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S Kano

Publications and source records attributed to S Kano.

At least 127 records · Page 7Linked to original sources

Suppressive role of endogenous endothelial monocyte chemoattractant protein-1 on monocyte transendothelial migration in vitro.

Monocyte chemoattractant protein-1 (MCP-1, or monocyte chemotactic and activating factor) is thought to play an important role in monocyte infiltration into tissue, but little is known about its effect on monocyte-endothelium interaction. We examined the effect of MCP-1 produced by cytokine-activated endothelial cells (ECs) on monocyte-endothelium adhesion and subsequent transendothelial migration by using a double-chamber vessel model. Unstimulated ECs showed no MCP-1 expression, but exposure to interleukin-1 beta (IL-1 beta, 25 U/mL) induced marked MCP-1 mRNA expression and protein synthesis. When placed in the lower compartment, recombinant human (rh) MCP-1 (100 ng/mL) produced a 1.9-fold and a 2.7-fold increase in adhesion and migration, respectively, compared with a corresponding 51% and 59% decrease when placed in the upper compartment. Migration of monocytes was dependent on a gradient of rh-MCP-1 from the apical to basilar side of the EC layer. Furthermore, a forward gradient of MCP-1 induced adherent cells to increase their subsequent migration, whereas a reverse gradient induced the cells to detach and completely inhibited their subsequent migration. Pretreatment with IL-1 beta for 4 and 24 hours produced a 20% and 63% increase in monocyte migration, respectively. In the presence of anti-MCP-1 antibody, the increase was further enhanced by 52% and 152%, respectively. These results suggest that endogenous endothelial MCP-1, when secreted by IL-1-stimulated ECs, suppresses monocyte migration in the presence of MCP-1 on the basilar side of the EC layer.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies↗

Induction of monocyte chemoattractant protein-1 synthesis in human monocytes during transendothelial migration in vitro.

Monocyte chemoattractant protein-1 (MCP-1, or monocyte chemotactic and activating factor) plays important roles in the recruitment of monocytes and thus in the development of atherosclerosis. In this study, we determined whether MCP-1 synthesis was induced by the cellular interaction between monocytes and endothelial cells during the process of transendothelial migration. We found that when human peripheral blood monocytes (2.5 x 10(6) cells) and umbilical vein endothelial cells (HUVECs; 5.0 x 10(5) cells) were cocultured for 5 hours, 7.9 ng/mL MCP-1 was secreted into the medium, whereas when the two were cultured separately, MCP-1 levels were 1.0 and 0.9 ng/mL, respectively. Furthermore, the use of interleukin-1 beta (IL-1 beta)-pretreated HUVECs in cocultures induced twice the levels of MCP-1 as in unstimulated HUVEC culture. Conditioned medium had transendothelial chemotactic activity for monocytes, and this activity was completely abolished by addition of anti-MCP-1 antibody. Although MCP-1 mRNA levels were very low or undetectable in HUVECs or monocytes alone, message could be detected after 2 hours of coculture in total mRNA preparations from both monocytes and HUVECs. mRNA levels increased by 4 hours and had declined slightly by 24 hours. The rapid induction of message suggests that cell contact between monocytes and HUVECs induces the de novo synthesis of MCP-1 protein. Anti-interleukin (IL)-1 alpha/beta and anti-tumor necrosis factor-alpha antibodies, or anti-lymphocyte function-associated antigen-1 and very late antigen-4 antibodies, had little or no inhibitory effects on MCP-1 secretion by cocultures.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion Molecules↗

Changes in respiratory mechanics in children undergoing cardiopulmonary bypass.

Congenital heart malformations are often associated with altered pulmonary hemodynamics. Lesions associated with increased pulmonary blood flow (PBF) or increased mean pulmonary artery pressure (MPAP) may in turn alter respiratory mechanics. Surgical correction of these cardiac defects frequently involves the use of cardiopulmonary bypass (CPB), during which the lung may be partially or completely atelectatic for lengthy periods, further compromising lung mechanics. The aims of this study were to document the effect of PBF on respiratory mechanics in children and to determine whether the detrimental effects of CPB were outweighed by the potentially positive effects of the corrective surgery. Twenty-three children (2-120 mo) undergoing surgery were studied while anesthetized, paralyzed, and mechanically ventilated. Pulmonary to systemic blood flow ratio was used as an index of PBF. Seventeen children had lesions associated with increased PBF (group 1), while six had decreased or normal PBF (group 2). Respiratory mechanics were measured just before the commencement of CPB and within approximately 2 h after the cessation of CPB, with the chest closed. Dynamic elastance (Ers,dyn) and resistance (RRS) were calculated from flow, volume (V), and pressure (Pao) measurements, using multiple linear regression with a volume-dependent single compartment model. Static elastance (ERS,st) was calculated from Pao and V measurements obtained when deflating the lung in steps from a maximal Pao of 30 cm H2O. ERS,dyn, ERS,st, and RRS increased significantly with increasing PBF to 220-330% predicted. There was no correlation between MPAP and respiratory mechanics. After CPB, ERS, dyn and RRS fell to normal levels in group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Rosette formation by Plasmodium coatneyi-infected erythrocytes of the Japanese macaque (Macaca fuscata).

