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Biomedical subjects

K Chida

Publications and source records attributed to K Chida.

At least 109 records · Page 6Linked to original sources
PubMed1997

High incidence of positive autoantibodies against thyroid peroxidase and thyroglobulin in patients with sarcoidosis.

OBJECTIVE: Although abnormalities of the humoral immune system, such as increased immunoglobulin production, are known in sarcoidosis, the relationship between sarcoidosis and autoimmune disorders in uncertain. We studied the incidence of thyroid autoantibodies and the prevalence of Hashimoto's thyroiditis in patients with sarcoidosis. PATIENTS AND MEASUREMENTS: Sixty-two patients with pulmonary sarcoidosis, diagnosed by a combination of clinical, radiographic and histological findings were studied. As controls, three groups of subjects aged 40 and over without a known history of thyroid disease (60 patients with pulmonary diseases other than sarcoidosis, 88 hospital employees and 82 company workers), were also analysed. Antibodies against thyroid peroxidase (TPO-Ab) and purified thyroglobulin (Tg-Ab) were measured by radioimmunoassay and antibodies against microsomal antigen (MCHA) and thyroglobulin (TGHA), by haemagglutination. RESULTS: Seventeen of 62 patients (27.4%) had either positive TPO-Ab or Tg-Ab or both. All the patients with positive thyroid autoantibodies were of middle or advanced age, and the incidence of positive TPO-Ab/Tg-Ab in patients with sarcoidosis aged 40 and over was 54.5% in males, 32.4% in females and 37.8% overall. The prevalence was significantly higher in males compared to age-matched control males (0-7.7% in the controls), and in female patients was twice that found in controls (11.8-16.3%). Seven patients had Hashimoto's thyroiditis, indicating that the prevalence was 11-3%, and much higher than that previously reported. CONCLUSIONS: The data show a remarkably high incidence of thyroid autoantibodies in patients of middle of advanced age with sarcoidosis, especially in males, and a higher prevalence of Hashimoto's thyroiditis than in previous reports.

Age Factors↗
PubMed1997

Effect of 6-fluoro-8-methoxy quinolone (AM-1155) against chronic airway infection with Pseudomonas aeruginosa in a rat model.

We studied the effect of AM-1155, a newly developed quinolone, against chronic airway infection with Pseudomonas aeruginosa using a previously described rat model. AM-1155 (25 mg/kg) or ciprofloxacin (25 mg/kg) or saline (controls) were injected s.c. for 14 days (from day 4 to day 17) after the inoculation of agar beads containing P. aeruginosa. The number of viable cells of intrapulmonary P. aeruginosa, histological findings of the lungs and immunoglobulin levels of serum and bronchoalveolar lavage fluid were examined in rats 11 and 18 days after the treatment. The findings indicated that the number of viable cells of P. aeruginosa in lungs was significantly decreased in the AM-1155- or ciprofloxacin-treated group compared with the non-treated control group. Histological examination in the non-treated control group showed hyperplasia of bronchus-associated lymphoid tissue as well as cellular infiltration in airways, but not prominently in the AM-1155- or ciprofloxacin-treated group. The IgG and IgA levels in serum and bronchoalveolar lavage fluid were significantly lower in the AM-1155- and ciprofloxacin-treated groups than in the control group. These in-vivo effects of AM-1155 were comparable to those of ciprofloxacin. These findings suggest that treatment with AM-1155 and ciprofloxacin suppressed excessive immune responses, preventing progression of airway damage in the chronic infectious state.

Animals↗
PubMed1997

Dysphasia accompanied by periodic lateralized epileptiform discharges.

We encountered a 67-year-old man who presented with repetitious dysphasia accompanied by periodic lateralized epileptiform discharges (PLEDs) on the electroencephalogram. A good correlation was established between the dysphasia and the PLEDs. A persistent partial seizure accompanied by PLEDs originating in the left hemisphere presented with dysphasia clinically. None of the previously reported patients with epileptic dysphasia had accompanying PLEDs. The administration of carbamazepine was successful to terminate the seizure, however valproate was not. This case indicates that PLEDs may produce significant, however reversible, functional damage, and may advance our understanding of the pathophysiology of epileptic dysphasia.

