses and endocrinological data are suggestive as to the roles of environmental and hereditary factors in the etiology of bulimia nervosa.

Adolescent↗
PubMed1992

Changes in the microvasculature after mechanical pressure on the hamster cheek pouch.

The reaction of the microvasculature in the periodontal ligament to mechanical pressure is considered a very important phenomenon with respect to the biological background to orthodontic tooth movement. For clarification of the microvascular reaction to mechanical pressure, an experimental model that incorporated a hamster cheek pouch was established. This in vivo model solves some of the problems of other experimental models of the microvasculature of the periodontal ligament. Blood plasma permeation in this model was examined by means of a blue dye (pontamine sky blue), and histological observation was performed by light and transmission electron microscopy. Increased vascular permeability was observed within 30 min after removal of the mechanical stimulation. The threshold weight resulting in dye leakage was between 1 and 5 g applied for 60 min. From the histological observations, some large gaps between the endothelial cells in venules were found, while most basement membranes remained undisturbed. These observations suggest that the plasma leakage was due to mild traumatic injury to the endothelial cells. Both leukocytes and platelets were observed in the gaps between the endothelial cells in the venule. These types of microvascular reactions to mechanical pressure could initiate tissue changes in the periodontal ligament during orthodontic tooth movement.

Animals↗
PubMed1991

Tumor cell adhesive mechanisms and their relationship to metastasis.

Despite recent advances in the diagnosis and therapy of many forms of cancer, metastasis remains the major cause of death in cancer patients. As tumors progress they become increasingly heterogeneous, giving rise to aggressive subpopulations of tumor cells that subsequently invade local tissues, the lymphatics, and the circulatory system. This invasive behavior can ultimately lead to the widespread dissemination and metastasis of the primary tumor. In hematogenous metastasis, emboli consisting of tumor cells, host cells, platelets, and fibrin are transported to distant sites where they arrest in the microvasculature prior to extravasation. It is well accepted that tumor cell adhesion plays a fundamental role in many of the stages of the metastatic process. Tumor cell interactions with extracellular matrix components of tissue, tissue boundaries (basement membranes), or cell adhesion-promoting components of plasma; influence tumor cell motility, invasiveness, and many other important aspects of the metastatic tumor cell phenotype. Tumor cell adhesion also has a rate-limiting influence at various stages within the metastatic process, such as tumor cell arrest and extravasation. In addition, the ability of the immune system to recognize and successfully eradicated tumors is also highly dependent on the adhesion of activated lymphocytes to target tumor cells. Despite the rapid accumulation of information on the molecular basis of cell adhesion, our understanding of the relationship between tumor cell adhesion and hematogenous metastasis per se is fragmented and incomplete. Nevertheless, clear progress has been made, both in understanding the molecular basis of tumor cell adhesion and its relationship to the biology of tumor metastasis. New and exciting directions have been identified that are likely to yield direct benefits in developing new therapeutic or diagnostic approaches for malignant neoplasms. Our purpose is to briefly review the molecular basis of tumor cell adhesion from the standpoint of many of the receptors involved as well as their putative ligands. The relationship between specific tumor cell adhesion events and the formation of metastatic lesions is also addressed.

Animals↗
PubMed1990

Prophylactic activity of dihydroheptaprenol, a synthetic polyprenol derivative, against Sendai virus infection in mice.

The effect of a chemically synthesized polyprenol derivative, dihydroheptaprenol (DHP), on the non-specific resistance of mice to Sendai virus infection was investigated. The mice that received 200 micrograms of DHP intranasally twice, at 3 days and 1 day before the infection, showed a significant protection against Sendai virus infection. Treatment of mice twice even with as much as 2000 micrograms of DHP through the subcutaneous route, however, had no protective effect against infection. Excess interferon and tumour necrosis factor production in intranasally DHP-treated mice was seen 1 day after the infection when compared with Sendai virus alone controls or with DHP alone controls. Variance analysis of these findings indicates a prophylactic activity of DHP in pulmonary viral infections.

Administration, Intranasal↗
PubMed1990

Tracheostomy--the horizontal tracheal incision.

