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Biomedical subjects

H Nishimura

Publications and source records attributed to H Nishimura.

At least 127 records · Page 7Linked to original sources
PubMed2000

[Three-dimensional imaging of hepatic and intrahepatic portal veins with helical CT: determination of optimal volume of contrast medium by intravenous injection using MIP technique].

In this study, the optimal volume of contrast medium in the liver for three-dimensional (3D) imaging of the hepatic and portal veins by helical CT were determined by intravenous injection using the MIP technique. In the 48 cases examined, CT images of the liver were obtained following the administration of contrast medium (90, 120, or 150 ml and 1.0 <, < or = 1.5 ml; 1.5 <, < or = 2.0 ml; 2.0 <, < or = 2.5 ml or 2.5 <, < or = 3.0 ml/kg) for determination of the optimal volume. The mean body weight of the patients was 59 kg. Contrast medium (Iopamidol 300 mgl/ml) was injected at a rate of 3 ml/sec, and scanning was initiated 70 sec after the beginning of injection. Images were obtained throughout the entire liver using 5-mm collimation. MIP images were graded from poor to excellent based on their visualization of the hepatic vessels. Images produced with 120 ml of contrast medium presented excellent images of hepatic vessels, superior to those produced with 90 ml (hepatic vein: p < .001, portal vein: p < .001). Images produced with 2.0 <, < or = 2.5 ml/kg of contrast medium presented excellent images of the portal vein, superior to those produced with 1.5 <, < or = 2.0 ml/kg ml (p < 0.05). It is evident from the present data that a contrast medium volume of more than 120 ml or 2.0 <, < or = 2.5 ml/kg is sufficient for three-dimensional imaging of hepatic vessels. These images may be a useful diagnostic tool in patients with hepatic disease.

Contrast Media↗
PubMed2000

Polyethylene glycol-modified concanavalin A as an effective agent to stimulate anti-tumor cytotoxicity.

The jack bean lectin, concanavalin A (Con A), was modified with 2,4-bis[O-methoxypoly(ethylene glycol)]-6-chloro-s-triazine, activated PEG2, to form PEG-Con A. The immunoreactivity of PEG-Con A towards anti-Con A antibodies was reduced by increasing the degree of modification of amino groups in the Con A molecule. PEG-Con A had a complete reduction of the immunogenicity in mice and prolonged the clearance-time in blood. Although the mitogenic activity of Con A towards murine spleen cells was reduced by the conjugation with activated PEG2, the administration of PEG-Con A to mice enhanced the anti-tumor cytotoxicity of peripheral lymphocytes against melanoma B16 cells.

Animals↗
PubMed2000

[A case of far advanced breast cancer with distant metastases which had mostly disappeared after chemoendocrine therapy].

We report a case of far advanced breast cancer showing an excellent response to chemo-endocrine therapy. A 40-year-old female with a huge ulcerated tumor on her left anterior chest visited our hospital. Distant metastases were found in the lymph nodes, liver and bone. Therefore, endocrine therapy (toremifene and medroxyprogesterone acetate) and chemotherapy (cyclophosphamide, Therarubicin and 5-fluorouracil) were started as a combination treatment. As a result, the main tumor and metastatic lesion were remarkably reduced, and extended mastectomy with resection of right axillary lymph nodes was performed. Histologically, cancer cells in the primary lesion mostly disappeared, and only one lymph node in the left axillary lesion showed metastasis. No recurrence was found for 16 months after the surgical treatment. The combined therapy in the present case was extremely effective.

Adult↗
PubMed2000

[Two cases of pyogenic cervical discitis presenting tetraparesis].