Aged↗
PubMed1997

[Clinicopathological features of interstitial pneumonia associated with amyopathic dermatomyositis].

We studied clinicopathological characteristics of interstitial pneumonia associated with amyopathic dermatomyositis. The subjects comprised two men and three women, and their mean age was 58.2 years. All subjects had cruptions specific for dermatomyositis, but had no signs of myositis. They all presented with acutely or subacutely developed coughing and dyspnea. Results of tests for anti-Jo-1 antibody were negative in all cases. Chest X-ray films showed infiltrations or streaky shadows, or both in the middle and lower lung fields. Analysis of bronchoalveolar lavage fluid revealed abnormally high percentages of lymphocytes and neutrophils. In one patients a specimen obtained by open lung biopsy showed homogeneous cell infiltrations in alveolar septa and regional alveolar damage. That patient was successfully treated with cyclosporin and corticosteroids in early phase of the disease. The other four patients received immunosuppressive agents after respiratory failure developed. All four died despite having received high-dose corticosteroid and immunosuppressive therapy. Examination of autopsy specimens showed diffuse alveolar damage.

Acute Disease↗
PubMed1997

[A case of Ki-1 lymphoma-associated eosinophilic polymyositis].

We report on a patient of Ki-1 lymphoma-associated hypereosinophilic syndrome and eosinophilic polymyositis. A 22-year-old male was admitted to a hospital because of anterior chest pain, when he had a white cell count of 12,000 with 33% of eosinophils. He first noticed muscle weakness in the right shoulder at age 23 years. At the age of 25, he experienced marked muscle weakness in his arms and neck, which brought him to our hospital. Neurological examination on admission revealed moderate muscle atrophy and weakness in the neck flexors and both upper extremities, and marked muscle hypertrophy in the sternocleidomastoideus and trapezius muscles. Laboratory studies showed a white blood cell count of 17,700 with 56% of eosinophils. His serum creatine kinase (CK) level was elevated to 347 units. A muscle biopsy specimen showing active myositis infiltrated by eosinophils confirmed the diagnosis of eosinophilic myositis. Although eosinophilia and serum CK activity decreased markedly with corticosteroid treatment, his muscle weakness was unchanged. At the age of 27 years, lymphadenopathy developed. Immunocytochemical examination on a biopsied neck lymph node indicated Ki-1 lymphoma with positive Ki-1, CD45 and epithelial membrane antibodies. In spite of chemotherapy and local irradiation treatment, he died four months after the emergence of Ki-1 lymphoma. We discussed the relationship between hypereosinophilic syndrome, eosinophilic polymyositis and Ki-1 lymphoma on pathogenetic mechanism.

Adult↗
PubMed1997

[Prediction of outcome after acute exacerbation of idiopathic interstitial pneumonia].