The complication rate after emergency tracheostomy is two to five times greater than after elective procedures. One of the main causes of the high risk of complications in emergency tracheostomy appears to be the amount of time required to open the trachea. Therefore, simple and fast procedures are mandatory. We have developed a new procedure as follows: A horizontal skin incision is performed. Strap muscles are dissected and retracted laterally. A transverse cut between tracheal rings below the thyroid isthmus is performed up to membranous portion of the trachea. The cut ends of the trachea remain open naturally because of the elasticity of the trachea. Skin and tracheal cut-ends are then joined by interrupted sutures. We have used this procedure during the past three years and have not experienced any major complications. This demonstrates the clear advantage and the more physiological nature of the procedure over various other incisions of the tracheal wall.

Adult↗
PubMed1989

Induction of an endogenous tumor necrosis factor in mice by murine recombinant interferon-gamma combined with a lipid A subunit analog (GLA-60) of low toxicity.

We have investigated the endogenous production of a serum cytotoxic factor when recombinant interferon-gamma (rIFN-gamma) is combined with synthetic lipid A subunit analogs of low toxicity (GLA compounds). The cytotoxic activity of the serum was measured by the crystal violet staining method with L929 cells as a target. Intravenous administration of rIFN-gamma followed by intravenous administration of lipopolysaccharide induced the endogenous production of a cytotoxic factor in the serum. The priming effect of rIFN-gamma appeared immediately and persisted for approximately 20 h after the injection. Administration of lipopolysaccharide as a trigger enhanced the production of the cytotoxic factor in the serum maximally 2 h after the injection. The cytotoxic activity in the serum was completely inhibited by anti-(mouse tumor necrosis factor) (TNF) antibody. A synthetic lipid A subunit analog (GLA-60), which is much less toxic in its endotoxin activities than lipopolysaccharide or synthetic lipid A (compound 506), induced the endogenous production of serum TNF in rIFN-gamma-primed mice. GLA-60 entrapped within liposomes induced the production of serum TNF in rIFN-gamma-primed mice more effectively than GLA-60 solubilized in phosphate-buffered saline. Intravenous or intranasal administrations of rIFN-gamma followed by intranasal administration of GLA-60 produced TNF in the lung washing fluid but not in the serum, indicating that TNF production can be induced locally rather than systemically by the alteration of the administration route of the primer and trigger. These results indicate that GLA-60, a lipid A subunit analog of low toxicity, is a beneficial triggering agent in the production of endogenous TNF, as well as having other immunopharmacological properties, and may provide a basis for cancer (metastases) treatment as a result of its ability to induce endogenous TNF.

Animals↗
PubMed1989

Biological activities of synthetic polypeptides containing a repetitive core sequence (Arg-Gly-Asp) of cell adhesion molecules.

A unique polypeptide containing the repeated structure of core sequence from cell adhesion molecules, poly(Arg-Gly-Asp), was successfully prepared by the polymerization procedure with diphenylphosphoryl azide. This polypeptide dramatically inhibited the aggregation of platelets induced by adenosine diphosphate (ADP) or malignant melanoma cells.

Adenosine Diphosphate↗
PubMed1989

Inhibition of tumour cell adhesion by anti-metastatic polypeptide containing a repetitive Arg-Gly-Asp sequence.

Anti-cell adhesive activity was examined by the synthetic polypeptide, containing repetitive Arg-Gly-Asp sequence of cell attachment site from fibronectin, poly (Arg-Gly-Asp). The attachment of tumour cells to fibronectin substrate was specifically inhibited by adding poly (Arg-Gly-Asp) in cell surface receptor-mediated and divalent cation-dependent manners, but not by unrelated peptides. In our previous study, the lung metastatic formation of tumour cells was dramatically reduced by intravenous co-injection of anti-cell adhesive poly (Arg-Gly-Asp) with B16-BL6 melanoma cells. These findings suggest that polypeptide-mediated inhibition of pulmonary metastasis is partly due to interference with tumour cell adhesion to the substrates including fibronectin in target organs or tissues.

Amino Acid Sequence↗
PubMed1989

Macrophage activation and host augmentation against Sendai or herpes simplex virus (HSV) infections with synthetic polypeptides in mice.

