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Biomedical subjects

N Niimi

Publications and source records attributed to N Niimi.

At least 37 records · Page 2Linked to original sources
PubMed1996

Development in lung function of the affected side after repair of congenital diaphragmatic hernia.

The widespread use of newly developed techniques including extracorporeal membrane oxygenation (ECMO) has led to the survival of a number of patients with congenital diaphragmatic hernia (CDH) and associated hypoplastic lung. However, it is not fully recognized whether the hypoplastic and small lung of the affected side has the ability to develop its function after repair of CDH. The authors studied the lung function of 32 patients with CDH in whom these new methods were used. Two parameters, lung volume and pulmonary perfusion amount, were used to evaluate lung function. The former (checked by computed tomography scan) was used to evaluate the size of lung; the latter (checked by perfusion scintigram) was used to assess vascular density. The patients were divided into two groups, based on values of alveolar-arterial difference in oxygen content (AaDo2) at the time of admission. In group A (AaDo2 < 500 mm Hg; 12 cases), whose respiratory distress was mild and could be managed with ventilator care alone, the mean lung volume value for the affected side was 86% of the contralateral lung value from the initial study, and reached 93% at the time of follow-up study. The perfusion amount also exceeded 80% of the contralateral lung value from the initial study. Thus, it is likely that group A's affected-side lung is not small and has developed at a rate similar to that of the contralateral lung. However, in group B patients (AaDo2 > 500 mm Hg; 20 cases), who had severe respiratory distress at the admission and were managed with new techniques including ECMO, both lung volume and perfusion amount of the affected side initially were low in all cases (ie, mean values were 61% and 53% of contralateral-lung values, respectively). At the time of follow-up, the lung volume had increased in most cases (mean value, 88% of the contralateral lung value), but the perfusion amount of the affected side had not increased in most cases. It remained low, or decreased to below the initial value; the mean was 53% of the contralateral lung value. The initial mean perfusion: volume ratio (87%) had decreased significantly (to 62%) by the time of follow-up. This tendency was exaggerated in the 11 ECMO cases. These data might indicate that in most group B cases, the lung of the affected side has little ability to develop arterial branches, or certainly will be delayed in comparison to the contralateral lung, and that enlargement of lung volume may depend on overexpansion or emphysematous change rather than cellular growth. The present data also suggest that, in group B cases, total lung function will depend on the contralateral lung for a relatively long time.

Child↗
PubMed1996

CD4 expression is important but not essential for infection with exogenous mouse mammary tumor virus.

We studied local events in the popliteal lymph nodes of CD4-deficient mice following foot pad injection with an MMTV strain which carries the gene for a V beta 14-specific superantigen. Injection of the V beta 14-specific MMTV induced vigorous expansion of V beta 14+ CD4+ T cells and B cells in their lymph nodes of CD4+/- heterozygous control mice. On the other hand, CD4-/- mice injected with the MMTV showed a proliferation of V beta 14+ T cells among the population of TCR alpha beta + CD4-CD8- T cells, although to a lesser extent. This phenomenon was not accompanied by vigorous B cell expansion. A PCR assay revelated that the MMTV definitely infected the lymph nodes cells of the CD4-/- mouse. However, the infectivity of the MMTV in CD4-/- mice was approximately 20 times lower than that in CD4+/- mice. These findings indicate that, in MMTV infection of CD4-deficient mice, the superantigen-reactive T cells among the population of TCR alpha beta +CD4-CD8- T cells substitute for the superantigen-reactive CD4- T cells of normal mice, and that the absence of CD4 molecules decreased the infectivity of MMTV because of insufficient expansion of the superantigen-reactive T cells.

Animals↗
PubMed1996

Dermal mast cell activation by autoantibodies against the high affinity IgE receptor in chronic urticaria.

