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Biomedical subjects

M Kohno

Publications and source records attributed to M Kohno.

At least 127 records · Page 7Linked to original sources
PubMed1999

Postoperative prognosis of Brown-Séquard-type myelopathy in patients with cervical lesions.

BACKGROUND: Postoperative prognosis of the hemihypalgesia in patients with Brown-Séquard-type myelopathy (BSM) caused by cervical lesions is of great interest to surgeons. However, there are very few reports discussing the postoperative prognosis of BSM. METHODS: We evaluated the prognosis of BSM using the criteria of the Japanese Orthopaedic Association (JOA) score in 16 (seven ossification of the posterior longitudinal ligament [OPLL], 5 cervical spondylosis [CS], and 4 disc herniation patients) out of 233 surgically treated patients with cervical diseases. The mean follow-up duration was 2 years and 11 months. RESULTS: After surgery, none of these patients showed complete resolution of hemihypalgesia, although the most rostral level of hemihypalgesia moved in a caudal direction in 13 patients (81%), whose recovery ratios of JOA score were significantly better than those of hemihypalgesia-level-persisted patients. In our BSM series, OPLL occurred most frequently and the anterior element compressing the spinal cord existed most frequently in the central area of the vertebra (44%). Postoperative improvement in the motor function of the legs in the disc herniation group was significantly better than in the OPLL and CS groups (p < 0.05, respectively). There were no significant differences in the functional prognosis between the BSM and non-BSM patient groups. CONCLUSIONS: BSM patients can expect almost the same functional outcome as non-BSM patients, with the exception of the disappearance of hemihypalgesia.

Adult↗
PubMed1999

Effect of angiotensin II receptor antagonism on vascular hypertrophy and aortic impedance in abdominal aortic-banded rat.

Vascular hypertrophy is considered to be an adaptive response to increased arterial wall stress in hypertension. Although there are several reports concerning the effect of angiotensin II inhibition on the development of vascular hypertrophy, little information is available as to its effect on vascular hypertrophy in parallel with the evaluation of arterial wall characteristics. The goal of this study was to evaluate the effect of angiotensin II type 1 receptor antagonist TCV-116 on pressure overload-induced vascular hypertrophy in parallel with the assessment of aortic impedance. Low dose (LD; 0.3 mg/kg/day) or high dose (HD; 3.0 mg/kg/day) of TCV-116 was administered to abdominal aortic-banded rats over 4 weeks; then hemodynamics and morphology were evaluated. In both the LD and HD groups, blood pressures were decreased to a similar extent compared with those of the vehicle-treated group (P < .05). Left ventricular (LV) weight and LV weight/body weight ratio was inhibited in both TCV-116-treated groups (P < .05), whereas the media cross-sectional area of the aorta was inhibited only in the HD group (P < .05). After the treatment of TCV-116 (LD, HD), total systemic resistance was decreased compared with the vehicle-treated group (P < .05), but there was no significant difference between the TCV-116-treated groups. In contrast, the first harmonic of the impedance modulus revealed the decrease only in the HD group (P < .05). TCV-116 attenuated the development of pressure overload LV hypertrophy and vascular hypertrophy as well; however, the dose of TCV-116 required for the inhibition of vascular hypertrophy was significantly higher than that for LV hypertrophy. Vascular hypertrophy may be less pressure dependent than cardiac hypertrophy. On chronic addition of high dose of TCV-116, arterial wave reflection was decreased in association with the attenuation of vascular hypertrophy.

Angiotensin Receptor Antagonists↗
PubMed1999

Histopathological characterization of spontaneously developing osteoarthropathy in the BCBC/Y mouse established newly from B6C3F1 mice.