Some patients with chronic idiopathic interstitial pneumonia (IIP) experience acute exacerbations (AE). Because the precise mechanisms of AE in patients with IIP remain unclear, the treatment for AE is not established and the efficacy of steroids is controversial. Consequently, it is difficult to predict outcomes in patients with AE of IIP. We therefore studied the relationship between clinical findings, efficacy of treatment, and clinical outcome in patients with AE of IIP. Thirty-two patients were enrolled, and were divided into two groups: 10 who were alive more than one year after the onset of the AE survivors, 8 men and 2 women, and 22 who died within one year of the AE (non-survivors, 17 men and 5 women). Survivors were significantly younger than non-survivors (59.7 +/- 9.9 vs 67.5 +/- 8.2 years, respectively, p < 0.05). The values of PaCO2 measured before the AE were higher in survivors than in non-survivors (43.0 +/- 3.7 vs 38.4 +/- 4.0 torr, respectively, p < 0.05). At the onset of the AE the levels of C-reactive protein in serum were higher in survivors than in non-survivors (13.9 +/- 7.9 vs 7.3 +/- 5.8 mg/dl, respectively, p < 0.05). Chest X-ray films showed progression of ground-glass shadows in both groups when the AE occurred; the radiographic findings did not differ markedly between groups. Of the 22 non-survivors, 7 had received medication before the AE; none of the survivors had received medication before the AE. At the time of the AE all patients were treated with steroid pulse therapy, and the dose of methylprednisolone used, did not differ significantly between groups. These data suggest that three factors are closely related to responsiveness to steroid therapy and to clinical outcomes after AE in patients with IIP: 1) age at the onset on IIP, 2) respiratory status before the AE, and 3) disease activity as reflected by inflammatory reactions.

Age Factors↗
PubMed1997

[Nasopharyngeal myiasis during mechanical ventilation].

We report a case of myiasis caused by Phaenicia sericata during mechanical ventilation. An 86-year-old woman with bronchiectasis was admitted to our hospital with severe respiratory failure. Treatment with mechanical ventilation and sedatives was initiated. On the 10th day of hospitalization, about 20 white larvae were found in the patient's oral or nasal cavities. The larvae were removed and identified as Phaenicia sericata. No mucosal injury was found in the patient's oral or nasal cavity by endoscopic examination. The patient died of multiple organ failure caused by sepsis that had no association with myiasis. From the clinical course and the fly's life cycle, it is considered that the fly laid eggs in the patient's oral or nasal cavity while she was sedated during mechanical ventilation. Myiasis can occur even in a hospital.

Aged↗
PubMed1996

Pathologic implications of restored positive T waves and persistent negative T waves after Q wave myocardial infarction.

OBJECTIVES: We sought to study the pathologic implications of restored positive T waves and persistent negative T waves in the chronic stage of Q wave myocardial infarction. BACKGROUND: Some inverted T waves (coronary T waves) become positive after acute myocardial infarction; others retain their negative T wave component for a long time. The pathologic implications of the difference between restored positive T waves and persistent negative T waves in leads with Q waves has not, until now, been given much careful study. METHODS: Of 17 patients with anterior or anteroseptal myocardial infarction confirmed by autopsy, 8 (group P) had positive and 9 (group N) had negative T waves in precordial leads with Q waves > or = 1 year after the onset of myocardial infarction. The appearance and extent of the infarct area and the degree of coronary artery stenosis were evaluated in both groups. RESULTS: At autopsy, seven of eight patients in group P had nontransmural fibrotic changes in the anteroseptal or anterior wall. However, seven of nine patients in group N had a transmural myocardial infarction consisting of only a thin fibrotic layer in the anteroseptal or anterior wall. The left anterior descending coronary artery showed 75% stenosis in 1 patient in each group but > 90% stenosis in the remaining 15 patients. CONCLUSIONS: Persistent negative T waves in leads with Q waves in the chronic stage of myocardial infarction indicate the presence of a transmural infarction with a thin fibrotic layer, whereas positive T waves indicate a nontransmural infarct containing viable myocardium within the layer.

Aged↗
PubMed1996

Possible involvement of an environmental agent in the development of acute eosinophilic pneumonia.

BACKGROUND: Although the pathogenesis of acute eosinophilic pneumonia remains largely unknown, it has been suggested that it may include a hypersensitivity phenomenon induced by inhaled environmental antigens. METHODS: To investigate this possibility, we studied the effect of environmental challenges in three patients with acute eosinophilic pneumonia. Symptoms and laboratory findings were evaluated before and after the challenge tests in the patient's homes and their places of work. RESULTS: After the provocation challenges to their homes, all three patients developed fever, cough, and fatigue and two of them presented with dyspnea. Inspiratory crackles became audible in all cases, and there was a decreased Pao2 level in two. Similar challenges at their workplaces were negative. After moving out of their homes, the patients engaged in their usual work but had no recurrent episodes. CONCLUSIONS: These results suggest that environmental factors in the home can be the cause of acute eosinophilic pneumonia. In order to elucidate the pathogenesis of the disease, it is important to further investigate environmental factors.

