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Biomedical subjects

N Aoki

Publications and source records attributed to N Aoki.

At least 235 records · Page 13Linked to original sources

Primary directional coronary atherectomy for acute myocardial infarction.

The effectiveness of primary coronary angioplasty for acute myocardial infarction (AMI) is now widely recognized. However, the reocclusion rate is as high as 10%. Directional coronary atherectomy (DCA), now used widely in the treatment of stable and unstable angina pectoris, has not been recommended as the primary reperfusion therapy for AMI. This report describes the first preliminary study of primary DCA for AMI without any antecedent thrombolytic therapy or balloon coronary angioplasty. Five patients received primary DCA. The initial results were very good, but further study is necessary to determine the efficacy, particularly the long-term results, of primary DCA in the treatment of AMI.

Atherectomy, Coronary↗

Acute myocardial infarction in a young adult due to solitary giant cell arteritis of the coronary artery diagnosed antemortemly by primary directional coronary atherectomy.

It has been reported sporadically that several types of coronary arteritis can result in myocardial infarction. Recently, we treated a 27-year-old with acute anterior myocardial infarction. Primary directional coronary atherectomy was performed in order to recanalize the totally occluded coronary artery. The atherectomized tissue consisted of thrombi and intima infiltrated with inflammatory cells and multinucleated giant cells. Underlying diseases which can result in giant cell arteritis were excluded. This report documents that coronary arteritis can induce acute myocardial infarction, and that directional coronary atherectomy can be an effective tool in the diagnostic method for coronary arteritis.

Adult↗

Papovavirus detection by electron microscopy in the brain of an elderly patient without overt progressive multifocal leukoencephalopathy.

Virions resembling papovavirus were demonstrated in glial cells in the brain of an aged patient without overt progressive multifocal leukoencephalopathy. The patient was not in a severely immunocompromised state. On histological examination, only a few tiny incomplete necrotic foci were found in the subcortical area. These foci were widely dispersed. Rare, swollen oligodendroglial cells and astrocytes in which papovavirus capsid protein (VP-1) was demonstrated immunohistochemically were present around the foci. The two typical types of virus particles i.e. 35 to 40 nm round particles and elongated particles, were observed in the nuclei of the swollen glial cells. The latter were in the minority. Distinct crystals were also found in the nuclei. The centre-to-centre distance of the particles in the crystals, about 40 nm, and the electron-opaque spots of the round-shaped virions and of the elongated particles, were indicative of structural subunits of papovavirus capsids. This case provides further evidence that papovavirus, possibly JC virus, may be reactivated in the brains of aged patients who are not in an immunocompromised state.

Aged↗

Plasma thrombomodulin as an indicator of thromboembolic disease in systemic lupus erythematosus.

We serially measured the plasma thrombomodulin (TM) levels in systemic lupus erythematosus (SLE) patients and assessed them clinically. The patients who responded to medical treatment experienced a decrease in plasma TM levels. Patients who developed exacerbations of SLE, thrombotic thrombocytopenic purpura or thrombosis, displayed increased plasma TM levels. There was no significant difference between the plasma TM levels of the lupus anticoagulant-positive (LAC-positive) patients and the LAC-negative patients or between the plasma TM levels of the anticardiolipin antibody-positive (aCL-positive) patients and the aCL-negative patients. While LAC and aCL titers did not always coincide with improvement in the patients' clinical course or with aggravation of the disease, the TM values correlated well with the patients' clinical condition. Plasma TM values may be used to evaluate disease activity and may predict the occurrence of thrombosis in SLE.

Antibodies, Anticardiolipin↗

Plasma thrombomodulin as a marker of vascular injuries in collagen vascular diseases.