A new breed of mouse showing cinnamon-color of hair and osteoarthropathy was born from mouse of the B6C3F1 strain, and was named the BCBC/Y mouse. The incidence and severity of the articular lesions increased with aging, and by 10 to 22 months of age, many mice showed moderate-severe motor paresis with ankylotic changes of the limb joints. Abnormal radiographic changes were observed at many joints with increasing age. There was bone and joint deformity, followed by progressive osteoarthritic changes and ankylosis of the limb joints. Histopathologically, degenerative changes, followed by loosening, fissuring and erosion of the articular cartilage were observed at early stage of articular lesions. Unilateral progressive changes, characterized by joint fusion with abnormal osteophytes, were observed at late stage of articular lesions with aging. For successive breeding to establish a homogeneous strain, generation mice retained the symptoms of the primary mice. Thus, these BCBC/Y mice may be a useful as mode to elucidate the hereditary background and hyperplastic changes of the osteochondrocytes for pathogenesis of the osteoarthropathy.

Aging↗
PubMed1999

Three cases of palatal polyps in infants.

Fibrous lesions are common in the oral cavity, however, in infants they are rarely reported. We present three cases of palatal polyps in infants aged 2 days, 3 months and 7 months. In two cases, the treatment was surgical removal and in one case the polyp decreased in size and surgical removal was not required. In two infants, the diagnosis was confirmed histologically as fibroepithelial hyperplasia.

Gingival Hyperplasia↗
PubMed1999

Bone morphogenetic protein-2 promotes survival and differentiation of striatal GABAergic neurons in the absence of glial cell proliferation.

We examined the potential neurotrophic effects of bone morphogenetic protein (BMP)-2 on the survival and differentiation of neurons cultured from the rat developing striatum at embryonic day 16, a period during which the mRNAs for BMP-2 and its receptor subunits (types IA, IB, and II) were detected. BMP-2 exerted potent activity to promote the survival of striatal neurons and increased the number of surviving microtubule-associated protein-2-positive cells by 2.4-fold as compared with the control cultures after 4 days in vitro. Although basic fibroblast growth factor (bFGF) also showed relatively high activity to promote the survival of striatal neurons, transforming growth factor-beta1, -beta2, and -beta3, glial cell line-derived neurotrophic factor, or brain-derived neurotrophic factor promoted their survival weakly. Striatal neurons cultured in the presence of BMP-2 or bFGF possessed extensive neurite outgrowths, the majority of which were GABA-immunoreactive. Inhibition of glial cell proliferation by 5-fluorodeoxyuridine did not affect the capacity of BMP-2 to promote the survival of striatal GABAergic neurons. In contrast, the ability of bFGF to promote the survival of striatal neurons was inhibited significantly by the treatment of cells with 5-fluorodeoxyuridine. All these results suggest that BMP-2 exerts potent neurotrophic effects on the striatal GABAergic neurons in a glial cell-independent manner.

Animals↗
PubMed1999

The putative mechanism of thrombosis in antiphospholipid syndrome: impairment of the protein C and the fibrinolytic systems by monoclonal anticardiolipin antibodies.

The mechanism of thrombosis in patients with antiphospholipid syndrome is not clear. To investigate it, we examined the effect of monoclonal anticardiolipin (aCL) antibodies and beta2-glycoprotein I (beta2-GPI), which is required for formation of the aCL epitopes, on activated protein C (APC) and on fibrinolytic activity. First, APC activities were measured in the presence and absence of beta2-GPI or gamma M immunoglobulin (IgM) monoclonal aCLs (EY1C8 and EY2C9), or both, established from peripheral blood lymphocytes obtained from a patient with aCL. beta2-GPI exhibited a procoagulant activity by inhibiting APC activity as well as an anticoagulant activity by inhibiting thrombin generation. Any further inhibition of APC activity was caused by monoclonal aCL, and then only in the presence of beta2-GPI. The remaining tissue plasminogen activator (t-PA) of the sample consisting of beta2-GPI, two-chain recombinant t-PA, and plasminogen activator inhibitor (PAI)-1 was measured by a chromogenic assay using the synthetic substrate S-2251, Glu-plasminogen, and soluble fibrin monomer. beta2-GPI protected t-PA activity from inhibition by PAI-1. However, monoclonal aCLs (EY1C8 and EY2C9) inhibited the effect of beta2-GPI on fibrinolytic activity; that is, monoclonal aCLs inhibited fibrinolytic activity by elevating PAI-1 activity. Thrombosis in patients with aCL can be explained in part by both the inhibition of APC anticoagulant activity and the impairment of fibrinolytic activity by aCL.

