Biomedical subjects

M Nose

Publications and source records attributed to M Nose.

At least 109 records · Page 6Linked to original sources

PubMed1995

High-energy underwater shock wave treatment for internal iliac muscle metastasis of prostatic cancer: a first clinical trial.

The first clinical trial of high-energy shock wave (SW) combined with chemotherapy to treat metastasis of prostate cancer in the internal iliac muscle was conducted. The patient, a 57-year-old man, diagnosed as having mucin-producing, poorly differentiated adenocarcinoma of the prostate invading the bladder wall, had been treated by total cystoprostatectomy. Five months later, metastatic tumors were found in the left axillar subcutaneous tissue and the right internal iliac muscles. For the axillar metastasis we performed radiation and left subclavicular arterial infusion of cisplatin 70 mg, THP-adriamycin (THP) 50 mg and methotrexate 50 mg. For the right internal muscular metastasis, 10,000 to 20,000 shots of SW and simultaneous intravenous injection of carboplatin 100 mg and THP 10 mg were carried out. Neither of the tumors decreased in size, but on magnetic resonance images, the SW-treated tumor exhibited a central low-intensity area. The SW-treated tumor was resected and central necrosis and a collection of mucin in the central area were observed. Hormone-resistant prostate cancer is well-known to be a multidrug-resistant tumor. It is noteworthy that SW and chemotherapy induced necrosis in such a refractory cancer without any significant side effects.

Adenocarcinoma↗

PubMed1995

Sequence analysis of the germ-line VH gene corresponding to a nephritogenic antibody in MRL/lpr lupus mice.

In order to investigate the genetic origin of nephritogenic antibodies in MRL/Mp-lpr/lpr (MRL/lpr) lupus mice, we isolated the germ-line heavy chain variable region (VH) gene corresponding to the nephritogenic antibody, B1, derived from an unmanipulated MRL/lpr mouse. Injection of this antibody into C.B-17/Icr-scid/scid mice resulted in the generation of wire loop-like glomerular lesions resembling those of lupus nephritis. Nucleotide sequences of this germ-line VH gene showed no replacement mutation in the VH region of the B1 antibody. Furthermore, this gene was identical to that found in the C3H/HeJ-lpr/lpr strain of mice. Our results suggest that germ-line VH genes can encode nephritogenic antibodies without somatic mutation, even in a mouse strain not prone to lupus.

Animals↗

PubMed1995

[An autopsy case of segmental mediolytic arteritis (SMA) accompanied with microscopic polyarteritis nodosa].

Segmental Mediolytic Arteritis (SMA) is a very rare arterial lesion which is limited in adults to the involvement of the intra-abdominal muscular arteries. The pathology is characterized by segmental disruption of the arterial media which leads segmental mediolysis, with subsequent dissecting aneurysm or rupture. A 73-year-old man was admitted to a hospital because of high fever, general fatigue and weight loss. These symptoms were resistant to antibiotic therapy, and soon after, renal insufficiency developed. Three months after the onset of symptoms, he died suddenly of hemorrhagic shock. Autopsy revealed rupture of the splenic artery and systemic necrotizing arteritis in the small-sized arteries of liver, pancreas and kidneys, as well as in the connective tissues around the adrenal glands. Histopathology of the splenic artery was consistent with SMA, and that of the systemic vascular lesions, with microscopic polyarteritis nodosa. Focal glomerular lesions characteristic of crescentic and/or granulomatous glomerulonephritis were present. A developmental mechanism for SMA is discussed with respect to this case together with a review of previous reports of this disease.

Adult↗

PubMed1994

In vitro effects of OK-432 on irradiated mouse bone marrow cells.