Thrombomodulin, a thrombin receptor on the vascular endothelial cell surface, is released into circulating blood. The plasma concentrations in patients with collagen vascular diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis, juvenile rheumatoid arthritis, Sjögren's syndrome, systemic sclerosis, polymyositis and/or dermatomyositis (PM/DM), Behçet's disease, and Wegener's granulomatosis, were measured and compared with those of healthy persons. The mean plasma thrombomodulin concentrations in patients with juvenile rheumatoid arthritis, systemic sclerosis, PM/DM, Wegener's granulomatosis, and active states of SLE, rheumatoid arthritis, and Beçhet's disease were significantly higher than those in the control group. Patients with Wegener's granulomatosis showed the highest mean value. The mean values in patients with inactive states of the diseases and Sjögren's syndrome were not significantly different from the values in the control group. In cases of juvenile rheumatoid arthritis, systemic sclerosis, PM/DM, and Wegener's granulomatosis, patients with active interstitial pneumonitis or extensive pulmonary lesions frequently showed higher values of plasma thrombomodulin than those without overt pulmonary involvement. Elevated plasma thrombomodulin values were decreased along with amelioration of the diseases by treatment. These results may indicate that plasma thrombomodulin measurement may be helpful for evaluating vascular injury in patients with collagen diseases.

Adult↗

Secretion of alpha 2-plasmin inhibitor is impaired by amino acid deletion in a small region of the molecule.

Alpha 2-plasmin inhibitor (alpha 2PI) deficiency Okinawa results from defective secretion of the inhibitor from the liver and appears to be a direct consequence of the deletion of Glu137 in the amino acid sequence of alpha 2PI. To examine the effects of replacing the amino acid occupying position 137 or deleting its neighboring amino acid on alpha 2PI secretion, we used oligonucleotide-directed mutagenesis of alpha 2PI cDNA to change the codon specifying Glu137 or delete a codon specifying its neighboring amino acid. The effects were determined by pulse-chase experiments and by enzyme-linked immunosorbent assay of media from transiently transfected COS-7 cells. Replacement of Glu137 with an amino acid other than Cys had little effect on alpha 2PI secretion. In contrast, deletion of an amino acid in a region spanning a sequence of less than 30 amino acids including positions 127 and 137 severely impaired the secretion. The results suggest that structural integrity of the region, rather than its component amino acids, is important for the intracellular transport and secretion of alpha 2PI.

Amino Acid Sequence↗

Ultrastructure of human skin by a rapid freezing technique: structural preservation and antigenicity.

To investigate the natural fine structure of skin, human skin biopsies were studied by electron microscopy and immunoelectron microscopy using rapid freezing and freeze-substitution techniques. Well-preserved structures were observed within a depth of 20 microns from the slammed surface of the samples. Epidermal cells were always closely located with very narrow intercellular spaces. Keratin filaments were distributed densely and homogeneously without forming bundles in the cytoplasm of epidermal keratinocytes. Langerhans cell granules were composed of a flat vesicular portion and an oval rod portion. The most striking finding was in the dermal-epidermal junction, where the lamina densa was present but no lamina lucida was observed. Further, by immunoelectron microscopy with anti-keratin monoclonal antibody, the 20-microns-deep part of the samples revealed the most significant staining. These findings indicate that the ultrastructure of routinely processed skin samples may be modified during the procedure for conventional chemical fixation and dehydration and that the ultrastructurally most preserved specimens, reflecting the conditions close to natural in vivo structures of the skin, can be obtained by the techniques described in this paper.

Adolescent↗

Rearrangement of bcl-2 is detectable in Hodgkin's disease by polymerase chain reaction.

The authors examined the occurrence of the t(14;18) chromosomal translocation in 44 cases of Hodgkin's disease (HD) using the polymerase chain reaction and Southern blot hybridization with non-radioactive oligonucleotide probes. DNAs were extracted from unfixed, fresh-frozen and formalin-fixed, paraffin-embedded biopsy specimens. Southern blot hybridization of the amplification product showed that, of 44 HD DNAs, three had a detectable t(14;18) breakpoint at the mbr (major breakpoint region), while none had a detectable t(14;18) breakpoint at the mcr (minor cluster region). Of the three cases positive for a t(14;18) breakpoint at the mbr, two were of lymphocyte predominance type, and the other was of mixed cellularity type.

Apoptosis↗

Variant translocation of the BCL6 gene to immunoglobulin kappa light chain gene in B-cell lymphoma.