The authors reported two cases of pyogenic cervical discitis presenting tetraparesis. Case 1: A 66-year-old male patient entered the hospital because of tetraparesis. Two weeks before the hospitalization, he had become feverish and awakened with motor weakness in all extremities. Magnetic Resonance Imaging (MRI) study revealed a lesion filling the anterior epidural space from C4 to C6 levels and posterior displacement of the spinal cord. Findings suggesting discitis of C5/6 and osteomyelitis of C5 and C6 were also obtained on MRI. These findings suggested that the tetraparesis was caused by cord compression by the epidural abscess as the acute stage of pyogenic spinal infection. On the day following admission, surgical removal of the epidural abscess and of the infected bodies was performed. Spinal fusion through C4 to C7 was also carried out with iliac bone graft. Antibiotic administration and Halo-vest application were performed after the operation. The postoperative course was good and the tetraparesis had completely disappeared within 12 months after the operation. Case 2: A 60-year-old male patient entered the hospital because of tetraparesis. Since 6 weeks before the hospitalization, he had become feverish and suffered from pain in the neck. He had also awakened with motor weakness of all extremities. The tetraparesis was progressive. Plain X-ray films of the cervical spine showed destructive change of C5 and C6 and kyphotic displacement. An epidural abscess of the cervical spine at the level of C4 to C6, discitis of C5/6 and osteomyelitis of C5 and C6 were diagnosed on MRI findings. The disarranged kyphotic vertebral bodies and the epidural abscess caused posterior displacement of the spinal cord. Based on these findings, it was concluded that the abscess and the kyphotic change of the bodies had been induced by spinal infection in the subacute stage. On the 8th hospital day, surgical removal of the anterior portion of the infected bodies as well as fusion of the vertebral column from C4 to C7 was performed. Iliac bone was used for the fusion graft. Postoperative administration of antibiotics and Halo-vest application for external fixation were carried out. On the 7th postoperative day, symptoms caused by radiculopathy of the left C5 appeared, but gradually ameliorated. The patient was free from motor weakness in the 8th month after the surgical treatment. Surgical intervention is a useful treatment for pyogenic cervical discitis with symptoms due to compression of the spinal cord both in the acute and subacute stages.

Acute Disease↗
PubMed2000

[A case of anterior mediastinal abscess with skin fistula resulting from descending necrotizing mediastinitis].

Descending necrotizing mediastinitis (DNM) is a serious, life-threatening infection. We present a case of anterior mediastinal abscess resulting from DNM. A 43-year-old woman, who had underwent cervical drainage for DNM 4 months ago, visited our hospital for cervical fistula. Chest CT revealed anterior mediastinal abscess. Mediastinal drainage through a subxiphoidal incision, debridement via the parasternal approach and resection of cervical fistula were performed without thoracotomy. A continuous mediastinal irrigation by acid water was performed postoperatively. The culture of the drain fluid became negative, and mediastinal abscess was disappeared. In conclusion, immediate and suitable drainage, debridement and postoperative-irrigation are important for DNM. On chronic stage, management to defend from extending infection is needed.

Abscess↗
PubMed2000

Induction of skin fibrosis in mice expressing a mutated fibrillin-1 gene.

BACKGROUND: Tight skin mice (TSK) bear a mutated Fibrillin-1 (Fbn-1) gene. Genetic studies show that the TSK mutation is closely associated with the Fbn-1 locus (0-0.7 cM). A previous study showed two recombinants between the Fbn-1 locus and the TSK mutation. TSK mutation and mutated Fbn-1 gene cosegregate in F1 mice. MATERIALS AND METHODS: To elucidate the role of the mutated Fbn-1 gene in occurrence of TSK syndrome, we generated transgenic (Tg) mice expressing mutated Fbn-1 gene. In another set of experiments, we injected normal mice after birth with a plasmid bearing mutated Fbn-1 gene (pdFbn-1). RESULTS: Our results demonstrate that the pdFbn-1 Tg mice developed permanent cutaneous hyperplasia that was permanent. In mice injected as newborns with a plasmid bearing the sense pdFbn-1 gene, cutaneous hyperplasia was transient. In contrast to TSK mice, neither Tg nor mice injected with plasmid developed lung emphysema. The pdFbn-1 Tg and TSK mice spontaneously produced anti-topoisomerase I and anti-Fbn- antibodies, as do humans afflicted by scleroderma; whereas, those injected with a plasmid containing the pdFbn-1 gene produced only anti-Fbn-1 autoantibodies. CONCLUSIONS: The results suggest that, although cutaneous hyperplasia is due to mutated Fbn-1 gene, the TSK syndrome may be multifactorial.

Animals↗
PubMed1999

Molecular cloning and expression of a mouse thiamin pyrophosphokinase cDNA.