Poly-L-Lys (mean mol. wt; 12,000), poly-L-Arg (5000) and poly-L-Orn were found to activate peritoneal macrophages effectively in vivo in 14 synthetic homo polypeptides. The ability of sequential poly(L-Arg-L-X) (5000) to activate macrophages was less than that of poly-L-Arg. Neither (L-Arg)12 nor (L-Arg)6 by themselves activated macrophages, but poly-D-Arg (5000) did, as also did poly-L-Arg; this suggests that the polycationic character of poly-L-Arg plays a role in the activation of macrophages. The intranasal administration of poly-L-Lys, -L-Arg, -L-Orn, -D-Arg, all of which activated macrophages, augmented host resistance against Sendai virus infection in mice. The protection afforded by poly-L-Arg seemed to depend on its mol. wt: the order of protection was poly-L-Arg greater than (L-Arg)12 greater than (L-Arg)6. The intranasal administration of poly-L-Arg 3 days before the infection was effective, while that 1 day before infection was not. There was no difference between the groups in the titer of interferon produced by the infection of Sendai virus given with poly-L-Arg either 3 days before or 1 day before the infection. The administration of poly-L-Arg 3 days before the infection caused a significant decrease of the virus titer in the lung 6 days after the infection when compared with the control or the mice given 1 day before. The intravenous administration of 2-chloroadenosine (2-Cl-Ade), which is a selective inhibitor of macrophages, into the mice which had received poly-L-Arg intranasally 3 days before the infection caused a significant decrease in the survival rate of the mice, indicating that the macrophages activated with poly-L-Arg are likely to be an important element in affording the protection. Subcutaneous administration of poly-L-Arg revealed protective activity against systematic infection with herpes virus-type 1.

2-Chloroadenosine↗
PubMed1989

Effect of N alpha-acetylmuramyl-L-alanyl-D-isoglutaminyl-N epsilon-stearoyl- L-lysine on resistance to herpes simplex virus type-1 infection in cyclophosphamide-treated mice.

The restoration of resistance by N alpha-acetylmuramyl-L-alanyl-D-isoglutaminyl-N epsilon-stearoyl-L-lysine [MDP-Lys(L18)] on herpes simplex virus (HSV) type-1 infection was examined in cyclophosphamide (CY)-treated mice. MDP-Lys(L18) was shown to restore the resistance to HSV infection in CY-treated mice when it was injected either subcutaneously, intravenously, or intraperitoneally before infection. Treatment with MDP-Lys(L18) in CY-treated mice restored impaired activity for inhibiting HSV growth in the liver.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1989

Prophylactic activity against Sendai virus infection and macrophage activation with lipophilic derivatives of N-acetylglucosaminylmuramyl tri- or tetrapeptides.

The efficacy of N-acetylglucosaminyl-beta (1----4)-N-acetylmuramyl tri- or tetrapeptides (GM) and the lipophilic derivatives for host augmentation against Sendai virus infection and for macrophage activation in vitro was examined. The anti-infectious activities of GM derivatives were shown to increase with the chain length of the fatty acid combined with the diaminopimelyl group. When the macrophages were activated with 1 U ml-1 murine interferon gamma (IFN-gamma) and 0.001 microgram ml-1 GM derivatives, the cytocidal ability of macrophages depended on the length of the side chain, and exhibited a positive relationship with the anti-infectious activity of GM derivatives against Sendai virus infection. These results indicated that the increment of lipophilicity of GM derivatives would play an important role in the anti-infectious activity and macrophage activation in vitro.

Adjuvants, Immunologic↗
PubMed1989

Protective activity of recombinant cytokines against Sendai virus and herpes simplex virus (HSV) infections in mice.

The efficacy of recombinant cytokines such as murine interferon-gamma (IFN-gamma), human granulocyte colony-stimulating factor (G-CSF), mouse granulocytic-macrophage colony-stimulating factor (GM-CSF) and human interleukin-1 beta (IL-1 beta) has been examined for augmentation of host resistance against Sendai virus and herpes simplex virus (HSV) infections. All four cytokines were found to protect mice against Sendai virus infection. IFN-gamma afforded protection when administered intranasally but not intravenously several days before the infection. Intranasal administration of G-CSF one day before the infection was the most effective administration route and timing. Intranasal administration of GM-CSF was found to afford protection 1 or 3 days before the infection. IL-1 beta demonstrated therapeutic activity against Sendai virus infection after intranasal administration on the same day as the infection. When each of the cytokines was administered subcutaneously four times daily into cyclophosphamide-treated mice before intravenous infection with HSV, only GM-CSF revealed any protective activity.