Antibodies, Anticardiolipin↗
PubMed1999

New aneurysm clip and applier for narrow spaces: technical note.

OBJECTIVE: Aneurysm surgery carries considerable risk to the patient, in part because the surgical field can be so constricted that accurate placement of the aneurysm clip is impeded. In fact, most aneurysm clip appliers are so bulky that they can impair the surgeon's view, if the field is tight. We describe a system of aneurysm clips and appliers that have a very low profile and consequently allow better visualization of the operative field at critical moments during surgery. INSTRUMENTATION: A new system of clips for aneurysm surgery was developed to overcome some of the deficiencies of conventional sets. The new clip blades are opened from inside the spring, so the clip blades are clearly seen as they are applied across the base of the aneurysm. In addition, these clips can be angled in any desired direction in the applier, which makes their application easier. A third advantage is that the clip applier is used as a clip remover should adjustment or reapplication of the clip be necessary. RESULTS: Thirty aneurysms were obliterated with the new clips without any complications attributable to the clips. The new instruments allowed the safe application of clips to aneurysms in deep, confined, and anatomically complex spaces, such as aneurysms of the basilar tip and anterior communicating artery. CONCLUSION: The newly described system of aneurysm clips and appliers appears to have significant advantages over other currently available systems.

Animals↗
PubMed1999

Plasma endothelin-1 level in chronic obstructive pulmonary disease: relationship with natriuretic peptide.

BACKGROUND AND OBJECTIVE: Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by the vascular endothelium. The purpose of this study was to elucidate the pathophysiological role of ET-1 in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD). METHOD: We measured plasma ET-1 levels during right heart catheterization both at rest and during exercise on room air and while breathing oxygen in patients with COPD. In addition, we simultaneously measured plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). RESULTS: Plasma ET-1 levels at rest were significantly higher in 21 patients with COPD than in 16 control subjects (p < 0.001). For COPD patients, there was no correlation between the plasma ET-1 level and pulmonary arterial pressure or pulmonary vascular resistance at rest. On the other hand, there was a significant negative correlation between plasma ET-1 level and mixed venous oxygen tension (r = -0. 503, p < 0.05). Also, the plasma ET-1 level was positively correlated with those of ANP (r = 0.540, p < 0.05) and BNP (r = 0. 533, p < 0.05) at baseline. Oxygen administration significantly decreased plasma ET-1 levels at rest (p < 0.05). Plasma ET-1 levels did not change significantly with exercise despite the progression of pulmonary hypertension and hypoxemia. In contrast, plasma ANP and BNP levels both increased markedly with exercise (p < 0.01). CONCLUSION: We conclude that in patients with COPD, the plasma ET-1 level is not affected by acute progression of pulmonary hypertension and hypoxemia during exercise, and persistent hypoxemia may be associated with an increase in the plasma ET-1 level. In addition, our findings suggest that ANP and BNP may modulate the pulmonary vascular tone by interacting with ET-1 in these patients.

Aged↗
PubMed1999

[Distribution of nitroxide radical compounds and its reducing activity in liver, spleen and kidney of rat by electron spin resonance (ESR) spectroscopy].

The time courses of intensity changes of X-band electron spin resonance (ESR) spectra in the blood, liver, spleen, kidney and porta hepatis of rats were examined after 3-carbamoyl-2,2,5,5-tetramethylpyrrolidin-1-yloxyl (carbamoyl-PROXYL) was perorally administered. The quenching activities of nitroxide radicals were determined using homogenate of the organs of individual rats. It was found that administrated nitroxide radicals were delivered to the liver, spleen, and kidney after peroral administration, where ESR signal intensities in the blood decreased gradually. The concentration of the elivered nitroxide radical varied with the individual organs. The quenching activity of the nitroxide radical for the homogenate of the porta hepatis was the highest before administration, while the concentration due to the reduced deoxidized-nitroxide radical compounds after 4 h of peroral administration was shown to be high in the kidney. It is concluded that the nitroxide radical compound is quenched in the porta hepatis of the liver, while the reduced nitroxide radical compound is delivered to the kidney.