Previous studies identified autoantibodies against the IgE high affinity receptor alpha-chain, Fc epsilon RI alpha, in sera of selected patients with severe chronic idiopathic urticaria. We have now determined the incidence of anti-Fc epsilon RI alpha autoantibodies in a group of 163 patients. Intradermal injection of autologous serum caused skin reactions indicative of mast cell degranulation in 98 (60%) patients. Based on histamine release from IgE-sensitized and nonsensitized basophil leukocytes of healthy donors, we detected anti-Fc epsilon RI alpha autoantibodies in sera from 38 (23%) urticaria patients and evidence for anti-IgE antibodies in a further nine patients. The sera that released histamine from basophils induced histamine release (4-34%, n = 12) from mast cells in incubated skin slices. Protein-G affinity chromatography of sera demonstrated that mast cell histamine release was IgG-mediated. Preincubation of sera or the IgG fraction with a recombinant alpha-chain of Fc epsilon RI inhibited histamine release from mast cells and basophils. Further studies with the mouse anti-human Fc epsilon RI alpha antibody 29C6 showed that mast cells and basophils were similarly sensitive to IgG-mediated direct cross-linking of Fc epsilon RI, with 0.01-1.0 micrograms/ml 29C6 evoking histamine release in each case. These studies demonstrate that circulating levels of anti-Fc epsilon RI alpha autoantibodies mediate histamine release from skin mast cells in vitro and, taken together with in vivo evidence of mast cell degranulation following intradermal injection of autologous serum, support the concept that anti-Fc epsilon RI alpha autoantibodies are relevant to the pathogenesis of severe chronic urticaria in about 25% of patients.

Adolescent↗
PubMed1995

Concomitant infection with exogenous mouse mammary tumor virus encoding I-E-dependent superantigen in I-E-negative mouse strain.

We found that milk from II TES mice contained two species of exogenous mouse mammary tumor viruses (MMTV). Sequence analysis of the open reading frame (ORF) in the MMTV 3' long terminal repeat indicated that the two MMTV, MMTV (II TES2) and MMTV (II TES14), encode superantigens specific for V beta 2+ T cells and V beta 14+ T cells, respectively. In an experiment of subcutaneous injection of II TES milk, both T cells bearing TCR V beta 2 and V beta 14 proliferated vigorously in the draining lymph node from BALB/c mice (H-2d I-E+), whereas only V beta 14+ T cells showed significant proliferation in C57BL/6 mouse (B6 H-2b I-E-) lymph nodes. These findings indicated that the superantigen encoded by MMTV (II TES2) required MHC class II I-E molecules exclusively for Ag presentation, but MMTV (II TES14) stimulated V beta 14+ T cells even in the absence of I-E molecules. Semiquantitative analysis of MMTV proviruses using PCR revealed that B6 mice were not infected with MMTV (II TES2) by injection of this MMTV alone. However, injection of II TES milk containing both MMTV (II TES14) and MMTV (II TES2) induced infection of B6 mice with MMTV (II TES2) besides MMTV (II TES14), in spite of no expansion of V beta 2+ T cells in this mouse strain. These results suggested that I-E-negative mice were concomitantly infected with MMTV (II TES2) with the help of I-E independent T cell activation mediated by MMTV (II TES14).

Amino Acid Sequence↗
PubMed1995

Antibodies against leukocyte function-associated antigen-1 and against intercellular adhesion molecule-1 together suppress the progression of experimental allergic encephalomyelitis.

We obtained the evidence that coadministration in vivo of mAbs against leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) suppressed the progression of experimental allergic encephalomyelitis (EAE) in rats. The suppressive effect in vivo of coadministration of the mAbs during the induction phase was not prominent, but the administration of these mAbs during the effector phase markedly suppressed the progression of clinical illness and prevented the infiltration of encephalitogenic cells into the central nervous system. However, administration of the mAb to LFA-1 alone or ICAM-1 alone did not show such suppressive effects. These findings suggest that LFA-1 and ICAM-1 are critically involved in the development of EAE and that the administration together of mAbs against adhesion molecules including LFA-1 and ICAM-1 might provide a new immunotherapeutic approach for the treatment of multiple sclerosis.

Animals↗
PubMed1995

A novel V beta 2-specific endogenous mouse mammary tumor virus which is capable of producing a milk-borne exogenous virus.