PURPOSE: In vitro effects of OK-432 on irradiated mouse bone marrow cells are examined. METHODS AND MATERIALS: Bone marrow cells of BDF1 mouse (1 x 10(6) cells/ml) were incubated with alpha medium, 2% fetal calf serum and OK-432 in a CO2 incubator at 37 degrees C for 24, 48 and 72 h, respectively. After centrifugation, each supernatant was collected and used for conditioned medium in CFU-GM assay: Changes in CFU-GM as a function of incubation time and OK-432 dose was examined; changes of CFU-GM according to various doses of OK-432 were examined in two mouse strains, BDF1 and BALB/c mouse; changes in protective effect of OK-432 in terms of CFU-GM as a function of administration timing of OK-432 in relation to irradiation. As a radiation source, 137Cs at a dose rate of 500 cGy/min was used. RESULTS: The CFU-GM decreased with the incubation time when OK-432 was not administered, while it significantly increased with incubation time when OK-432 was added at 0.5 and 1.0 KE/ml at 48-72 h of incubation. The former showed marked increase at 48-72 h of incubation. CFU-GM of BDF1 mouse was always higher than that of BALB/c mouse for any dose of OK-432. CFU-GM per femur according to the timing of administration of OK-432 from 24 h before to 24 h after irradiation showed 10299 +/- 2300 (24 h before), 10783 +/- 2463 (3 h before), 10045 +/- 1501 (immediately after), 8504 +/- 1188 (3 h after), 4898 +/- 1212 (6 h after), 1214 +/- 736 (12 h after) and 181 +/- 113 (24 h after irradiation), respectively. CONCLUSION: OK-432 stimulates cultured mouse bone marrow cells to produce GM-CSF in vitro by direct contact action. This direct stimulating action of OK-432 on GM-CSF production of bone marrow cells can be kept from 24 h before to at least 3 h after irradiation.

Animals↗

PubMed1994

A comparison of the antihepatotoxic activity between glycyrrhizin and glycyrrhetinic acid.

A comparison of antihepatotoxic activities between glycyrrhizin (18 beta-GL) and its genuine aglycone, glycyrrhetinic acid (18 beta-GA), was carried out using in vivo and in vitro assay methods. The oral administration of 18 beta-GA at 1, 24, and 48 h before D-galactosamine (GalN) treatment significantly reduced the increase of serum transaminase activities 24 h after GalN treatment, whereas 18 beta-GL did not inhibit the increase of serum transaminase activities. The intraperitoneal administration of 18 beta-GA 1 h before GalN treatment restored the increase of serum transaminase activities with lower doses than 18 beta-GL. In CCl4-induced cytotoxicity of primary cultured rat hepatocytes, 18 beta-GA protected the CCl4-induced leakage of transaminase at doses of 5 to 50 micrograms/ml, whereas 18 beta-GL inhibited slightly the leakage at a dose of 1000 micrograms/ml. In the same way, 18 alpha-GA, the alpha-isomer of 18 beta-GA, reduced the CCl4-induced cytotoxicity more strongly than 18 alpha-GL. Furthermore, the adsorbability of 18 alpha, beta-GA on primary cultured rat hepatocytes was higher than that of 18 alpha, beta-GL. These results suggest that 18 alpha, beta-GA is a more potent antihepatotoxic agent than 18 alpha, beta-GL, and that the potency of the antihepatotoxic compounds parallels their adsorbability in hepatocytes.

Animals↗

PubMed1994

Expression of mRNA for matrix gamma-carboxyglutamic acid protein during progression of atherosclerosis in aortae of Watanabe heritable hyperlipidemic rabbits.

In an effort to characterize mRNAs that are highly expressed during atherosclerosis, we employed differential hybridization screening of a cDNA library constructed from total RNA derived from the aorta of Watanabe heritable hyperlipidemic (WHHL) rabbits. Characterizing the cDNAs for mRNAs that are present in large amounts in WHHL rabbit aortae, we identified a positive clone encoding matrix gamma-carboxyglutamic acid protein (MGP). The primary structure of rabbit MGP was deduced from nucleotide sequence analysis of the cDNA. Northern blot analysis of total RNA prepared from aortae of WHHL and normal rabbits of various ages indicated that the expression of MGP mRNA increased in proportion to the progression of atherosclerosis in WHHL rabbits. Analysis of MGP mRNA by in situ hybridization revealed that a significant amount of MGP mRNA is accumulated in atherosclerotic lesions of WHHL rabbits, suggesting that the expression of MGP mRNA is correlated with the progression of atherosclerosis.