Animals↗
PubMed1999

Abnormal coronary flow profiles at rest and during rapid atrial pacing in patients with hypertrophic cardiomyopathy.

To examine the mechanism of myocardial ischemia in hypertrophic cardiomyopathy (HCM), coronary flow velocity was measured in the left anterior descending coronary artery (LAD) using a Doppler guide wire in 11 patients with HCM and in 8 normal controls. The average peak velocity (APV), percent increase of APV (%APV), and APV during systole (Vs) and diastole (Vd) were calculated at rest and during rapid atrial pacing. The APV in HCM reached a peak value at a heart rate of 90 beats/min, while in the controls the APV increased continuously until the heart rate reached 130 beats/min [%APV (130 beats/min); 103+/-30% in HCM vs 139+/-23% in controls, p<0.04]. During rapid atrial pacing, Vs in the controls increased, whereas Vs in HCM decreased further. During high-rate pacing, Vd in HCM reached a peak value at a heart rate of 90 beats/min, whereas in the controls, Vd increased continuously until the heart rate reached 130 beats/min. The acceleration rate of early diastolic flow was significantly lower in HCM than in the controls (1.85+/-0.66 vs 3.18+/-1.62 m/s2, p<0.03). This abnormal response might be due to an increase in the reverse systolic flow and a decrease in the diastolic flow, probably caused by a slow acceleration of early diastolic flow velocity in the LAD.

Adult↗
PubMed1999

Generation of reactive oxygen species and 8-hydroxy-2'-deoxyguanosine formation from diesel exhaust particle components in L1210 cells.

The generation of the reactive oxygen species during the interaction of diesel exhaust particles (DEP) with NADPH-cytochrome P450 reductase (P450 reductase) was investigated by electron spin resonance using the spin-trap 5,5'-dimethyl-1-pyrroline-N-oxide (DMPO). Addition of DEP extract to an incubation mixture of mouse lung microsomes in the presence of NADPH resulted in a time-dependent NADPH oxidation and acetylated-cytochrome c reduction. Using purified P450 reductase as the enzyme source, superoxide radicals which were detected as the spin adduct (DMPO-OOH) while metabolized by P450 reductase were dependent upon both DEP and enzyme concentrations. The ELISA method using a specific monoclonal antibody revealed that DEP produced 8-hydroxy-2'-deoxyguanosine (8-OHdG), which is formed from deoxyguanosine in DNA by hydroxyl radicals, in the culture medium of L1210 cells. Active oxygen scavengers such as superoxide dismutase and catalase effectively blocked the formation of 8-OHdG in culture medium, and deferoxamine, which inhibits hydroxyl radicals production by chelating iron, was also effective in inhibiting the DEP-produced 8-OHdG formation. These results indicate that DEP components produce 8-OHdG through the hydroxyl radical formation via superoxide by redox cycling of P450 reductase.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1999

Regulation of rat mesangial cell migration by platelet-derived growth factor, angiotensin II, and adrenomedullin.

This study sought to determine whether platelet-derived growth factor (PDGF) and angiotensin II (AngII) stimulate migration of cultured rat glomerular mesangial cells. After finding that this was so, the effects of adrenomedullin (ADM) and cAMP-elevating agents on basal and stimulated mesangial cell migration were examined. Two isoforms of PDGF, AB and BB, stimulated migration in a concentration-dependent manner between 1 and 50 ng/ml, while the AA isoform lacked significant effect. AngII modestly but significantly stimulated migration in a concentration-dependent manner between 10(-7) and 10(-6) mol/L. Rat ADM significantly inhibited the PDGF BB- and AngII-stimulated migration in a concentration-dependent manner between 10(-8) and 10(-7) mol/L. Inhibition by rat ADM was accompanied by an increase in cellular cAMP. cAMP agonists or inducers such as 8-bromo cAMP, forskolin, and prostaglandin I2 also significantly reduced the stimulated migration. H 89, a protein kinase A (PKA) inhibitor, attenuated the inhibitory effect of ADM, and a calcitonin gene-related peptide (CGRP) receptor antagonist, human CGRP (8-37), abolished the inhibitory effects of rat ADM. These results suggest that PDGF AB and BB as well as AngII stimulate rat mesangial cell migration and that ADM can inhibit PDGF BB- and AngII-stimulated migration, at least in part through cAMP-dependent mechanisms likely to involve specific ADM receptors with which CGRP interacts. The adenylate cyclase/cAMP/PKA system may be involved in the migration-inhibitory effect of ADM in these cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1999

Clinical findings in Japanese children with obstructive sleep apnea syndrome: focus on dental findings.

