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Biomedical subjects

K Fujii

Publications and source records attributed to K Fujii.

At least 253 records · Page 14Linked to original sources

Relationship between exercise capacity and ventilatory equivalent for carbon dioxide in patients with stable old myocardial infarction.

The aim of the present study was to evaluate the relationship between exercise capacity and ventilatory response in patients with stable old myocardial infarction. We performed cardiopulmonary exercise test in 61 patients with stable old myocardial infarction and in 30 healthy men. Each subject exercised on a bicycle ergometer until exhaustion. Patients who had anginal pain or electrocardiographic ischemic changes during exercise were excluded. The patients were classified into three groups according to peakVO2 achieved during exercise, using Weber's method: group A, peakVO2 > or = 21 ml/min/kg (n = 4); group B, 14 < or = peakVO2 < 21 ml/min/kg (n = 45); and group C, peakVO2 < 14 ml/min/kg (n = 12). With progressive increases in VCO2, VE increased linearly below the anaerobic threshold (AT) level. The slope of the linear regression line between VCO2 and VE (SLOPE) was calculated in each subject. The mean SLOPE of the healthy men (group N) and groups A, B and C were 25.8 +/- 0.5, 25.1 +/- 0.5, 28.9 +/- 0.8 and 37.1 +/- 1.7 (x 10(-3), respectively. Thus, the SLOPE was steeper in patients with lower peakVO2. It is difficult to perform a maximal exercise tolerance test on patients with chronic heart failure to evaluate their exercise capacity. We can assess exercise capacity by the slope of the linear regression line between VCO2 and VE (SLOPE) at the lower exercise level.

Aged↗

G-CSF induces apoptosis of a human acute promyelocytic leukemia cell line, UF-1: possible involvement of Stat3 activation and altered Bax expression.

Granulocyte colony-stimulating factor (G-CSF) is a cytokine that regulates the proliferation, differentiation and survival of cells in the granulocytic lineage. In this study, however, we found that G-CSF or interleukin-6 (IL-6) induced UF-1, a human acute promyelocytic leukemia cell line, into apoptosis that was confirmed by morphological features and DNA fragmentation. This rare response is demonstrated for the first time with human acute promyelocytic leukemia cell line. The apoptosis induced by G-CSF or IL-6 was not preceded by terminal differentiation characterized by morphological maturation, capability to reduce nitroblue tetrazolium, or surface CD11b expression. Interestingly, Western blot analysis revealed that the stimulation of UF-1 with either G-CSF or IL-6 resulted in excessive activation of both signal transducer and activator of transcription 3alpha (Stat3alpha) and Stat3beta. Furthermore, an additional 18 kDa Bax-related protein was expressed by the stimulation of G-CSF or IL-6, while Bcl-2 and Bcl-X proteins remained unchanged. These findings suggest that UF-1 may be a valuable tool in investigating the aberrant regulation of apoptosis, especially the Stat3 involvement in the mechanism of apoptosis induction.

Apoptosis↗

Lumbar spinal subdural hematoma following craniotomy--case report.

A 52-year-old female complained of lumbago and weakness in the lower extremities 6 days after craniotomy for clipping an aneurysm. Neurological examination revealed symptoms consistent with lumbosacral cauda equina compression. The symptoms affecting the lower extremities spontaneously disappeared within 3 days. Magnetic resonance (MR) imaging 10 days after the operation demonstrated a lumbar spinal subdural hematoma (SSH). She had no risk factor for bleeding at this site, the symptoms appeared after she began to walk, and MR imaging suggested the SSH was subacute. Therefore, the SSH was probably due to downward movement of blood from the cranial subdural space under the influence of gravity. SSH as a complication of cranial surgery is rare, but should be considered if a patient develops symptoms consistent with a lumbar SSH after craniotomy.

Brain↗

Bow hunter's stroke associated with an aberrant course of the vertebral artery--case report.

A 53-year-old male presented with repeated vertebrobasilar insufficiency on turning the head to the left. Angiography revealed severe stenosis of the dominant right vertebral artery at the atlantoaxial level in this position. Decompression surgery for the affected vertebral artery at the transverse foramen of the atlas was planned. However, surgery revealed an aberrant course of the artery, turning at the orifice of the transverse foramen of the atlas and perforating the dura at the occipitoatlantal level after passing through the bony canal of the atlas. Therefore, decompression was performed at the bony canal, which was the contributing site, and the symptoms improved. Bow hunter's stroke may be caused by atlantoaxial arterial anomalies, so accurate preoperative evaluation of the region is necessary to avoid anatomical confusion at surgery.

Atlanto-Axial Joint↗

[A case of mixed connective tissue disease with microscopic polyarteritis nodosa associated with perinuclear-antineutrophil cytoplasmic antibody and anti-glomerular basement membrane].