Amino Acid Sequence↗

PubMed1994

Immunopathological features of palatine tonsil characteristic of IgA nephropathy: IgA1 localization in follicular dendritic cells.

IgA nephropathy (IgAN) is generally thought to be mediated by the glomerular deposition of circulating immune complexes containing IgA as the major antibody component. Upper respiratory infections and tonsillitis often precede IgAN, and in some cases tonsillectomy is effective for the treatment of IgAN. Thus, the tonsil seems to be a unique organ causing initial and/or progressive events to generate nephritogenic immune complexes in IgAN. In this study we focused on the analysis of immunopathological features of the palatine tonsil characteristic of IgAN patients by using an immunohistochemical technique. The IgA1 subclass was demonstrated in follicular dendritic cells (FDC) of the tonsil of IgAN patients, but not in FDC of non-IgAN controls. On the other hand, IgA2, IgG, IgM and C3 did not show any differences in distribution between the two groups. Moreover, the expression of decay-accelerating factor (DAF), an inhibitor of homologous complement activation, and transforming growth factor-beta 1 (TGF-beta 1), an inducer of antibody-producing cells to IgA class switching, in FDC and interdigitating dendritic cells of the tonsil, respectively, which was also clarified in this study for the first time, was found to be identically distributed in the two groups. These findings may support the idea that IgA1, possibly in an immune complex form, is trapped by FDC and plays an important role in the persistent activation of particular B cell repertoires responsible for the onset and/or progression of IgAN.

Adolescent↗

PubMed1994

Immune complex-degradation ability of macrophages in MRL/Mp-lpr/lpr lupus mice and its regulation by cytokines.

Impaired clearance of circulating and/or deposited immune complexes (IC) by the mononuclear phagocytic system is one of the major factors in the pathogenesis of IC diseases. MRL/Mp-lpr/lpr (MRL/lpr) lupus mice spontaneously develop a lethal glomerulonephritis associated with IC deposition. The ability of macrophages to degrade phagocytozed IC and regulation of this degradation in MRL/lpr mice were examined. In 4-month-old MRL/lpr mice, macrophages accumulated in the affected glomeruli and these macrophages contained many phagosomes containing electron-dense bodies. When culture supernatant of human T cell line HUT102 was administered intraperitoneally into disease-bearing MRL/lpr mice, degradation of these electron-dense bodies in the macrophages in glomeruli was noted. We developed a quantitative in vitro assay for IC degradation activity of MRL/lpr resident peritoneal macrophages (RPM) using peroxidase-labelled IC derived from MRL/lpr mouse sera. The ability of the RPM to degrade IC was remarkably enhanced by the pretreatment with HUT102 cell products and the related human recombinant cytokines, lymphotoxin and IL-1 alpha. Moreover, pretreatment of RPM from non-diseased MRL/Mp-+/+ mice with the culture supernatant of spleen cells from diseased MRL/lpr mice reduced their IC degradation activity. These results suggested that the ability of macrophages to degrade IC in MRL/Mp strains of mice is under the regulation of cytokines, and the impaired ability in the disease-bearing mice may be the result of abnormalities in the cytokine system in these mice.

Animals↗

PubMed1994

Increased mRNA for CD63 antigen in atherosclerotic lesions of Watanabe heritable hyperlipidemic rabbits.