Thiamin pyrophosphokinase (EC 2.7.6.2) catalyzes the pyrophosphorylation of thiamin with adenosine 5'-triphosphate to form thiamin pyrophosphate. A mouse thiamin pyrophosphokinase cDNA clone (mTPK1) was isolated using a combination of mouse expressed sequence tag database analysis, a two-step polymerase chain reaction procedure, and functional complementation screening with a Saccharomyces cerevisiae thiamin pyrophosphokinase-deficient mutant (thi80). The predicted protein contained 243 amino acid residues with a calculated molecular weight of 27,068. When the intact mTPK1 open reading frame was expressed as a glutathione S-transferase fusion protein in Escherichia coli lacking thiamin pyrophosphokinase, marked enzyme activity was detected in the bacterial cells. The corresponding 2.5-kilobase pair mRNA was expressed in a tissue-dependent manner and was found at relatively high levels in the kidney and liver, indicating that the mode of expression of mTPK1 genes differs with cell type. The expression of mTPK1 genes in cultured mouse neuroblastoma and normal liver cells was unaffected by the thiamin concentration in the medium (10 microM versus 3.0 nM). This is the first report on identification of the primary sequence for mammalian thiamin pyrophosphokinase.

Amino Acid Sequence↗
PubMed1999

Activation of T cells recognizing an epitope of heat-shock protein 70 can protect against rat adjuvant arthritis.

We have previously reported that CD4+ T cells recognizing a peptide comprising residues 234-252 of the heat shock protein (HSP)70 of Mycobacterium tuberculosis (M.tb) in the context of RT1.B MHC class II molecule emerged in the peritoneal cavity during the course of Listeria monocytogenes infection in rats and suppressed the inflammatory responses against listerial infection via IL-10 production. We report in this work that pretreatment with peptide 234-252 of HSP70 derived from M.tb suppressed the development of adjuvant arthritis (AA) in Lewis rats induced using heat-killed M.tb. T cells from rats pretreated with peptide 234-252 produced a significant amount of IL-10 in response to the epitope. T cells from rats pretreated with the peptide and immunized with M.tb produced the larger amount of IL-10 in response to the peptide, but only a marginal level of IFN-gamma in response to purified protein derivative of M.tb. Administration of anti-IL-10 Ab partly inhibited the suppressive effect of pretreatment with peptide 234-252 on the development of AA. Furthermore, transfer of a T cell line specific for the epitope at the time of AA induction markedly suppressed AA. These findings suggested that T cells recognizing peptide 234-252 may play a regulatory role in inflammation during AA via the production of suppressive cytokines including IL-10.

Amino Acid Sequence↗
PubMed1999

Regulatory role of peritoneal NK1.1+ alpha beta T cells in IL-12 production during Salmonella infection.

NK1.1+ alpha beta T cells emerge in the peritoneal cavity after an i.p. infection with Salmonella choleraesuis in mice. To elucidate the role of the NK1.1+ alpha beta T cells during murine salmonellosis, mice lacking NK1.1+ alpha beta T cells by disruption of TCR beta (TCR beta-/-), beta 2m (beta 2m-/-), or J alpha 281 (J alpha 281-/-) gene were i.p. inoculated with S. choleraesuis. The peritoneal exudate T cells in wild type (wt) mice on day 3 after infection produced IL-4 upon TCR alpha beta stimulation, whereas those in TCR beta-/-, beta 2m-/-, or J alpha 281-/- mice showed no IL-4 production upon the stimulation, indicating that NK1.1+ alpha beta T cells are the main source of IL-4 production at the early phase of Salmonella infection. Neutralization of endogenous IL-4 by administration of anti-IL-4 mAb to wt mice reduced the number of Salmonella accompanied by increased IL-12 production by macrophages after Salmonella infection. The IL-12 production by the peritoneal macrophages was significantly augmented in mice lacking NK1.1+ alpha beta T cells after Salmonella infection accompanied by increased serum IFN-gamma level. The aberrantly increased IL-12 production in infected TCR beta-/- or J alpha 281-/- mice was suppressed by adoptive transfer of T cells containing NK1.1+ alpha beta T cells but not by the transfer of T cells depleted of NK1.1+ alpha beta T cells or T cells from J alpha 281-/- mice. Taken together, it is suggested that NK1. 1+ alpha beta T cells eliciting IL-4 have a regulatory function in the IL-12 production by macrophages at the early phase of Salmonella infection.