We evaluated clinical findings including those on dentistry and in the oral cavity of children with obstructive sleep apnea syndrome (OSA). This study examined twenty-seven OSA children, who were advised by otolaryngologists to be admitted for closer examination and showed an apnea index (AI) of 5 or more on polysomnographs. Their clinical history was obtained from their mothers, and oral findings were also evaluated. The patient consisted of 15 males (56%) and 12 females (44%). The mean body mass index (BMI) was 16.0 +/- 3.0. Of the clinical findings related to sleeping and the duration of sleeping, snoring was the most frequently observed finding (100%). The mean duration of sleep, calculated from the time they went to bed (9.2 +/- 0.8 p.m.) and the time they got up (7.1 +/- 0.8 a.m.), was 9.9 +/- 1.0 hours. Of the clinical findings obtained during the daytime, hyponasal speech was the most frequently observed finding (74%). In terms of dentistry, oral breathing was the most frequently observed finding (89%). The mean duration of meals was 31.7 +/- 13.8 minutes. Results of oral examination revealed that Hellman's dental age was most frequently IIA. According to the standardized grading classification, grade I was observed in 7%, II in 63%, and grade III in 30% of subjects.

Age Determination by Teeth↗
PubMed1999

A pilot study of a response oriented chemotherapeutic regimen combined with autologous peripheral blood progenitor cell transplantation in aggressive non-Hodgkin's lymphoma.

Fourteen consecutive patients with poor-risk aggressive NHL who at presentation had any one of four risk factors underwent response oriented induction chemotherapy and successive high-dose chemotherapy followed by autologous PBPC transplantation. After treatment with three cycles of conventional CHOP with G-CSF support (CHOP-G), the response was evaluated. For patients who achieved a complete remission (CR), an additional three cycles of CHOP-G were administered, while for partial response patients, another induction regimen including some non-cross-resistant agents was given; three cycles of VIPDexa-G (etoposide, ifosfamide, cisplatinum and dexamethasone) +/- two cycles of ENAP-G (mitoxantrone, etoposide, cytosine arabinoside and prednisone), were given. The scheduled induction chemotherapy, was followed by treatment with a high-dose cytoreductive regimen followed by autologous PBPC transplantation. After three cycles of CHOP-G, four patients (29%) achieved a CR, and 10 (71%) achieved a partial response (PR). When all scheduled induction therapy was completed, 10 patients (71%) had a CR. All 14 patients received high-dose therapy and obtained a complete hematologic recovery, except for one with a bone marrow relapse two months after transplantation. Evaluation of response after high-dose therapy showed 12 CRs (86%) which included three additional CRs, one PR, and one toxicity-related death. With a median follow-up of 12 months (range, 4 to 40), 12 are alive, with 11 in continuous first CR, and one relapse. The 2-year overall survival (OS) rate and event-free survival (EFS) rate are 77% and 79%, respectively, while the disease-free survival (DFS) rate is 92%. In conclusion, this pilot study suggests that response oriented induction chemotherapy and successive high-dose chemotherapy followed by autologous PBPC transplantation is commendable and can be associated with a high rate of remission and DFS for poor risk subjects with aggressive NHL.

Adolescent↗
PubMed1999

Surgical treatment for patients with cervical flexion myelopathy.