To identify a set of mRNAs that increases with the progression of atherosclerosis, differential hybridization screening of a cDNA library, constructed from total RNA in aortae of Watanabe heritable hyperlipidemic (WHHL) rabbits, was carried out. Here we report that one of the positive clones encodes a rabbit homologue of human CD63 antigen. Nucleotide sequence analysis of the cDNA revealed the primary structure of rabbit lysosomal membrane antigen CD63. Analysis of the mRNA by in situ hybridization revealed that a significant amount of the mRNA is accumulated in atherosclerotic lesions of WHHL rabbits. Northern blot analysis of total RNA prepared from aortae of WHHL and normal rabbits indicates that expression of the mRNA increased with age in WHHL rabbits, suggesting that expression of the mRNA is correlated with the progression of atherosclerosis.

Aging↗

PubMed1994

Effect of hachimijiogan, an oriental herbal medicinal mixture, on experimental amnesia in mice.

The effect of Hachimijiogan on cognitive disturbance was investigated using step-through passive avoidance failure techniques: scopolamine-, cycloheximide- and cerebral ischemia-induced amnesia. Pre-acquisition trial administration of Hachimijiogan (0.5 g/kg, p.o.) prolonged the step-through latency reduced by scopolamine and cycloheximide. Hachimijiogan (0.5 and 1.0 g/kg, p.o.) also ameliorated the cerebral ischemia-induced amnesia. Physostigmine (0.1 mg/kg, i.p.) ameliorated all three amnesia models. The ameliorating effects of Hachimijiogan and physostigmine on cycloheximide-induced amnesia were diminished by the combination with scopolamine. These results suggest that Hachimijiogan possesses a wide-ranging pharmacological profile in anti-amnesic actions and that its anti-amnesic activities may be related to the cholinergic neuronal system.

Amnesia↗

PubMed1994

Nephritogenic antibodies in MRL/lpr lupus mice: molecular characteristics in pathological and genetic aspects.

MRL/lpr mice spontaneously develop a lethal glomerulonephritis (GN). We found that IgG3 production in this strain of mice has a critical role on the development of GN; 1) IgG3 levels were high in kidney-extracted IgG and in circulating IgG immune complexes (IC), 2) serum IgG3 was selectively reduced by cyclosporin A treatment, associated with amelioration of GN, and 3) the mRNA levels of IgG3 correlated well with the severity of GN among the MRL/lpr x (MRL/lpr x C3H/lpr) F1 backcross mice with the rearranged genetic profile. Based on these results, we have successfully established five hybridoma clones which produce nephritogenic IgG3 antibodies from an unmanipulated MRL/lpr mouse. When they were injected to normal mice, four of the five clones generated cell-proliferative GN associated with the marked cellular infiltrates, while the remaining clone induced wire loop-like lesions. This result suggests that particular antibodies generated in MRL/lpr mice have a different pathogenic potency. The V-region sequence study of these nephritogenic antibodies revealed that the two types of the glomerular lesions were mediated by a different B cell precursor. In conclusion, GN in MRL/lpr lupus mice is thought to be generated by the expansion of clonally different B cells producing nephritogenic antibodies with a different pathogenic potency.

Amino Acid Sequence↗

PubMed1994

Involvement of the c-kit receptor in the adhesion of hematopoietic stem cells to stromal cells.

The proto-oncogene c-kit, encoding a receptor-type tyrosine kinase, is allelic with the W locus of the mouse. The stromal cell line OP9, capable of supporting long-term hematopoiesis, was newly established from a newborn B6C3F1-op/op mouse calvaria. When bone marrow cells of WBB6F1-W/Wv mice were cocultured with the OP9 cells in liquid medium, hematopoiesis declined to a level one-thousandth of that in the cocultures of bone marrow cells of WBB6F1-+/+ mice and stromal cells by day 21. In contrast, when bone marrow cells of W/Wv mice were cocultured with OP9 cells in semisolid medium, at least 61% of the number of colonies were detected until the end of our observation period of 42 days when compared with that in control cocultures, although colonies formed by hematopoietic stem cells of W/Wv mice were significantly smaller than those of normal stem cells. After a 24-hour incubation with OP9 cells, fewer stem cells of W/Wv mice than normal ones adhered to the stromal cells. Adhesion of normal stem cells to stromal cells was inhibited by the addition of an antagonists anti-c-kit monoclonal antibody, ACK2. These results demonstrate that the c-kit receptor plays an important role not only in the proliferative response of hematopoietic stem cells but also in their adhesion to stromal cells.