We have previously reported new Mtv loci, Mtv-48 and -51, in the Japanese laboratory mouse strains CS and NC. Here we show by backcross analysis that both Mtv-48 and -51 cosegregate with very slow deletion of T cells bearing V beta 2. The nucleotide sequences of the open reading frames in the 3' long terminal repeats of Mtv-48 and -51 were very similar to those of Mtv-DDO, mouse mammary tumor virus C4 [MMTV(C4)], and MMTV(BALB/cV), which encode V beta 2-specific superantigens. Furthermore, backcross female mice carrying Mtv-48 but not Mtv-51 were found to be able to produce milk-borne MMTV(CS), which can vigorously stimulate V beta 2-expressing T cells after local injection in vivo in an I-E-dependent manner. On the other hand, mice carrying Mtv-51 but not Mtv-48 could not produce such an MMTV in milk. The nucleotide sequences of MMTV(CS) open reading frame were completely matched with those of Mtv-48. These results indicate that the provirus Mtv-48 but not Mtv-51 is capable of producing a milk-borne virus of which the superantigen stimulates V beta 2-expressing T cells.

Amino Acid Sequence↗
PubMed1994

Delay in expression of a mammary tumor provirus is responsible for defective clonal deletion during postnatal period.

A gene-encoding ligand for deletion of T cells bearing TcRV beta 6 and V beta 8.1 cosegregates a new mammary tumor provirus locus, Mtv-50 in NC mice. The sequence of the open reading frame (ORF) in the 3' long terminal repeat (LTR) of Mtv-50 was strikingly similar to those of Mtv-7, Mtv-43 and exogenous mouse mammary tumor virus (SW) with properties of minor lymphocyte stimulating antigen 1a. Consistent with previous reports, clonal deletion of mature thymocytes bearing TcRV beta 6 was defective during the early postnatal period of mice carrying Mtv-50. Appreciable levels of mRNA corresponding to common Mtv ORF and Mtv-6 ORF were expressed in the neonatal thymus, while little, if any, mRNA corresponding to Mtv-50 ORF was detected in the thymus at the early postnatal stage. Delay in expression of Mtv-50 ORF during the postnatal period may be responsible for the failure of clonal deletion of V beta 6-T cells in the early postnatal life of mice carrying Mtv-50.

Amino Acid Sequence↗
PubMed1994

Intercellular adhesion molecule-1 and leukocyte function-associated antigen-1 are involved in protection mediated by CD3+TCR alpha beta- T cells at the early stage after infection with Listeria monocytogenes in rats.

To investigate the significance of intercellular adhesion molecule-1 (ICAM-1) and leukocyte function-associated antigen-1 (LFA-1) in host defense against infection with intracellular parasites, we examined the effects of in vivo pretreatment with mAbs to ICAM-1 (1A29) and LFA-1 alpha (WT-1) on the protection against infection with Listeria monocytogenes in Fisher F344/N rats. Expression of ICAM-1 and LFA-1 alpha molecules on T cells in spleen, liver and peritoneal cavity of rats was down-regulated after i.p. administration with daily doses of 300 micrograms of either 1A29 or WT-1 for 10 days. The survival rate of rats inoculated with viable Listeria was significantly reduced by in vivo pretreatment with 1A29 together with WT-1 for 10 days but not by in vivo pretreatment with control mAb. The numbers of bacteria in the spleen in rats pretreated with both 1A29 and WT-1 were significantly increased on day 3 and day 6 after infection with 1 x 10(7) of viable Listeria corresponding to 1/30 of LD50 to normal rats. Thus, the resistance against listerial infection was severely impaired by combinational pretreatment with mAbs in ICAM-1 and LFA-1 alpha. As shown in our previous report, the early appearance of CD3+TCR alpha beta- T cells, presumably TCR gamma delta T cells, was evident in the peritoneal cavity and liver of control rats at the early stage after listerial infection, while this was suppressed at this stage in rats pretreated with both 1A29 and WT1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Cefotiam-induced IgE-mediated occupational contact anaphylaxis of nurses; case reports, RAST analysis, and a review of the literature.