OBJECT: Cervical flexion myelopathy is a rare condition that mainly affects adolescent boys. In recent years, avoidance of neck flexion has been advocated as the treatment for cervical flexion myelopathy, and treatment with a cervical collar and surgery in which fusion of the cervical spine is performed have been found to be effective. However, previously reported series contained only a limited number of patients. The authors report their experience with treating 10 male patients in whom surgery was performed to correct cervical flexion myelopathy, and they evaluate the patients' surgical outcome. METHODS: The authors performed anterior decompressive surgery and fusion in the cervical spine by using a long bone graft after resection of one or two vertebrae in seven patients. The other three patients underwent posterior fusion of four or five laminae. After surgery, symptom progression was stopped in all patients, muscle strength improved in seven, and sensory disturbance was alleviated in another two. However, the muscular atrophy in the upper extremities, which was evident in nine patients preoperatively, improved in only two. CONCLUSIONS: Because some neurological improvement was seen in nine of 10 patients, it is believed that surgical fusion of the cervical spine is an effective treatment for patients with cervical flexion myelopathy.

Adolescent↗
PubMed1999

Excimer laser-induced hydroxyl radical formation and keratocyte death in vitro.

PURPOSE: To characterize the type of reactive oxygen species (ROS) produced by excimer photoablation of aqueous solutions and to show the effects of ROS and antioxidants on corneal stromal cells in vitro. METHODS: Electron spin-resonance spectroscopy was performed using the spin-trapping agent 5,5-dimethyl-1-pyrroline N-oxide (DMPO) for the detection of the superoxide anion and the hydroxyl radical in an acellular DMPO solution irradiated with the excimer laser. Hydroxyl radicals were produced by the Fenton reaction in vitro by the mixture of hydrogen peroxide and ferrous iron (Fe2+), and the effects on cultured corneal fibroblasts were observed by fluorescent microscopy using the cell death marker, propidium iodide (PI) and TdT-mediated dUTP nick-end labeling (TUNEL). RESULTS: Excimer photoablation of a 1% DMPO solution produced a species-specific spin-trapping adduct for the hydroxyl radical ('OH), but not for the superoxide anion or other unidentified free radical. The signals were inhibited dose dependently by the hydroxyl radical scavenger dimethylsulfoxide (DMSO) and an L-ascorbic acid analogue, EPCK-1. The production of *OH in the supernatant of cultured rabbit corneal fibroblasts by the Fenton reaction caused an increase in PI (+) and TUNEL (+) cells by 90 minutes, which was significantly inhibited by the addition of DMSO. CONCLUSIONS: Hydroxyl radicals may be partly responsible for stromal fibroblast cell apoptosis after excimer photoablation.

Animals↗
PubMed1999

Anti-atherosclerotic action of vascular D1 receptors.

1. Vascular smooth muscle cell (VSMC) migration and proliferation are believed to play key roles in atherosclerosis. To elucidate the role of vascular dopamine D1-like (D1 and D5) receptors in atherosclerosis, the effects of dopamine and the specific D1-like receptor agonists SKF 38393 and YM 435 on platelet-derived growth factor (PDGF)-BB-mediated VSMC migration, proliferation and hypertrophy were investigated. 2. We observed that cell stimulated by 5 ng/mL PDGF-BB showed increased migration, proliferation and hypertrophy. These effects were prevented by co-incubation with dopamine, SKF 38393 or YM 435 at 1-10 mumol/L and this prevention was reversed by Sch 23390 (1-10 mumol/L), a specific D1-like receptor antagonist. These actions of D1-like receptor agonists were mimicked by 1-10 mumol/L forskolin, a direct activator of adenylate cyclase, and 0.1-1 mmol/L 8-bromo-cAMP. The actions were blocked by the specific protein kinase A (PKA) inhibitor N-[2-(p-bromocinnamylamino) ethyl]-5-isoquinoline-sulphonamide (H 89), but were not blocked by its negative control N-[2-(N-formyl-p-chlorocinnamylamino) ethyl]-5-isoquinoline sulphonamide (H 85). Platelet-derived growth factor-BB (5 ng/mL)-mediated activation of phospholipase D (PLD), protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) activity was significantly suppressed by co-incubation with dopamine. 3. These results suggest that vascular D1-like receptor agonists inhibit migration, proliferation and hypertrophy of VSMC, possibly through the activation of PKA and the suppression of activated PLD, PKC and MAPK activity.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