Administration, Intranasal↗
PubMed1987

Suppression of Sendai virus growth by treatment with N alpha-acetylmuramyl-L-alanyl-D-isoglutaminyl-N epsilon-stearoyl-L-lysine in mice.

Mice that received N alpha-acetylmuramyl-L-alanyl-D-isoglutaminyl-N epsilon-stearoyl-L-lysine [MDP-Lys (L18)] were resistant to Sendai virus infection. In these protected mice, a significant growth inhibition of the virus was confirmed repeatedly at 10(0.2) to 10(0.4) of haemadsorbing units at an early non-specific phase but not at a late virus-eliminating phase of the infection. Virus growth was enhanced by treatment with silica but not by treatment with anti-asialo GM1 serum in MDP-Lys (L18)-treated mice. Peritoneal adherent cells activated by MDP-Lys(L18) showed an enhanced uptake and ability to inactivate Sendai virus in vitro. Excess interferon production in MDP-Lys (L18)-treated mice was seen on day 1 but not on days 2 to 7 of the infection. The possible role of macrophages and interferon in providing non-specific protection against Sendai virus in the MDP-Lys (L18)-treated mice is discussed.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1985

Effect of muramyl dipeptide and its stearoyl derivatives on resistance to Sendai virus infection in mice.

The efficacy of N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP), 6-O-stearoyl-MDP (L18-MDP), N alpha-acetylmuramyl-L-alanyl-D-isoglutaminyl-N epsilon-stearoyl-L-lysine (MDP-Lys-L18) and N-stearoylmuramyl-L-alanyl-D-isoglutamine (2N-L18-MDP) for augmenting host-resistance to viral infection was examined in Sendai virus infected mice. L18-MDP and MDP-Lys-L18 augmented the non-specific host-resistance to infection with Sendai virus. MDP showed a slight enhancement of host-resistance to this infection but 2N-L18-MDP was ineffective. The protective effect of MDP-Lys-L18 was seen only when the drug was administered a few days before the virus challenge. The intranasal administration of MDP-Lys-L18 was effective at 1 microgram but only slight activity was observed in mice treated intravenously or intraperitoneally even at the 100 microgram dose level. MDP-Lys-L18 treatment preceding infection augmented interferon production in the lung of the mice but MDP-Lys-L18 treatment alone induced no interferon.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1979

[Decrease of ACh response in isolated duodenum from SART stressed (repeated cold stressed) mice (author's transl)].

ACh response in the isolated duodenum from SART stressed (repeated cold stressed) mice was remarkably decreased in comparison to normal mice 5 days after onset of loading SART stress, and maximal contraction in SART stress mice duodenum was about 37% of that in non-stressed mice. Pilocarpine and KCl responses were also considerably decreased, but BaCl2 response was much the same as in the controls. Thus, the contraction system of the muscle is apparently not damaged by SART stress. Though body weights decreased, the daily intake of food incressed in SART stressed mice. Length of small intestine from SART stressed mice was much the same as in controls, but wet weights of small intestines were larger than in controls. Autonomic agonists, antagonists, tranquilizers and other drugs were given intraperitoneally to mice once daily during SART stress, and the ACh responses in the isolated duodenum were investigated. Pretreatment with adrenergic and anticholinergic drugs inhibited the decrease of ACh response, but antiadrenergic and cholinergic drugs had no effects. Pretreatment with tranquilizers such as reserpine, chlorpromazine, carpipramine and imipramine inhibited the decrease of ACh response in the isolated duodenum, but diazepam, meprobamate and benadryl had no influence. Pretreatment of neurotropin, a neurosedative had good inhibitory effects. Our results suggest that SART stressed mice may be in a state of unbalance regarding sympathetic and parasympathetic nerves, particularly with regard to abnormal tension in the parasympathetic nervous system, in part of duodenum. Pretreatment with most of the above drugs had no influence on loss of body weight in SART stressed mice while pretreatment with neurotropin inhibited body weight to a considerable extent.

Acetylcholine↗