Cefotiam (CTM) is one of the most popular cephem antibiotics in Japan. Recently we experienced two cases of nurses with CTM-induced contact anaphylaxis. When they were preparing drip infusions of antibiotics or working around other nurses doing so, they suddenly fell into shock with other symptoms such as flushing, urticaria, abdominal distress, vomiting, dyspnoea and/or loss of consciousness. The symptoms never occurred after they avoided exposure to CTM. Passive cutaneous or open patch tests were positive for CTM. Histamine release was induced by CTM from washed leucocytes. RAST analysis using CTM-human serum albumin-coupled discs showed high % RAST count, suggesting that these reactions were mediated by IgE antibodies. A RAST inhibition test suggested that the methyl-thiotetrazole side-chain was the main antigenic determinant. Both patients had hand dermatitis that had appeared preceding the episodes of anaphylaxis. Although the dermatitis had been resistant to treatments, it also disappeared after they avoided exposure to CTM. It seemed likely that it was also induced or exacerbated by CTM and facilitated the penetration of CTM to cause anaphylaxis. The literature is also reviewed.

Adult↗
PubMed1993

Involvement of cytokines in N-methyl-N'-nitro-N-nitrosoguanidine-induced plasminogen activator activity in acute disseminated encephalomyelitis and multiple sclerosis lymphocytes.

In order to examine the plasminogen activator (PA) induction involved in the pathogenesis of acute disseminated encephalomyelitis (ADEM) and multiple sclerosis (MS), PA activity in peripheral blood lymphocytes derived from 5 ADEM and 3 MS patients was investigated. There was no PA induction in any ADEM, MS or control lymphocytes treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) alone. PA activity, however, in lymphocytes exposed to human interferon-gamma (HuIFN-gamma) prior to MNNG treatment was elevated during the active phase of ADEM and MS, whereas the PA induction disappeared in association with improvement of the neurologic symptoms. The PA activity was abolished by mixed treatment with HuIFN-gamma and anti-HuIFN-gamma antibody. No such PA induction by any HuIFN was observed in any normal controls or cases of other neurologic diseases. Among the cytokines tested other than HuIFN, tumor necrosis factor-alpha, in combination with MNNG, also induced PA activity in lymphocytes from ADEM and MS patients during the active phase. Thus, the PA induction observed in lymphocytes on combined treatment with MNNG and cytokines may be involved in the progression of neurologic disorders in these demyelinating diseases, and indicates the possibility of therapeutic strategies involving anticytokine usage.

Acute Disease↗
PubMed1992

The effect of histamine on cultured endothelial cells. A study of the mechanism of increased vascular permeability.

The role of endothelial cells in the histamine-induced vascular response was investigated using cultured endothelial cells obtained from human umbilical veins. A single population of histamine H1 receptors was detected in these cells by means of a [3H]mepyramine binding assay. Its Kd was 0.74 +/- 0.07 nM and Bmax was 41.4 +/- 8.68 fmol/mg protein. Actin filaments were distributed as dense bands at the margin of the cells and as sparse microfilament bundles traversing the center of the cells. Histamine caused a decrease in peripheral bands and an increase in longitudinal bands. The changes evoked by histamine were dose-dependent, related to the duration of incubation of the cells with histamine, and blocked by mepyramine, a histamine H1 receptor antagonist. The results suggest that the endothelial cells respond to histamine through the histamine H1 receptor. This may explain one of the mechanisms of histamine-induced vascular response including vascular permeability increase.

Actins↗
PubMed1978

Computational reconstruction of body surfact isopotential maps in myocardial infarction: comparison between nontransmural and transmural infarction.

The relationship between the lack of electromotive force in myocardial infarction and body surface potential distribution was investigated on maps reconstructed from a simulated heart model and transfer impedance vectors of human torso model. The heart model, a cluster of 3-mm cubic blocks, was stored in the memory of a computer. Transfer impedance vectors between 81 lead points on the human torso model and 392 positions covering ventricular areas in the torso were measure. Body surface potential values were calculated mathematically by summing up scalar products between the electromotive force of the heart model and the measured transfer impedance vectors. Thus, reconstructed maps changed in their patterns with the alternation in lacation and/or extent of infarcted region in the heart model. In particular, the appearance of the abnormal potential minimum, which projects the infarcted region in the heart model onto the torso surface, was characteristic in both transmural and subendocardial infarction. In addition, delayed activation in the intact layer of the epicardium overlying the infarcted region produced a potential maximum on the same place as the abnormal potential minimum appeared previously.

Action Potentials↗