Adoptive Transfer↗
PubMed1999

ATF-2-binding regulatory element is responsible for the Ly49A expression in murine T lymphoid line, EL-4.

To understand the mechanism of Ly49A-expression and its significance in T-cell differentiation, we analyzed the 5'-flanking region of the Ly49A gene in a search for the Ly49A-regulatory element. Since very few known regulatory elements have been found in this region, presumably a novel regulatory sequence(s) could exist. Accordingly, we defined the 13-bp regulatory element, 5'-ATGACGAGGAGGA-3', restricted to Ly49A-expression in EL-4 cells in comparison with two other representative cell lines tested. This element, designated as EL13, proved to be previously undiscovered by homology search and is highly homologous with several virus DNAs. Using EL13 as a probe we have cloned a cDNA encoding a binding protein to EL13. Its deduced nucleotide sequence revealed that EL13-binding protein is almost identical with rat ATF-2. Although ATF-2 is known to bind to cyclic AMP responsive element (CRE), EL13 shares five out of eight nucleotides with this consensus sequence. Our results suggested that ATF-2 may play an important role via binding to EL13 for the expression of Ly49A. These data will provide useful information for understanding T-cell and NK-cell differentiation in murine immune system.

Activating Transcription Factor 2↗
PubMed1999

MHC class II-dependent NK1.1+ gammadelta T cells are induced in mice by Salmonella infection.

We observed the emergence of a novel population of gammadelta T cells expressing NK1.1 Ag in the peritoneal cavity of mice infected with Salmonella choleraesuis. The NK1.1+gammadelta T cells accounted for approximately 20% of all gammadelta T cells emerging in the peritoneal cavity of C57BL/6 mice and expressed preferentially rearranged Vgamma4-Jgamma1 and Vdelta6.3-Ddelta1-Ddelta2-Jdelta1 genes with N diversity. The gammadelta T cells proliferated vigorously in response to PHA-treated spleen cells and produced IFN-gamma in the culture supernatant. However, spleen cells from Abetab-deficient mice were unable to stimulate the gammadelta T cells. Furthermore, the NK1.1+gammadelta T cells were stimulated not only by Chinese hamster ovary (CHO) cells expressing wild-type IAb but also by those expressing IAb/Ealpha52-68 or IAb/pigeon cytochrome c-derived analogue peptide complex. These proliferation activities were inhibited by mAb specific for IAb chain. Consistent with these findings, the emergence of NK1.1+gammadelta T cells was reduced in the peritoneal cavity of Abetab-deficient mice after Salmonella infection, whereas NK1.1+gammadelta T cells were rather abundant in the peritoneal cavity of Salmonella-infected beta2m-deficient mice. Moreover, the NK1.1+gammadelta T cells were easily identified in the thymus of beta2m-deficient but not Abetab-deficient mice. Our results indicated that MHC class II expression is essential for development and activation of NK1. 1+gammadelta T cells in the thymus and the periphery.

Animals↗
PubMed1999

Immunogene therapy of murine fibrosarcoma using IL-15 gene with high translation efficiency.

We have recently found that translational efficiency is up-regulated by an alternative exon in IL-15 mRNA in mice. In a malignancy model using BALB/c mice and syngeneic Meth A fibrosarcoma (Meth A), we successfully applied immunological gene therapy with IL-15 protein using alternative IL-15 cDNA with high translational efficiency. Two expression vectors carrying the murine IL-15 gene were constructed for use in tumor immunotherapy, one utilizing IL-15 cDNA with alternative exon 5 and the second utilizing IL-15 cDNA with normal exon 5. The first vector induced the production of a large amount of IL-15 protein in Meth A cells, whereas tumor cells transfected by the second vector produced only a marginal level of IL-15 protein. Although cell growth of both transfectants in vitro remained unchanged, inoculation of clones transfected with normal IL-15 cDNA resulted in progressive tumor growth, while clones transfected with alternative IL-15 cDNA led to the rejection of the tumor. The clone producing high levels of IL-15 grew progressively in nude mice and mice treated with anti-CD4 monoclonal antibodies (mAb), whereas the growth of the transfectants was retarded in anti-CD8 mAb- or anti-asialo GM1 antibody-treated mice. Cured mice were shown to have generated immunity against a subsequent challenge with the wild type of Meth A but not against Meth 1 tumor cells, another type of fibrosarcoma derived from BALB/c mice. Thus, tumor therapy based on IL-15 gene transfection was effective against Meth A tumor cells, suggesting a possible application to human neoplasms.