Acute Disease↗
PubMed1996

Absence of down-regulation and translocation of the eta isoform of protein kinase C in normal human keratinocytes.

Among 11 isoforms of protein kinase C (PKC), we previously reported that the eta isoform of PKC plays a crucial role in mediating differentiation of keratinocytes. Activation of PKC is associated with its intracellular translocation from the cytoplasm to the plasma membrane, followed by down-regulation through proteolytic cleavage of the PKC molecules. In the present study, we demonstrated that the eta isoform of PKC is unique in that it is not translocated nor down-regulated upon stimulation. The level of the eta isoform, assayed by immunoblotting, remained unchanged during the first 12 h and then increased slightly up to 24 h when treated with tumor promoters or activators of PKC in constitutively expressing normal human keratinocytes. The activity of the eta isoform also remained unchanged after the 12-O-tetradecanoyl-phorbol-13-acetate treatment, as judged by binding ATP analog, autophosphorylation, and phosphorylation of an exogenous substrate. The alpha isoform of PKC, however, was rapidly down-regulated and was undetectable by 6 h after the treatment. These observations were further confirmed by immunohistochemical staining of normal human keratinocytes and transiently expressing COS1 cells. In addition, although the alpha isoform rapidly translocated to the plasma membrane, the eta isoform remained in the cytoplasm.

Amino Acid Sequence↗
PubMed1996

The recessive phenotype displayed by a dominant negative microphthalmia-associated transcription factor mutant is a result of impaired nucleation potential.

In the DNA binding domain of microphthalmia-associated transcription factor (MITF), four mutations are reported: mi, Mi wh, mi ew, and mi or. MITFs encoded by the mi, Mi wh, mi ew, and Mi or mutant alleles (mi-MITF, Mi wh-MITF, Mi ew-MITF, and Mi or-MITF, respectively) interfered with the DNA binding of wild-type MITF, TFE3, and another basic helix-loop-helix leucine zipper protein in vitro. Polyclonal antibody against MITF was produced and used for investigating the subcellular localization of mutant MITFs. Immunocytochemistry and immunoblotting revealed that more than 99% of wild-type MITF and Mi wh-MITF located in nuclei of transfected NIH 3T3 and 293T cells. In contrast, mi-MITF predominantly located in the cytoplasm of cells transfected with the corresponding plasmid. When the immunoglobulin G (IgG)-conjugated peptides representing a part of the DNA binding domain containing mi and Mi wh mutations were microinjected into the cytoplasm of NRK49F cells, wild-type peptide and Mi wh-type peptide-IgG conjugate localized in nuclei but mi-type peptide-IgG conjugate was detectable only in the cytoplasm. It was also demonstrated that the nuclear translocation potential of Mi or-MITF was normal but that Mi ew-MITF was impaired as well as mi-MITF. In cotransfection assay, a strong dominant negative effect of Mi wh-MITF against wild-type MITF-dependent transactivation system on tyrosinase promoter was observed, but mi-MITF had a small effect. However, by the conjugation of simian virus 40 large-T-antigen-derived nuclear localization signal to mi-MITF, the dominant negative effect was enhanced. Furthermore, we demonstrated that the interaction between wild-type MITF and mi-MITF occurred in the cytoplasm and that mi-MITF had an inhibitory effect on nuclear localization potential of wild-type MITF.

3T3 Cells↗
PubMed1996

Bronchiolar disease in rheumatoid arthritis.