We studied in vitro the spontaneous rosette formation by red blood cells of a Japanese macaque infected with Plasmodium coatneyi, which occurred after 30 hr of incubation. Rosette formation involved 88% of parasitized red blood cells (PRBCs). Spontaneous rosettes were formed when the ring-stage parasites developed into late trophozoites or schizonts. A rosette usually consisted of a PRBC surrounded by three or more uninfected erythrocytes. Electron microscopic examination revealed that interaction with adjacent uninfected erythrocytes in rosettes appeared to be mediated by knobs of PRBCs. Protruding ends of these knobs attached to the membranes of adjacent uninfected erythrocytes. In the present study, we have also obtained evidence that another pattern of cell adhesion was mediated by flat and focal electron-dense knobs that had formed on the membranes of PRBCs.

Animals↗

Effects of endogenous endothelial interleukin-8 on neutrophil migration across an endothelial monolayer.

OBJECTIVE: Recent studies suggest that interleukin-8 (IL-8) is involved in the neutrophil infiltration of subendothelial myocardial tissue in the ischaemia/reperfusion injury associated with acute myocardial infarction. The aim of this study was to investigate the effects of IL-8 on transendothelial neutrophil migration using an in vitro three dimensional double chamber migration assay system. METHODS: Human neutrophils were incubated with human endothelial cell monolayers for 1 h, and adherent and migrated neutrophils were then counted. Expression of IL-8 mRNA and secretion of its protein by endothelial cells were analysed respectively by northern blotting and ELISA. RESULTS: Recombinant human (rh) IL-8 (50 ng.ml-1) placed in the lower compartment significantly increased neutrophil adhesion 1.7-fold and transmigration 2.3-fold, compared with control conditions using medium alone in both compartments. In contrast, rh IL-8 (50 ng.ml-1) in the upper compartment significantly inhibited neutrophil adhesion and transmigration by 53% and 61% respectively compared with controls. Neutrophil adhesion and transmigration was dependent on the IL-8 concentration gradient between upper and lower compartments. Unstimulated endothelial cells showed no IL-8 expression, but endothelial cells pretreated with IL-1 beta (25 U.ml-1) markedly induced endogenous IL-8 mRNA and protein accumulation. When endothelial cells were cocultured with neutrophils, enhanced endogenous IL-8 production was observed. Pretreatment of endothelial cells with IL-1 beta for 4 and 24 h increased neutrophil transmigration 2.8-fold and 3.0-fold respectively, compared with unstimulated endothelial cells. The addition of anti-IL-8 monoclonal antibody (12.5 micrograms.ml-1) to the upper compartment with IL-1 beta-pretreated endothelial cells further enhanced transmigration from 2.8- to 3.3-fold and from 3.0- to 4.3-fold respectively. CONCLUSIONS: Endogenous endothelial IL-8, secreted from activated endothelial cells into the apical side of endothelial cell monolayers, has an inhibitory effect on transendothelial migration of neutrophils, suggesting that IL-8 may prevent excessive neutrophil infiltration of myocardial tissue from circulating blood in the reperfusion injury associated with acute myocardial infarction.

Blotting, Northern↗

[Spontaneous regression in a case of primary pulmonary lymphoma with Sjögren's syndrome].

A 62-year-old asymptomatic woman had a nodular shadow approximately 3 cm in diameter in the middle lung field on chest roentgenogram. The shadow gradually grew over 1.5 years. She was then admitted to our hospital for evaluation of the abnormal shadow. Transbronchial biopsy specimens showed a diffuse, small, lymphoid infiltrate with predominance of B-cells. These findings suggested neoplastic proliferation. Further examinations revealed the presence of Sjögren's syndrome. Four months later, she was readmitted for surgical resection. Chest roentgenogram on the second admission disclosed that the mass shadow had shrunk slightly. Histopathological examination of the resected specimen led to the diagnosis of malignant lymphoma, diffuse small cell type (IgG kappa type). Gene analysis revealed the presence of heavy chain gene rearrangements, which confirmed the diagnosis of B-cell lymphoma. In this case, no contraction or necrosis of the lesion was observed, and the change in the shadow size was probably due to partial or transient spontaneous regression.