A 46-year-old female was admitted to our hospital due to general fatigue, systemic edema and dyspnea with history of systemic sclerosis (SSc). The patient was diagnosed as mixed connective tissue disease (MCTD) based on Raynaud phenomenon, a high anti-RNP antibody level and clinical symptoms and laboratory findings suggesting SSc, dermatomyositis (DM) and systemic lupus erythematosus (SLE). After the admission, both alveolar hemorrhage and a rapidly progressive glomerulonephritis (RPGN) also developed and laboratory findings showed a positive remark of myeloperoxydase-antineutrophil cytoplasmic antibody (MPO-ANCA) and anti-glomerular basement membrane (GBM) antibody. She was therefore re-diagnosed as microscopic polyarteritis nodosa (microscopic PAN) combined with MCTD and treatment with high dose prednisolone and steroid pulse therapy dramatically improved general conditions and lung symptoms, but maintenance dialysis was persistent because of irreversible renal failure. However, 3 months after the admission, she died of acute exacerbation of interstitial pneumonitis that was unresponsive to steroid pulse therapy. Autopsy revealed interstitial pneumonitis with alveolar hemorrhage and crescentic glomerulonephritis (CrGN), in which immunofluorescent microscopy showed no deposition in agreement with pauciimmune type. The histological findings supported the diagnosis; primary microscopic PAN combined with MCTD, which is a quite rare case, to our knowledge. Furthermore, co-existence of MPO ANCA and anti-GBM antibody, clinical and histological findings of the case also lead us to reconsider the relevance of these antibodies to pathogenesis and/or categories of microscopic PAN and Goodpasture's syndrome.

Antibodies, Antineutrophil Cytoplasmic↗

Effects of thermal cycling on dynamic viscoelastic properties of four commercial resins for crown and bridge.

To elucidate the effects of thermal cycling on the viscoelastic properties of four commercial resins for crown and bridge, dynamic shear modulus (G'), mechanical loss tangent (tan delta), Knoop hardness, water sorption and appearance of specimen surfaces before and after thermal cycling test were determined. The changes of G' and tan delta for two materials were insignificant with increased repetitions of thermal cycling. Those of the other two materials were statistically significant: in particular, G' at temperatures above 60 degrees C was inclined to increase slightly and tan delta decreased considerably. While the Knoop hardness of the materials was a little decreased over a number of 75,000 thermal cycles, the water sorption almost attained an equilibrium in uptake after 14,000 thermal cycles. Furthermore, cracks on the specimen surface were observed after 37,500 to 75,000 thermal cycles. From these results, the deterioration of materials was observed as damage to the specimen surface. Moreover, it could be presumed that the materials would be further polymerized during the period of thermal cycling.

Analysis of Variance↗

Tissue response of a small saccular aneurysm after incomplete occlusion with a Guglielmi detachable coil.

A 49-year-old woman had a small saccular aneurysm that was incompletely occluded with a Guglielmi detachable coil (GDC). She died from rupture of another aneurysm 42 days after the treatment. Autopsy for the embolized aneurysm revealed no neoendothelium at the aneurysmal neck, but an organized thrombus was observed limited to the periphery of the aneurysmal lumen. Although isolation of the aneurysm was not apparent, loose embolization with this method may help to reinforce the aneurysmal wall.

Aneurysm, Ruptured↗

[Prolonged effects of vecuronium in a patient with Crow-Fukase syndrome].

We gave anesthesia to a patient with the Crow-Fukase syndrome. A patient with this syndrome shows polyneuropathy, endocrinological symptoms, skin change, hypertrichosis, organomegaly and osteosclerotic change. We monitored the effects of vecuronium using a neuromuscular blockade monitor. The patient with this syndrome was hypersensitive to vecuronium and its effects lasted longer than usual. It is important to monitor neuromuscular blockade carefully in patients with this syndrome.

Anesthesia, General↗

Novel patterns of amino acid mutations in the hepatitis B virus polymerase in association with resistance to lamivudine therapy in japanese patients with chronic hepatitis B.

Lamivudine is effective in suppressing replication of hepatitis B virus (HBV). However, the emergence of HBV variants resistant to lamivudine is a concern. Lamivudine resistance has been attributed mainly to a substitution of isoleucine or valine for methionine at residue 550 (M550I or M550V) in the catalytic site of the virus polymerase. A substitution of methionine for leucine at residue 526 (L526M) has also been identified. To examine such virus genotypic mutations in Japanese patients, we studied five patients with chronic hepatitis B, who showed HBV breakthrough while on a 1-year lamivudine treatment. The entire nucleotide and deduced amino acid sequences of the proposed reverse transcriptase domain of the polymerase gene were determined on HBV DNA amplified by polymerase chain reaction from patient sera collected at the start and at the end of therapy. The HBV sequences from all five patients were of genotype C. In four patients, a substitution of valine or isoleucine for leucine at residue 426, which has not been reported previously, emerged in combination with M550I. One also harbored L526M. In the remaining patient, an alteration of leucine to methionine at residue 428 co-occurred with M550V. Longitudinal study of the mutations showed that the two or three mutations in each patient emerged almost simultaneously 4 weeks before or at the time of breakthrough and were replaced by wild-type virus after completing the therapy. Our results indicate that occurrence of HBV polymerase mutations at residue 426 in combination with M550I is frequent in Japanese or genotype C virus-in- fected patients who develop resistance to lamivudine.

Adult↗

Etretinate therapy for papuloerythroderma.