The pulmonary manifestations of rheumatoid arthritis (RA) include bronchiolar diseases such as follicular bronchiolitis (FB) and bronchiolitis obliterans (BO). In this study, we investigated the clinical and pathologic features of FB and BO, as well as the effect of erythromycin (EM) on these diseases. The subjects included 15 RA patients with biopsy-proven bronchiolar disease (eight with FB, seven with BO). None of the patients had Sjögren's syndrome. Eleven patients (73%) had chronic sinusitis, and 14 (93%) had a chronic cough with sputum. Bacterial culture of sputum was positive in 50% and 71% of the FB and BO patients, respectively. High-resolution computed tomography (HRCT) revealed small nodular shadows in the centrilobular regions (FB and BO), patchy areas of low attenuation (BO), and peribronchial thickening (FB and BO). Eleven patients who received EM therapy showed a significant improvement of symptoms. In addition, none of the 15 patients died of the bronchiolar disease during follow-up. In conclusion, RA patients with FB or BO basically have a chronic clinical course with main complaint of productive cough, and EM may be useful for the management of these diseases.

Anti-Bacterial Agents↗
PubMed1996

Cellular distribution of bronchus-associated lymphoid tissue in rheumatoid arthritis.

Bronchus-associated Lymphoid tissue (BALT) has been reported to be present in the lungs of patients with rheumatoid arthritis (RA). However, little is known about the structure and cellular distribution of BALT in this disease, so we investigated these points using immunohistochemical methods. The subjects were eight RA patients with BALT in biopsy specimens and a histologic diagnosis of follicular bronchiolitis. Seven patients had cough and purulent sputum, and four patients had positive sputum cultures. BALT was histologically composed of four distinct regions, which were the lymphoepithelium, the dome area, the follicular area, and the parafollicular area. Surface IgM+ B cells were predominant in the follicular area, whereas IgA+ cells were scattered in the dome and parafollicular areas. T cells were mainly found in the parafollicular area (CD4+ > CD8+), and most of them expressed the T Cell receptor alpha beta (alpha beta TCR). These findings were similar to those described previously for BALT in diffuse panbronchiolitis, which manifests as a chronic respiratory infection. The present study indicated that extrinsic stimulation as well as alterations of the immune response are involved in the development of BALT in RA, although the exact mechanism requires further clarification.

Adult↗
PubMed1996

A clinical study of minocycline-induced pneumonitis.

We studied the clinical features of minocycline-induced pneumonitis in seven patients. Acute symptoms included fever, dry cough and dyspnea, indicating acute respiratory failure. Diffuse ground glass shadows with Kerley's B lines, bronchial wall thickening, swelling of vascular bundles and pleural effusion were visible on radiography. Bronchoalveolar lavage or transbronchial lung biopsy confirmed pulmonary eosinophilia. Cessation of minocycline led to rapid remission with no treatment or only short-term steroid therapy. The lymphocyte stimulation test for minocycline with peripheral blood lymphocytes was not found to be useful for diagnosis.

Acute Disease↗
PubMed1996

[Clinicopathologic study of mitral regurgitation due to abnormal chordae tendineae].

Severe mitral regurgitation (MR) due to abnormal chordae tendineae as a primary cause is rare. This clinicopathologic study included four such cases which occurred among 6,500 consecutive autopsies on persons older than 60 years. This paper describes three of these cases. Case 1 was a 76-year-old woman with congestive heart failure, MR and atrial fibrillation. She died of acute myocardial infarction. The heart weighed 360 g. Mitral regurgitation was caused by a thick and long abnormal chorda originating from the posteromedial papillary muscle and protruding into the atrial surface of the middle scallop of the posterior mitral leaflet associated with prolapsed anterior mitral leaflet. Case 2 was an 81-year-old woman with MR and congestive heart failure. She died of acute myocardial infarction. The heart weighed 480 g. There were abnormal chordae tendineae with very few branches at the posterior commissure. Parts of both mitral leaflets on the sides of posterior commissure were also prolapsed. Case 3 was a 91-year-old man with MR and atrial fibrillation. He died of congestive heart failure. The heart weighed 530 g. Abnormal chordae tendineae with reticular structures originated from the anterolateral papillary muscle and protruded into the anterior mitral leaflet, which induced severe MR. These cases had abnormally protruding chordae tendineae, abnormal branching, and abnormal structures of the chordae tendineae, respectively. These abnormal chordae tendineae were considered to be congenital anomalies. Clinically all patients had a holosystolic murmur (Levine III-IV degrees), refractory congestive heart failure and atrial fibrillation. The etiology of the MR in these three patients was suspected to be ruptured chordae tendineae demonstrated on echocardiograms. These patients had heavy hearts (mean 457 g) with enlarged left atria and thickened mitral valves, which corresponded to the appearance of severe MR.