A lymphoma cell line with a variant type of translocation, t(2;3)(p11;q27), was established from a patient who had received liver transplantation. To elucidate the molecular mechanism of the t(2;3)(p11;q27) chromosomal translocation, we compared the structures of both derivative (der) chromosomal breakpoints with those of their germline predecessors. We noted that the BCL6 gene on chromosome 3 was juxtaposed with the immunoglobulin kappa light chain (Ig kappa) gene on chromosome 2 in a head-to-head configuration. The breakpoint of the BCL6 gene was within a previously reported breakpoint cluster region. The breakpoint on chromosome 2 was within the intron between the leader (L) and variable (V) sequences of one of the V kappa genes, which was fused to the J kappa 3 (J = joining) segment. At chromosomal junctures, a direct repeat duplication of chromosome 3 sequences and a deletion of chromosome 2 sequences were discovered. These results are consistent with a translocation model with illegitimate pairing of staggered double-stranded DNA breaks at 3q27 and 2p11, repair, and ligation to generate der(3) and der(2) chromosomes.

Base Sequence↗

Determination of plasma tissue factor antigen and its clinical significance.

To investigate the clinical significance of determination of plasma tissue factor (TF) antigen, we have developed a highly sensitive enzyme-linked immunosorbent assay (ELISA) for plasma TF, using two different monoclonal antibodies against TF apoprotein, 6B4 (catching antibody) and 5G9 (detecting antibody), and tetramethyl benzidine/H2O2 as substrates. Titration curves of recombinant human TF in buffer containing Triton X-100 were linear within the range from 50 to 2000 pg/ml. The total assay time was 3 h. Ultracentrifugation and immunoblot analysis indicated that human plasma and urine contained 50,000 g sedimentable and non-sedimentable forms of TF, both of which were detected by our ELISA method. Plasma and urine concentrations of TF in healthy subjects and patients with various diseases were measured by the ELISA method. In healthy subjects, plasma and urinary TF levels were found to be 149 +/- 72 pg/ml (n = 30) and 175 +/- 60 pg TF/urine creatinine mg (n = 95), respectively. TF was increased in plasma of patients with disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura, vasculitis associated with collagen diseases, diabetic microangiopathy and chronic renal failure receiving haemodialysis, but not in the plasma of endotoxaemic patients without DIC. The plasma TF/serum creatinine ratio did not show a positive correlation. Measurement of TF antigen in plasma may be useful for evaluating the endothelial damage and cell destruction in TF-containing tissues.

Adult↗

Plasma thrombomodulin in Wegener's granulomatosis as an indicator of vascular injuries.

OBJECTIVE: To compare the concentrations of thrombomodulin (TM) and titers of antineutrophil cytoplasmic antibodies (ANCA) in plasma of patients with Wegener's granulomatosis (WG). PATIENTS: Nine patients with WG were diagnosed according to the clinical criteria and histologic findings of biopsy specimens. MEASUREMENTS AND RESULTS: The concentrations of plasma TM were measured by enzyme-linked immunosorbent assay (ELISA). Titers of ANCA were determined by immunofluorescence technique (cANCA) and by ELISA (anti-PR-3 Ab). The mean plasma TM concentration in patients with WG at an active stage was significantly higher than that of normal control, but that in remission was not significantly different from the normal value. More organs were involved, higher plasma TM levels were observed. The elevated plasma levels of TM returned to normal when the patients were treated successfully and in remission. The cANCA and anti-PR-3 Ab did not correlate with the severity of vasculitis in patients with active WG, although the antibodies determined by both methods were always negative in patients with inactive WG. Postmortem examination of one patient, who died of respiratory failure resulting from diffuse pulmonary hemorrhage, revealed pulmonary capillaritis with the total absence of TM in the lesions involved, suggesting that TM had been released totally from injured capillary endothelial cells. CONCLUSIONS: These results suggest that the plasma TM level may be a useful indicator of the extent of vascular injury in WG.

Adult↗

Evolution of chronic subdural hematoma after burr-hole exploration for subdural effusion--case report.

A 57-year-old male developed subdural effusion after head trauma, which remained asymptomatic and unchanged in volume during a follow-up period of 3 months. A typical chronic subdural hematoma (CSDH) developed 6 weeks after burr-hole exploration in spite of the absence of hematoma capsule or blood components in the effusion. The CSDH was successfully treated by irrigation and drainage. This case suggests that the presence of blood in subdural effusion may be the trigger for evolution of CSDH. We recommend that asymptomatic subdural effusion should be followed up without surgical intervention.

Brain↗

Extracerebral fluid collections in infancy: role of magnetic resonance imaging in differentiation between subdural effusion and subarachnoid space enlargement.