Animals↗

PubMed1994

[Animal models for intractable vasculitis: significance of genetic background].

Almost all of intractable vasculitis have been thought to develop mainly in immunological mechanisms, based on the data from several animal models previously established. Serum sickness models, microbe-induced models and others have contributed to supporting this idea. These models have furthermore indicated that vasculitis could be generated by exogenous factors in normal individuals, and that vasculitis might be explained in monism. However, recent studies in murine lupus suggest that intractable vasculitis requires endogenous factors involving retroviruses and/or genetic background under the control of polygene system. In this review, although not comprehensive, significance of background genes in vasculitis will be focused.

Animals↗

PubMed1994

[An autopsy case of AIDS with hemophilia A who died of DIC and gastrointestinal bleeding associated with gastric carcinoma (signet ring cell carcinoma)].

We describe a 39 years-old male hemophilia A patient with acquired immunodeficiency syndrome (AIDS) developing to disseminated intravascular coagulation (DIC) due to gastric carcinoma. He had been diagnosed as human immunodeficiency virus (HIV) sero-positive in 1990. Since then, he has been treated by the oral administration of zidovudine (AZT), dideoxyinosine (ddI) and intravenous administration of glycyrrhizin. In September 1990, he suddenly complained abdominal pain with bloody stool. His condition deteriorated in spite of our intensive treatment for DIC. He died of multiple organ failure (MOF) due to DIC. The autopsy findings showed gastric carcinoma, defined of signet ring cell carcinoma histopathologically. But neither opportunistic infection nor other cause of DIC were observed.

Acquired Immunodeficiency Syndrome↗

PubMed1994

Interstitial nephritis in Aleutian mink disease. Possible role of cell-mediated immunity against virus-infected tubular epithelial cells.

Aleutian mink disease (AD) has been characterized by immune complex glomerulonephritis associated with persistent infection of Aleutian mink disease parvovirus (ADV). Histopathological examination of kidneys from ADV-infected mink in this study revealed that interstitial nephritis characterized by prominent damage of renal tubuli and lymphocyte infiltration was also common in AD along with glomerulonephritis. By using strand-specific in situ molecular hybridization technique, replication of ADV was observed in tubular epithelial cells, in addition to epithelial cells of Bowman's capsules and some glomerular cells of the infected mink. Analysis of tubular lesions by a combination of immunohistochemistry and in situ hybridization revealed that the renal tubuli positive for virion DNA or replicative form DNA/mRNA of ADV were also positive for an activation marker of immunocompetent cells, which is shared by B lymphocytes and thymic epithelial cells. Infiltration of a subpopulation of T lymphocytes around infected renal tubuli were observed but deposition of immune complexes in these tubular lesions was not demonstrable. ADV replication in epithelial cells of renal tubuli and cell-mediated immune responses to the infected epithelial cells may play a role in the pathogenesis of interstitial nephritis in Aleutian mink disease.

Aleutian Mink Disease↗

PubMed1993

Antibody feedback regulation in MRL/lpr mice.