Aged↗
PubMed1996

[Immunoadsorption therapy for Fisher's syndrome: analysis of the recovery process of external ophthalmoplegia and the removal ability of anti-GQ1b antibodies].

The beneficial effect of plasma exchange, plasmapheresis or immunoadsorption therapy on Fisher's syndrome, suggested previously, has not been proved since no controlled studies have been conducted. In order to assess the effect of any treatment on Fisher's syndrome, simple and reasonable grading scales for evaluating the major neurological signs are needed. We tried immunoadsorption therapy in four patients with Fisher's syndrome, whose sera had anti-GQ1b antibodies. The clinical course was observed, with assessment of the severity of the major neurological signs based on grading scores; ranging from 0 to 30 for external ophthalmoplegia, from 0 to 10 for ataxia, and from 0 to 16 for areflexia. Tryptophan- or phenylalanine-linked polyvinyl alcohol gel column (TR-350, PH-350) was used as an adsorbent. In a patient who had IgG anti-GQ1b antibody and another patient who had both IgG and IgM anti-GQ1b antibodies, we compared the effectiveness of TR-350 and PH-350 to remove the anti-GQ1b antibody during the therapy. Two patients underwent immunoadsorption therapy at the height of clinical manifestations: in one patient, the therapy was discontinued because of critical hypotension and arrhythmia; the other was given only three sessions of therapy. The other two patients received six or seven sessions during the early recovering stage. All patients recovered without major neurological sequelae. Since ataxia was improved earlier than external ophthalmoplegia, the duration of hospitalization and the time of return to social life depended upon the recovery of external ophthalmoplegia. Analysis of the time course of external ophthalmoplegia score indicated that the improving period and the 50%-recovery day came earlier in the patients who were given a sufficient number of sessions than those who received an insufficient number of sessions. The treatment with TR-350 reduced the IgG anti-GQ1b antibody titer more than that with PH-350, but reduced the IgM anti-GQ1b antibody titer similarly. Immunoadsorption therapy using TR-350 has a probable beneficial effect on Fisher's syndrome even though it is carried out after the height of illness. The evaluation method for the severity of external ophthalmoplegia that we used in the present study is useful for assessing the effect of therapy on Fisher's syndrome.

Adult↗
PubMed1996

[Follicular bronchiolitis associated with rheumatoid arthritis].

A 52-year-old man with an 8-year history of rheumatoid arthritis was admitted to the hospital because of coughing and purulent sputum. A chest X-ray film obtained on admission showed small nodular shadows without overinflation in both lower lung fields, and a high-resolution CT scan showed many micronodular shadows in the centrilobular regions. Follicular bronchiolitis was diagnosed from the results of an open-lung biopsy, and prednisolone therapy was started at a dosage of 40 mg/day. Sinusitis developed 4 years later. Five years after the start of steroid therapy, dilation of bronchi and thickening of bronchial walls appeared on a CT scan, which also showed areas of low attenuation that were presumed to be bronchiolitis obliterans. These findings suggest that the pattern of airway disease can vary during the course of rheumatoid arthritis.

Anti-Inflammatory Agents↗