Female↗

[Autopsy of a patient with rheumatic fever, who initially presented with acute respiratory failure].

A 59-year-old man was admitted to the hospital because of dyspnea, fever, and general erythema. He had hypoxemia on admission. Chest X-ray film showed diffuse reticulonodular shadows in both lungs. Chest CT showed a diffuse increase in density, predominantly in both lower lobes. The respiratory failure had rapidly progressed, and the patient died only 40 hours after admission. Autopsy revealed diffuse alveolar damage in the lung, and Aschoff's bodies in the cardiac muscle. Aschoff's bodies are specific for rheumatic fever, and consist of Aschoff's cells with owl-eye-like or caterpillar-like nuclei. We diagnosed this patient's condition as rheumatic fever because of the presence of Aschoff's bodies. Rheumatic fever is generally seen as a disease of younger people, and these patients rarely present with respiratory signs, but this case shows that we have to recognize the possibility of rheumatic fever in adults with respiratory signs and skin lesions.

Acute Disease↗

[Progressive systemic sclerosis (PSS) and cancer--increasing coincidence rate of cancer in 67 PSS patients].

The coincidence rate of cancer and PSS has been increasing according to reports from Nippon Byori Boken Shuho (Annual of Pathological Autopsy Cases in Japan), reaching 12.3% in the most recent report. Therefore we reviewed the histories of 67 PSS patients seen at our division over an 18-year period between 1974 and 1992, and found a high coincidence rate (14.6%) of cancer, reflecting the increasing tendency reported in the Nippon Byori Boken Shuho. The most frequent type of cancer was gastrointestinal cancer, including gastric and colon cancer and duodenal carcinoid. There were no significant differences in the clinical and laboratory findings between PSS patients with cancer and those without. Twenty-six of the 67 PSS patients died. Cancer was the cause of death in four, ranking second behind respiratory failure. The reason for the increasing coincidence rate of cancer and PSS is unclear at present. However, it is very important to discover cancer in PSS patients as early as possible, since it has a marked effect on prognosis.

Adult↗

Classification criteria for polymyositis and dermatomyositis.

OBJECTIVE: The establishment of classification criteria for polymyositis (PM) and dermatomyositis (DM). METHODS: Questionnaires inquiring about patients with DM, PM, systemic lupus erythematosus, progressive systemic sclerosis and noninflammatory neuromuscular diseases were distributed to the main medical institutes in Japan. Data were collected and analyzed by computer. RESULTS: Among skin lesions of DM, heliotrope rash, Gottron's sign and erythema or purpura on the extensor surfaces of the extremity joints were shown to be distinguishing criteria. In both DM and PM, proximal muscle weakness, muscle grasping and spontaneous pain, nondestructive arthritis or arthralgia, elevated CK or aldolase level, presence of systemic inflammatory signs, myogenic changes on EMG, positive and anti Jo-1 antibody and pathologic findings compatible with inflammatory myositis were distinguishing criteria items. CONCLUSION: When a patient satisfies one of 3 skin lesion items and at least 4 other items, he or she shall be classified as having DM, sensitivity 94.1%. When a patient satisfies at least 4 items other than skin lesion items, he or she shall be classified as having PM, sensitivity 98.9%. Specificity of DM and PM is 95.2%.

Dermatomyositis↗

Quantification of antiribosomal P0 protein antibodies by ELISA with recombinant P0 fusion protein and their association with central nervous system disease in systemic lupus erythematosus.

OBJECTIVE: Using solid phase ELISA with recombinant P0 fusion protein as the antigen for detecting antiribosomal P0 protein antibody, we analyzed the association of this antibody and anticardiolipin antibody (aCL) with central nervous system (CNS) disease in patients with active systemic lupus erythematosus (SLE). METHODS: Sera from 70 randomly selected Japanese patients with active SLE were assayed for IgG and IgM antiribosomal P0 protein antibody titers and IgG aCL. RESULTS: IgG and IgM antiribosomal P0 protein antibodies were present in 29 and 12 (41.4 and 17.1%) of the 70 patients, respectively. The incidence of CNS disease, excluding lupus psychosis, was significantly higher in patients with IgG and IgM antiribosomal P0 protein antibodies than in those who lacked them (IgG antiribosomal P0 protein antibody 11/29 vs 3/41; IgM antiribosomal P0 protein antibody 7/12 vs 7/58). In addition, both IgG and IgM antiribosomal P0 protein antibody titers were significantly higher in patients with CNS disease, excluding lupus psychosis, than those without. No significant association was observed between antiribosomal P0 protein antibodies and lupus psychosis. No significant association was observed between IgG aCL and CNS disease. Serial studies of antiribosomal P0 protein antibodies and aCL in patients with transverse myelopathy also showed that IgG and IgM antiribosomal P0 protein antibodies, but not IgG aCL, were associated with CNS disease, excluding lupus psychosis. CONCLUSION: These data suggest a strong association of IgG and IgM antiribosomal P0 protein antibodies with CNS disease, excluding lupus psychosis, in SLE.

