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Biomedical subjects

T Miyazaki

Publications and source records attributed to T Miyazaki.

At least 343 records · Page 19Linked to original sources
PubMed1996

[CD45 gating for flow cytometric analysis of acute leukemia].

Gating of leukemic cells for immunophenotyping by flow cytometry is currently set on two dimensional display of forward scatter (FSC) and side scatter (SSC). However, this gating method can not descriminate leukemic cells from contaminated normal cells (especially normal lymphocytes). Thus, in this paper, we used CD45 monoclonal antibody to detect leukemic cells (CD45dim cells) in conjunction with SSC parameter. This CD45-SSC gating revealed that this method is very useful in AML and ALL, especially leukemia with low percentage blasts. We recommend that this new gating method should be employed for more accurate immunophenotyping of acute leukemia.

Antibodies, Monoclonal↗
PubMed1996

[A case of carcinoid tumor of left superior trunk treated by sleeve upper lobectomy].

A case of bronchial carcinoid was reported. A 39-year-old male was suffered from recurrent pneumonia. Bronchofiberscopy revealed a polipoid tumor nearly obstructing left superior bronchial trunk. CT scan showed a round tumor about 1 cm in diameter. Resection of the tumor was carried out by sleeve upper lobe loectomy. Histological diagnosis was typical carcinoid, and there was no lymph node matastasis. Postoperative course was uneventful. Granulation and stenosis were not observed at the part of anastomosis.

Adult↗
PubMed1996

[Transverse lesion of the spinal cord due to mucormycosis in an AML patient].

A 54 year old man complained exertional dyspnea and palpitation since November 1989. As he was diagnosed with marked anemia, leukocytosis and thrombocytopenia by his work place doctor, he was admitted to our hospital. Acute myelogenous leukemia was diagnosed based on laboratory findings. BHAC-DMP, BHAC-MEP and A triple V therapies were only partially effective. Fine nodular shadows in all lung fields and a semicircular mass in the right lower lobe next to the thoracic vertebra were evident on the chest X-P since the end of March 1990. He was treated with antibiotics and amphotericin B but the abnormal lung shadows did not disappear. He had sudden onset of paraplegia and loss of all sensation below Th6 on May 1. Aparavertebral mass in the right lower lobe was detected by CT and MRI, for which radiotherapy was performed but without improvement. He died of respiratory failure on May 12. Autopsy showed that the semicircular paravertebral mass continued to the main pulmonary vein and epidural area of the thoracic cord (Th6-8). Microscopically, mucormycosis was found. Necrosis due to mucor embolism was found in the thoracic cord. It is usually difficult to diagnose mucormycosis in immunocompromised patients while they are alive. It is important to suspect mucormycosis if any infarction symptoms or infections resistant to antibiotics develop in immunocompromised patients.

Fatal Outcome↗
PubMed1996

Antioxidants inhibit tumor necrosis factor-alpha mediated stimulation of interleukin-8, monocyte chemoattractant protein-1, and collagenase expression in cultured human synovial cells.

OBJECTIVE: To study whether the induction of mRNA for interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and collagenase by tumor necrosis factor-alpha (TNF-alpha) is suppressed by antioxidants in human synovial cells. TNF-alpha has been shown to exert some of its effects by stimulating production of reactive oxygen intermediates in some cell lines other than synovial cells. METHODS: Amounts of mRNA for IL-8, MCP-1, and collagenase were determined by Northern blot analysis. Electrophoretic mobility shift assays were performed for the detection of a transcription factor, nuclear factor-kappa B(NF-kappa B). The concentration of IL-8 in the medium was determined by ELISA. RESULTS: TNF-alpha increased the expression of IL-8, MCP-1, and collagenase mRNA in human synovial cells. NF-KB known to induce IL-8 gene transcription was also increased in nuclear extracts from the synovial cells treated with TNF-alpha. Prior addition of antioxidant, N-acetyl-L-cysteine (NAC) or 2-oxothiazolidine-4-carboxylate (OTC), suppressed TNF-alpha stimulated expressions of IL-8, MCP-1, and collagenase mRNA in a dose dependent manner. Treatment with NAC also suppressed TNF-alpha induced increase in NF-kappa B. The changes of IL-8 in the medium reflected the mRNA levels. Hydrogen peroxide (H2O2) induced the expression of mRNA for the cytokines but not collagenase mRNA, and NAC suppressed the effect of H2O2. CONCLUSION: Our data suggest that TNF-alpha induces expression of proinflammatory cytokines such as IL-8 and MCP-1 through generation of reactive oxygen intermediates and subsequent activation of NF-kappa B in human synovial cells, and the antioxidants may inhibit, at least in part, the activation of NF-kappa B by TNF-alpha. These results indicate that antioxidants such as NAC may be useful in treating rheumatoid arthritis.