Papuloerythroderma, first reported by Ofuji et al. (1984), is a rare cutaneous disorder whose pathogenesis remains unknown. Owing to the small number of cases, there is no recommended choice of treatment. This is the first report on the efficacy of etretinate for papuloerythroderma. Seven male cases ranging in age from 65 to 84 years were treated with moderate doses (0.2-0.6 mg/kg/day) of etretinate. All but one case showed quick and excellent responses and the chronic recalcitrant erythrodermatous lesions disappeared within 2-5 weeks. Eventually all the seven cases could be brought into remission. Once remission was achieved, etretinate was tapered by 0.1-0.2 mg/kg/day over a period of 2-4 weeks. One case remained in complete remission after cessation of etretinate without any treatment for 16 months. Another case could stop etretinate treatment and the subsequent recurrence of papular eruption could be managed by topical steroids. In the other five cases remission could be maintained by daily doses of 0.16-0.36 mg/kg etretinate. None of the patients developed severe side effects. Our observation suggests that etretinate is a safe and effective agent for papuloerythroderma.

Aged↗

Crosslinking of CD44 on rheumatoid synovial cells augment interleukin 6 production.

CD44 is a ubiquitous molecule also known as hyaluronic acid or homing receptor. However, its cellular functions and its role in inflammation, for example rheumatoid synovitis, are currently unknown. Here we propose a novel function for CD44. Using synovial cells from patients with rheumatoid arthritis (RA), we demonstrated that CD44 crosslinking and binding to hyaluronan augmented IL-6 production. Briefly, we found that (a) rheumatoid synovial cells highly expressed CD44; (b) crosslinking of CD44 augmented IL-6 production and its mRNA transcription; (c) hyaluronan, especially when fragmented, also increased IL-6 production; and (d) CD44 activated the transcription factor activator protein-1 and CAMP-responsive element binding protein. These results indicate that the adhesion of RA synovial cells to matrices such as hyaluronic acid through CD44 could activate transcription factor, resulting in cytokine production. We therefore propose that the function of adhesion molecules as a signaling molecule may be pivotal in the pathogenesis of inflammation, including RA synovitis.

Arthritis, Rheumatoid↗

Differential regulation of monocyte matrix metalloproteinase and TIMP-1 production by TNF-alpha, granulocyte-macrophage CSF, and IL-1 beta through prostaglandin-dependent and -independent mechanisms.

Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) produced by monocytes are believed to be involved in the migration of these cells through the basement membrane and the ensuing destruction of connective tissue in chronic inflammatory lesions. Because monocytes encounter a variety of cytokines at these sites, we examined the effect of cytokines either alone or in combination on the production of monocyte MMPs and TIMP-1. TNF-alpha, granulocyte-macrophage-CSF (GM-CSF), or IL-1 beta when added individually enhanced the endogenous levels of 92-kDa gelatinase (MMP-9) and TIMP-1 but failed to induce interstitial collagenase (MMP-1). However, GM-CSF, when added with either TNF-alpha or IL-1 beta, induced MMP-1 and synergistically enhanced MMP-9 and TIMP-1. Th2 cytokines, such as IL-4, inhibited the induction of MMPs and TIMP-1 by TNF-alpha, GM-CSF, and IL-1. Cytokine stimulation of MMP-1 was due, at least in part, to an increase in the release of arachidonic acid and PG E2 (PGE2), because inhibition of MMP-1 by indomethacin could be reversed by exogenous PGE2. In contrast to MMP-1, cytokine stimulation of MMP-9 and TIMP-1 was unaffected by indomethacin. The PGE2-independent induction of monocyte MMP-9 and TIMP-1 by these cytokines differed from stimulation of MMP-9 and TIMP-1 by LPS, which is in large part PG-dependent. In addition, LPS stimulated higher levels of MMP-1 whereas cytokines induced higher levels of MMP-9 and TIMP-1. This is the first demonstration that monocyte MMP-1 can be induced by cytokines and that MMP-1, MMP-9, and TIMP-1 are differentially regulated by cytokines through PG-dependent and -independent mechanisms.

Arachidonic Acid↗

Role of IQGAP1, a target of the small GTPases Cdc42 and Rac1, in regulation of E-cadherin- mediated cell-cell adhesion.

The small guanosine triphosphatases (GTPases) Cdc42 and Rac1 regulate E-cadherin-mediated cell-cell adhesion. IQGAP1, a target of Cdc42 and Rac1, was localized with E-cadherin and beta-catenin at sites of cell-cell contact in mouse L fibroblasts expressing E-cadherin (EL cells), and interacted with E-cadherin and beta-catenin both in vivo and in vitro. IQGAP1 induced the dissociation of alpha-catenin from a cadherin-catenin complex in vitro and in vivo. Overexpression of IQGAP1 in EL cells, but not in L cells expressing an E-cadherin-alpha-catenin chimeric protein, resulted in a decrease in E-cadherin-mediated cell-cell adhesive activity. Thus, IQGAP1, acting downstream of Cdc42 and Rac1, appears to regulate cell-cell adhesion through the cadherin-catenin pathway.

Animals↗