Adolescent↗

Increase in oxygen tension after intraperitoneal N-methyl-DL-aspartate in rat cerebral cortex.

An oxygen electrode equipped with a thermocouple enabled us to determine the absolute oxygen tension (PO2) in brain regions by taking account of local changes in temperature. Under urethane anesthesia, the PO2 of rat cerebral cortex was significantly increased up to 90 min after N-methyl-DL-aspartate administration (200 mg/kg, i.p.). This suggests that stimulation of NMDA receptors enhances oxygen supply to the cerebrum in vivo.

Animals↗

Involvement of LDL receptor in the proliferation of vascular smooth muscle cells.

To study the involvement of the low-density lipoprotein (LDL) receptor in the growth of vascular smooth muscle cells (VSMC), we compared the proliferation of cultured VSMC from Watanabe heritable hyperlipidemic (WHHL) rabbits, which lack the LDL receptor, and VSMC from normal Japanese white rabbits in response to platelet derived growth factor (PDGF). The increase in the number of VSMC from WHHL rabbits in response to PDGF (10(-8) M) was significantly lower than that of VSMC from normal rabbits. PDGF stimulated the synthesis of DNA in VSMC from both normal rabbits and WHHL rabbits, but the response was significantly lower in the latter. To determine the involvement of the LDL receptor in the decreased mitogenic response of WHHL rabbit VSMC, we used an anti-LDL receptor monoclonal antibody (MAb) to normal rabbit VSMC; DNA synthesis of VSMC was stimulated by PDGF, but the effect was significantly blocked by the anti-LDL receptor MAb. Mitogen-activated protein (MAP) kinase activity in normal rabbit VSMC was increased by exposure to PDGF, but the effect was significantly suppressed in the presence of the MAb. The anti-LDL receptor MAb markedly inhibited LDL binding to the surface of normal rabbit VSMC. These results suggest that the LDL receptor influences the proliferation of VSMC and thus might be involved in the pathogenesis of atherosclerosis.

Animals↗

Validation of esophageal pressure occlusion test after paralysis.

Measurements of respiratory mechanics are frequently made in ventilated infants and children. Esophageal pressure measurements (Pes) using a balloon on a catheter have been used to partition the respiratory mechanics into lung and chest wall components. Appropriate positioning of this balloon is crucial to obtain accurate estimates of pleural pressure. Traditionally, in spontaneously breathing subjects the balloon position is assessed with an occlusion test. In ventilated subjects, it is not always possible to perform an occlusion test prior to paralysis, and even if such a test is performed it may be relevant under conditions of positive pressure ventilation. By occluding the airway opening and applying gentle pressure to the abdomen or rib cage, positive swings in pressure can be measured by both Pes and airway opening pressure (Pao). We compared traditional occlusion tests measured in 16 spontaneously breathing puppies to the positive pressure occlusion test performed after paralysis. In 2 pups we were unable to obtain a reasonable traditional occlusion test (> 15% difference between Pes and Pao) but we obtained 10 traditional occlusion tests in each of the remaining 14 pups (2.1-14 kg). In 11 of these animals delta Pes was within 10% of delta Pao. This compared well to positive pressure occlusion test using abdominal pressure performed after analysis, where delta Pes was within 10% of delta Pao in 10 animals. In 9 of these pups occlusion tests were also performed by applying pressure on the rib cage, where delta Pes was within 10% of delta Pao in 6 animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Nasal response to inhaled histamine measured by acoustic rhinometry in infants.