Acetylcysteine↗
PubMed1996

[Monoamine imbalance of the central nervous system in a case of Shy-Drager syndrome with recurrent attacks of a neuroleptic malignant syndrome].

A 79-year-old male suffering from Shy-Drager syndrome was treated with a daily dosage of 300 mg of L-threo-3,4-dihydroxyphenylserine (L-DOPS). He developed a neuroleptic malignant syndrome (NMS) like state 1 month after teh initiation of L-DOPS therapy. And recurrent attacks of NMS occurred subsequently despite discontinuation of L-DOPS administration. We measured homovanillic acid (HVA), 3 methoxy 4 hydroxyphenylethylenglycol (MHPG), and 5-hydroxyindoleacetic acid (5-HIAA) in this corrected brospinal fluid (CSF), both during his 2 attacks of NMS and after recovery. The HVA and 5 HIAA levels after recovery were low compared with those in age-matched normal controls. However, his levels in the active phase were not different from those after recovery. In contrast, MHPG levels were elevated and his HVA/MHPG ratios decreased in the active phase compared with those in the recovery phase. The results indicate that his symptoms of NMS are attributed to the imbalance between dopamine and noradrenalin rather than the dopamine receptor blockade in the central nervous system. We suggest further evaluations of CSF monoamine metabolites in similar cases to determine the pathogenesis of NMS.

Aged↗
PubMed1996

Coupling of the IL2 receptor complex with non-receptor protein tyrosine kinases.

IL2 induces the proliferation of T lymphocytes through the IL2 receptor (IL2R) following T lymphocyte activation. The IL2R consists of at least three subunits, IL2R alpha, beta and gamma chains. The cytoplasmic regions of the IL2R beta and gamma chains are critical for transduction of the IL2 signal to the cell interior. Although IL2R beta and gamma chains lack an intrinsic protein tyrosine kinase (PTK) domain, these chains recruit various non-receptor type PTKs, such as p56lck (and other Src family PTKs), Jak PTKs and Syk PTKs. The recruited PTKs are then activated following ligand stimulation to invoke intracellular signalling for the cell proliferation. Furthermore, it has been demonstrated that the IL2R is linked to at least three distinct signalling pathways leading to the induction of the c-fos/c-jun genes, c-myc gene induction and bcl-2 gene induction. All these pathways are essential for IL2 mediated proliferative signalling and co-operate with each other to ensure a full scale signal transduction. These signalling pathways, except that for bcl-2 pathway, appear to be mediated by multiple PTKs: p56lck is critical for the induction of the c-fos/c-jun genes, the activation of Syk PTKs results in the induction of the c-myc gene and Jak3 PTK is required for the induction of both c-fos and c-myc genes. Finally, the IL2 system may serve as a prototype in understanding the pleiotropic function of cytokine receptors that lack intrinsic PTK domains; the cytoplasmic structures of these cytokine receptors have evolved to allow the combined action of different PTK family members (and other signalling molecules) expressed in different cell types, which may determine the activity of cytokines.

Humans↗
PubMed1996

[Congenital esophago-bronchial fistula in the adult: a case report].

A 45-year-old female with congenital esophago-bronchial fistula was reported. She had suffered from common cold and recurrent bouts of coughing during meals since infancy. An esophago-bronchial fistula was detected by esophagography accidentally. The fistula was connected with right lower lobe bronchus (B6). CT scan showed the cystic change of the right lower lobe. The fistula was surgically removed and right lower lobe lobectomy was carried out. The adhesion of the lower lobe to the chest wall was recognized, but there were no inflammatory signs around the fistula. The isolation of the fistula was very easy. The postoperative course was uneventful.

Bronchial Fistula↗
PubMed1995

Detection of amphetamines in urine using head space-solid phase microextraction and chemical ionization selected ion monitoring.

An accurate, simple and rapid method for qualitative and quantitative analysis of amphetamine and methamphetamine in urine was developed using head space-solid phase microextraction and gas chromatography-mass spectrometry/chemical ionization selected iron monitoring. A vial containing a urine sample potassium carbonate and pentadeuterated methamphetamine which was used as an internal standard was heated at 80 degrees C for 20 min. The needle of a solid phase microextraction device was passed through the septum, and the extraction fiber in the needle was exposed for 5 min in the head space of the vial. The needle was removed from the vial and inserted into the injection port of gas chromatograph or gas chromatograph/mass spectrometer. The compounds adsorbed on the fiber were detached by exposing the fiber in the injection port, and analyzed. The proposed method was more than 20 times more sensitive than the conventional head space method.

Amphetamine↗
PubMed1995

Changes in epidural pressure during walking in patients with lumbar spinal stenosis.