MRL/Mp-lpr/lpr (MRL/l) mice spontaneously develop autoimmune disease, characterized by glomerulonephritis, polyarteritis and polyarthritis. The lpr mice have defects in the Fas antigen, which plays a role in apoptosis, and it has been suggested that lack of negative selection of autoreactive T cells explains the initiation of the disease. The extremely high amount of autoantibodies may reflect additional immunoregulatory abnormalities. Antibody feedback regulation is an efficient way of up- or downregulating antibody responses. We have for the first time determined whether IgG-mediated suppression as well as IgM-mediated enhancement operates normally in these mice. MRL/l and MRL/Mp(-)+/+ (MRL/n) mice of different ages were therefore immunized with sheep erythrocyte (SRBC)-specific IgG or IgM antibodies followed by SRBC. Control groups received antigen alone. Five days later, the antigen-specific plaque-forming cell response was measured. IgG induced more than 90% suppression in both MRL/l and MRL/n in mice of all ages tested. This degree of suppression is in the same range as for other, normal mouse strains. In contrast, IgM-mediated enhancement was completely absent in 12-week-old MRL/l mice but normal in 8-week-old MRL/l as well as in MRL/n mice of all ages tested. When spleens and lymph nodes were immunohistochemically studied using a mAb specific for complement receptors 1 and 2 (CR1/CR2), an abnormal follicular structure was demonstrated in 12-week-old MRL/l mice. The antibody response of both 8- and 13-week-old MRL/l mice in vivo, after downregulation of these receptors, was inhibited by 85-96%. Thus, the presented data demonstrate that MRL/l mice with overt autoimmune disease are refractory to IgM-mediated enhancement of antigen-specific antibody production. We believe that this abnormal antibody feedback regulation is due to abnormal follicular structure in lymphoid organs of old MRL/l mice, hence the inability to localize and present antigen in a normal way.

Animals↗

PubMed1993

A case of fatal infectious mononucleosis presenting with fulminant hepatic failure associated with an extensive CD8-positive lymphocyte infiltration in the liver.

We describe a fatal case of infectious mononucleosis presenting with fulminant hepatic failure associated with extensive CD8-positive lymphocyte infiltration and diffuse karyorrhexis in the liver. Immunohistochemical analysis of mononuclear cells showed that Leu-2a (CD8)-positive lymphocytes were heavily distributed in the portal areas and the sinusoidal spaces, but Leu-3a (CD4)-, Leu-14 (CD22)-, or My 4 (CD14)-positive cells were undetectable in sections of the liver. Southern blot hybridization studies disclosed the presence of Epstein-Barr virus DNA fragments in the liver tissue. The unusual pathologic and immunologic responses observed in this case could not simply be explained by severe Epstein-Barr virus infection. Some superimposed factors should be considered.

CD8 Antigens↗

PubMed1993

Cloning and cDNA sequence analysis of nephritogenic monoclonal antibodies derived from an MRL/lpr lupus mouse.

Production of IgG3 in MRL/Mp-lpr/lpr (MRL/lpr) lupus mice is one of the major factors to develop glomerulonephritis (GN) in these mice. To examine molecular characteristics of IgG3 responsible for GN in these mice, hybridoma clones producing IgG3 antibodies were prepared from one unmanipulated MRL/lpr mouse. Two clones, 2B11.3 and 7B6.8, were nephritogenic; that is, they caused severe glomerular lesions when injected to normal mice, moreover with a different histopathological manifestation. The 2B11.3 clone generated diffuse cell-proliferative lesions, while those induced by the 7B6.8 clone resembled wire loop lesions in human lupus nephritis. The cDNA sequence analysis of 7B6.8 antibody and the other IgG3 antibody, 1G3, non-nephritogenic, revealed that the C regions of the heavy and light kappa chains were completely the same between them. Furthermore, they were identical in deduced amino acid sequences to those from non-autoimmune BALB/c mice, indicating no allelic difference of Igh-8 between these two strains. The V regions of 2B11.3 and 7B6.8 antibodies were composed of different sets of VH, D, JH, Vk and Jk. Although both of the VH belonged to the J558 family, they seemed to use a different VH germline gene. These findings suggest that GN in MRL/lpr mice is generated by the expansion of clonally different B cells producing particular antibodies possibly with a different pathogenetic potency.

Amino Acid Sequence↗