Aerosolized histamine, delivered via a face mask, is commonly used to evaluate bronchial responsiveness in infants. To investigate nasal response to inhaled histamine we have measured nasal passage geometry in 32 infants by the use of acoustic reflections. Satisfactory data were obtained from only 17 infants (12 males, 5 females, 6.6 +/- 4.4 months), because of awakening prior to completing the study in the remaining 15 infants. Acoustic rhinometry provided nasal cavity volume at 4 cm from the entrance of the nostril (V04), the minimum cross-sectional area (Amin), and the distance from the nostril to Amin (Dmin). Nasal geometry and lung function (maximum expiratory functional residual capacity [VmaxFRC] were measured before and immediately after a histamine challenge test using rapid thoratic compression. The histamine aerosols decreased both VO4 and Amin significantly by a mean of 17% and 13%, respectively (P < 0.001). There was a small, but significant increase (mean = 0.19 cm) of Dmin in the right side only, indicating a posterior dislocation of the narrowest site with swelling of the mucous membrane. In general, we found a dose-response relationship in grouped data, with a greater fall in VO4 with increasing dose of histamine, but there was no correlation between percent fall in VO4 and VmaxFRC. This pilot study suggests that histamine aerosol affects nasal cavity geometry and that of acoustic rhinometry in infants and children warrants further investigation.

Acoustics↗

Prevalence of antihuman parvovirus B19 IgG antibodies in patients with refractory rheumatoid arthritis and polyarticular juvenile rheumatoid arthritis.

We investigated the prevalence of antihuman parvovirus B19 immunoglobulin G (IgG) antibody in 108 Japanese patients with rheumatoid arthritis (RA) and 11 patients with polyarticular juvenile rheumatoid arthritis (JRA). Seropositivity of anti-B19 was significantly higher in patients with refractory RA (57.6%, 38/66) compared with patients with remittent RA (19.0%, 8/42; P < 0.001) or age-matched controls (24.3%, 19/78; P < 0.001). Patients with refractory polyarticular JRA had a significantly higher frequency of anti-B19 seropositivity (71.4%, 5/7) than age-matched controls (8.3%, 5/60; P < 0.001), while none of the remittent group was positive for the antibody (0/4).

Adolescent↗

Involvement of adhesion molecules in human monocyte adhesion to and transmigration through endothelial cells in vitro.

Although the accumulation of monocyte-derived foam cells in the subendothelium is a key step in early atherogenesis, the mechanism responsible for monocyte adhesion to and subsequent transmigration through endothelial cells (ECs) has not been defined fully. We investigated the kinetics and the role played by adhesion molecules in the adhesion and transmigration of human monocytes using an in vitro three-dimensional model system comprising ECs cultured on collagen gels. Monocyte adhesion to untreated EC layers increased with time, reached a maximum after 3 h, and then declined. Monocyte transmigration through untreated EC layers also increased with time and reached a plateau after 3-4 h. Prestimulation of ECs with interleukin-1 beta (IL-1 beta; 25 U/ml) for 4 h enhanced monocyte adhesion (40.7 +/- 1.4%) and transmigration (37.9 +/- 1.6%) significantly compared with the value for untreated EC layers. In unstimulated EC layers, anti-leukocyte function-associated antigen-1 (LFA-1) plus anti-intercellular adhesion molecule-1 (ICAM-1) monoclonal antibodies (mAbs) inhibited monocyte adhesion and transmigration significantly by 19% and 20%, respectively, whereas anti-very late antigen-4 (VLA-4) plus anti-vascular cell adhesion molecule-1 (VCAM-1) mAbs did not. In IL-1 beta-stimulated EC layers, anti-LFA 1 plus anti-ICAM-1 mAbs inhibited the adhesion and transmigration by 32% and 30%, respectively and anti-VLA-4 plus anti-VCAM-1 mAbs did so by 18% and 27%, respectively. These results suggest that the monocyte-EC interaction in unstimulated ECs is mediated, in part, by the LFA-1-ICAM-1 pathway and in IL-1 beta-stimulated ECs, in part, by both LFA-1-ICAM-1 and VLA-4-VCAM-1 pathways.

Antibodies, Monoclonal↗

Interleukin 6 gene transcripts are expressed in human atherosclerotic lesions.

Factors controlling the proliferation of vascular smooth muscle cells (SMC) are thought to be key elements in the progression of atherosclerosis. We have previously shown that interleukin 6 (IL-6) stimulates the growth of SMC in vitro and that IL-6 gene transcripts are expressed in atherosclerotic lesions of genetically hyperlipidemic rabbits. To understand the involvement of IL-6 in the development of human atherosclerosis, we investigated IL-6 mRNA expression in atherosclerotic arteries from patients undergoing surgical vascularization, utilizing reverse transcription polymerase chain reaction (RT-PCR) and in situ hybridization analyses. In RT-PCR analysis, the atherosclerotic arteries showed 10- to 40-fold levels of IL-6 mRNA expression over the non-atherosclerotic artery. In in situ hybridization analysis, IL-6 gene transcripts were observed in the thickened intimal layer of atherosclerotic lesions. These results strongly suggest the involvement of IL-6 in the development of human atherosclerosis.

Actins↗