STUDY DESIGN: This study was done to assess the pathophysiology of neurogenic intermittent claudication by measuring the epidural pressure at walking. OBJECTIVES: Changes in epidural pressure during walking in patients with neurogenic intermittent claudication and in normal individuals were analyzed. SUMMARY OF BACKGROUND DATA: Neurogenic intermittent claudication may be caused by compression of the nerve roots or may be a result of nerve root ischemia. The exact pathogenesis of neurogenic intermittent claudication is uncertain. METHODS: Local epidural pressure changes at the stenotic level during walking were analyzed in 12 patients with lumber spinal stenosis and seven normal individuals. a flexible pressure transducer was inserted into the epidural space and placed at the L4-L5 level. The epidural pressure was monitored continuously during walking. The pattern of the pressure change was assessed by gait analysis using a foot switch. RESULTS: The pressure was changed during walking. The pressure had a wave pattern of increase and decrease, and this pattern was repeated during walking. Intermittent pressure increase was seen about 90 times per minute while walking at a velocity of 2 km/h. An increase in epidural pressure occurred at the double-supporting phase in each gait cycle. CONCLUSIONS: The pressure was high in spinal stenosis and low in normal individuals. The increase of epidural pressure at simple walking was higher than walking with lumbar flexion. Intermittent compression to the nerve roots during walking may be a cause of neurogenic intermittent claudication.

Aged↗
PubMed1995

New orally active serine protease inhibitors: structural requirements for their good oral activity.

Synthesis and structural requirements for good oral activity of a series of para-substituted benzoyl esters of 4-hydroxybenzamidine serine protease inhibitors are described. The structure required for good oral activity was found to be general formula II whose corresponding ester has to be hydrolyzed in the intestine before absorption through the mucous membranes or in plasma after absorption. Biological evaluation of oral absorption using plasma anti-trypsin activity was useful for rapid evaluation. By measuring their actual plasma concentrations after oral administration, compounds 14 and 16b were confirmed to show good area under the plasma concentration-time curves (AUC). Their plasma concentrations corresponded to their plasma anti-trypsin activity. Structure-oral activity relationships are discussed.

Administration, Oral↗
PubMed1995

Critical role of the interleukin 2 (IL-2) receptor gamma-chain-associated Jak3 in the IL-2-induced c-fos and c-myc, but not bcl-2, gene induction.

The interleukin 2 receptor (IL-2R) consists of three subunits, the IL-2R alpha, IL-2R beta c, and IL-2R gamma c chains. Two Janus family protein tyrosine kinases (PTKs), Jak1 and Jak3, were shown to associate with IL-2R beta c and IL-2R gamma c, respectively, and their PTK activities are increased after IL-2 stimulation. A Jak3 mutant with truncation of the C-terminal PTK domain lacks its intrinsic kinase activity but can still associate with IL-2R gamma c. In a hematopoietic cell line, F7, that responds to either IL-2 or IL-3, overexpression of this Jak3 mutant results in selective inhibition of the IL-2-induced activation of Jak1/Jak3 PTKs and of cell proliferation. Of the three target nuclear protooncogenes of the IL-2 signaling, c-fos and c-myc genes, but not the bcl-2 gene, were found to be impaired. On the other hand, overexpression of the dominant negative form of the IL-2R gamma c chain, which lacks most of its cytoplasmic domain, in F7 cells resulted in the inhibition of all three protooncogenes. These results provide a further molecular basis for the critical role of Jak3 in IL-2 signaling and also suggest a Jak PTK-independent signaling pathway(s) for the bcl-2 gene induction by IL-2R.

Animals↗
PubMed1995

IL-2 signaling involves recruitment and activation of multiple protein tyrosine kinases by the IL-2 receptor.

The IL-2 receptor (IL-2R) consists of three subunits, the IL-2R alpha, IL-2R beta, and IL-2R gamma chains, the last of which is also used in the receptors for IL-4, IL-7, IL-9, IL-13, and IL-15. The IL-2-induced proliferative signals emanate from the cytoplasmic domains of IL-2R beta and IL-2R gamma, but the nature and function of the signaling molecules that transmit these signals are not fully understood. Here we summarize our current understanding of the mechanisms by which IL-2R transmit signals by using multiple protein kinases. In fact, at least four protein tyrosine kinases (PTKs) are physically associated with IL-2R: p56lck (and its members), Syk PTK, and the Janus kinases, Jak1 and Jak3. cDNA expression studies revealed that the activation of these PTKs is critical for IL-2-induced proliferative signal transmission. Our findings indicate that a unique property of the IL-2R cytoplasmic domains is to recruit a variety of signaling molecules, which may suggest a mechanism by which these PTKs and other signaling molecules function in concert.

Animals↗