Animals↗
PubMed1999

The roles of intrahepatic Valpha14(+) NK1.1(+) T cells for liver injury induced by Salmonella infection in mice.

To investigate the roles of intrahepatic T cells in liver injury after Salmonella infection, we examined serum alanine transaminase (ALT), histopathology, and bacterial numbers in liver after infection with Salmonella choleraesuis strain 31N-1 in mice genetically lacking TCRalpha beta+, CD4(+), CD8(+), or NK1.1(+)T cells with C57BL/6 background. In control (+/+) mice, serum ALT reached a peak level by day 7 after an intraperitoneal inoculation of 2 x 10(6) CFU Salmonella choleraesuis 31N-1. In TCR-beta-/- mice, liver injury, as assessed by serum ALT level and histological examination, was significantly suppressed on day 7 after Salmonella infection but the numbers of bacteria in liver did not differ from those in normal mice, suggesting that alpha beta T cells are responsible for liver injury induced by Salmonella infection. To further determine which subsets in alpha beta T cells are important for the liver injury, we compared serum ALT level in mice genetically lacking CD4, CD8, beta2-microglobulin (beta2m, IAbeta, or Jalpha281 after Salmonella infection. In CD4(-/-) mice, serum ALT was significantly lower in comparison with control mice, but there was no difference in serum ALT levels in CD8(-/-) and IAbeta-/- mice from that in control mice. Notably, serum ALT levels and pathological lesions in liver were significantly decreased in beta2m-/- or Jalpha281(-/-) mice, which lacked in NK1.1(+) T cells bearing TCR Valpha14-Jalpha281 specific for beta2m-associated CD1d, following Salmonella infection. Taken together, it is suggested that alpha beta T cells bearing NK1.1 and CD4 may be main effector cells for liver injury after Salmonella infection.

Alanine Transaminase↗
PubMed1999

Prostaglandin E(1) protects against liver injury induced by Escherichia coli infection via a dominant Th2-like response of liver T cells in mice.

Prostaglandin E series (PGEs) are known to protect against lipopolysaccharide (LPS)-induced liver injury by down-regulating the production of inflammatory cytokines. We show here a novel mechanism whereby prostaglandin E(1) protects mice against liver injury after Escherichia coli infection. Prostaglandin E(1) administration suppressed circulating interleukin 12 (IL-12) levels but increased the IL-10 production after E. coli challenge. Furthermore, prostaglandin E(1)-alpha-cyclodextrin (PGE(1)) shifted the Th1/Th2 balance of CD3(intermediate) IL-2Rbeta(+) T cells in the liver to a dominant Th2-like response. Neutralization of endogenous IL-4 by administration of anti-IL-4 monoclonal antibody (mAb) diminished the inhibitory effect of prostaglandin E(1) on liver injury after E. coli challenge. These results suggested that the Th2-like response of liver T cells may be at least partly involved in the mechanism whereby prostaglandin E(1) protects against E. coli-induced liver injury.

Alprostadil↗
PubMed1999

Endogenous IL-15 might be responsible for early protection by natural killer cells against infection with an avirulent strain of Salmonella choleraesuis in mice.

Interleukin (IL)-15 is a novel cytokine with growth factor activity for T cells, B cells, and natural killer cells (NK cells). We investigated the role of IL-15 in the host defense against infection with avirulent Salmonella choleraesuis strain 31N-1 cured of 50-kb virulent plasmid. IL-15 was abundantly expressed at transcription and protein levels in macrophages infected with S. choleraesuis 31N-1. The number of NK cells in the infected sites was increased during the course of infection coincident with IL-15 production. Anti-IL-15 mAb administration inhibited the emergence of NK cells and interferon-gamma (IFN-gamma) production in serum after infection with S. choleraesuis 31N-1 and concurrently impaired the clearance of the bacteria. These results suggested that IL-15 might be responsible for protection against avirulent S. choleraesuis infection at early stage of infection through activation of NK cells in the infected sites.

Animals↗