The pathological process of extracerebral fluid collections in infancy includes subdural effusion and enlargement of the subarachnoid spaces. Both conditions have traditionally been investigated as a single clinical entity, because of difficulty in differentiating between them. The prognosis of subdural effusion is not as benign as that of enlargement of subarachnoid spaces, requiring differential diagnosis between these disorders. The present study was conducted to elucidate whether this differentiation could be made on magnetic resonance (MR) images. The series consisted of 16 infants aged 10 months or younger, including eight with verified subdural effusion and eight in whom a diagnosis of enlargement of the subarachnoid spaces was achieved by neuroimaging studies other than MR imaging. In all eight patients with subdural effusion, the intensity of the fluid was greater than that of cerebrospinal fluid (CSF) in at least one of the sequences using T1-weighted, proton-density, and T2-weighted MR images. The flow-void sign, indicating vessels in the fluid spaces, was not seen in any of these eight patients. On the other hand, in all eight patients with enlargement of the subarachnoid spaces, the fluid was isointense in relation to CSF, and vascular flow-void areas were seen in at least one of the MR imaging sequences. Based on these observations, it is concluded that differentiation between subdural effusion and enlargement of the subarachnoid spaces can be established by focusing on two aspects of MR imaging findings: 1) the intensity of the fluid, which is either iso- or hyperintense relative to CSF, and 2) the presence or absence of vascular flow-void areas in the fluid spaces.

Contrast Media↗

Compound heterozygous protein C deficiency caused by two mutations, Arg-178 to Gln and Cys-331 to Arg, leading to impaired secretion of mutant protein C.

The protein C gene in a patient apparently homozygous for protein C deficiency was analyzed. Two different point mutations, each located in a different allele, were detected to reveal that the patient is a compound heterozygote. Mutation of Arg-178 (CGG) to Gln (CAG) [mutation I] was detected in exon VII, in the vicinity of activation peptide cleavage site by thrombin. Mutation of Cys-331 (TGC) to Arg (CGC) [mutation II] was found in exon IX, at one of the sites involved in disulfide bond formation in the catalytic domain of the heavy chain. The alteration of Cys-331 to Arg disables the formation of the disulfide bond and would alter the protein conformation. Transient expression assays using COS-7 cells transfected with protein C expression vectors containing each one of these two mutations suggested that each of the two mutations would lead to the protein C deficiency by an impairment of secretion of the respective mutant proteins.

Alleles↗

[Metastasis of an adenocarcinoma of unknown origin to mediastinal lymph nodes, and transient regression].

A 67-year-old woman was admitted to our hospital because of fever. Chest roentgenogram showed an enlargement of mediastinal lymph nodes. Despite thorough examination, no definite diagnosis could be made. The mediastinal lymph nodes got smaller over the next 3 weeks and a chest roentgenogram taken 4 months later showed no mediastinal lymphadenopathy. The mediastinal lymphadenopathy and fever recurred 5 months later. She underwent thoracotomy and the mediastinal lymph nodes were excised. Microscopic examination of pretracheal lymph node specimens showed invasion of poorly differentiated adenocarcinoma associated with abundant tumor-infiltrating lymphocytes. The other lymph nodes showed sarcoid reaction. Although she has been followed for one year and 11 months, no primary site of the cancer has been found. Metastasis of cancer of unknown origin to mediastinal lymph nodes is extremely rare. It is also interesting that the lymph node swelling diminished spontaneously. The tumor-infiltrating lymphocytes and sarcoid reactions may have been immunological responses to the cancer and may have caused the transient regression.

Adenocarcinoma↗

[Blood concentrations of thrombomodulin in patients with various diseases].

Concentrations of thrombomodulin in blood plasma were measured by a one-step sandwich enzyme immunoassay (EIA). The concentrations in normal healthy subjects were 9.9 +/- 2.9 ng/ml. The concentrations were found to be significantly higher in patients with SLE, RA and other collagen diseases in their active stages than at their non-active stages. The concentrations increased in patients with DIC, and significantly higher levels were observed when DIC was complicated by multiple organ failure. These findings indicate that plasma concentrations of thrombomodulin may be a useful parameter for vascular injuries caused by inflammatory processes or coagulation/fibrinolysis reactions.

Adult↗