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K Chida

Publications and source records attributed to K Chida.

At least 73 records · Page 4Linked to original sources
PubMed1994

[A case of recurrent pulmonary thromboembolism presenting with positive antiphospholipid antibodies].

A 76-year-old man was admitted to our hospital in December of 1990, for investigation of progressive dyspnea on exertion over the previous 3 months. Physical examination revealed cyanosis, but no edema. Cardiomegaly was seen on chest X-ray, and findings compatible with right-sided congestive heart failure were revealed by ECG and echocardiography. Lung perfusion scintigrams showed multiple defects in both lungs, but no abnormal findings were detected on a ventilation study. Venograms of the lower extremities disclosed thrombosis of the right femoral vein. Therefore, a diagnosis of recurrent pulmonary thromboembolism was made. Furthermore, lupus anticoagulant and IgG-class anticardiolipin antibody were noted in the serum. The patient was treated with intravenous heparin, long-term warfarin, and transvenous placement of a Greenfield filter in the inferior vena cava. The clinical symptoms and signs improved, and no recurrence has been seen during the 13 months since the onset. On discharge, both antiphospholipid antibodies were negative. This case of primary antiphospholipid syndrome without autoimmune disease, with transiently positive antibodies only in the exacerbation phase, is discussed herein.

Aged↗
PubMed1994

[A case of acute interstitial pneumonia caused by blasticidin S].

A 41-year-old male developed acute interstitial pneumonia after inhalation of Blasticidin S, an antibiotic effective against rice blast disease. He presented with diarrhea, followed by dry cough, dyspnea and fever. A chest roentgenogram showed bilateral diffuse ground glass appearance, superimposed by patchy shadows. Arterial blood gas analysis revealed severe hypoxemia. Bronchoalveolar lavage fluid specimen showed moderate increase in total cell count, lymphocytes, neutrophils and eosinophils with marked elevation of CD4/8 ratio. Antibiotic therapy with minocycline failed to improve his condition, and methylprednisolone pulse therapy followed by methylprednisolone (48 mg) resulted in clinical remission with resolution of the chest roentgenogram findings. Blasticidin S should be kept in mind as a causative agent of acute interstitial pneumonia.

Acute Disease↗
PubMed1994

[A case of so-called benign metastasizing leiomyoma].

A 44-year-old female was admitted to our hospital for the purpose of undergoing hysterectomy for removal of multiple uterine tumors. A chest X-ray film obtained on admission revealed a solitary nodule in the right lung field. The resected specimen containing the uterine tumors revealed well differentiated leiomyoma with no nuclear atypia or mitotic figures. The resected specimen from the pulmonary tumor revealed histologic findings similar to those of the uterine myomas, being devoid of any signs of mitosis. Similar cases have been reported as so-called benign metastasizing leiomyoma, and are generally regarded as low grade malignancy or leiomyomatosis. However, we consider this case to have had a primary pulmonary leiomyoma associated with uterine myoma since the pulmonary lesion was solitary and no mitotic figures were detectable. As the concept of metastasizing leiomyoma is confusing, the accumulation of additional case reports is necessary.

Adult↗
PubMed1994

[A case of eosinophilic pneumonia caused by inhalation of nickel dusts].

A 16-year-old male, an industrial high school student working at an ironworks, without a dust mask, began to complain of dry cough and fever several hours after inhalation of stainless steel dusts including 0.1% nickel. A chest X-ray film revealed ground glass shadows, patchy shadows and Kerley B lines in the right lung fields. A high resolution chest CT scan showed fusing panlobular densities, thickening of bronchial walls and thickening of interlobular septa. Blood cells counts revealed leucocytosis with eosinophilia. Arterial blood gas analysis revealed hypoxemia. A bronchoalveolar lavage fluid specimen showed a marked increase in the total cell count and in eosinophils. A transbronchial biopsy specimen showed eosinophilic and lymphocytic infiltration in the alveolar septa. Steroid therapy with methylpredonisolne (250 mg x three days) resulted in clinical remission. As we suspected nickel-induced eosinophilic pneumonia, an inhalation provocation test with 0.5% nickel sulfate solution was carried out with the patient's informed consent. Six hours after inhalation he developed a dry cough and fever with leucocytosis and A-aDo2 widening. The positive results of the inhalation provocation test provided a definite diagnosis of nickel induced eosinophilic pneumonia. A review of the world literature revealed three case reports of nickel induced PIE syndrome, all of whom were clinically diagnosed without biopsy however. We believe that this is the first case diagnosed by transbronchial biopsy-proven tissue eosinophilia and a positive nickel inhalation provocation test.

Adolescent↗
PubMed1994

[A case of eosinophilic pneumonia, showing a positive environmental provocation test].

A 23-year-old woman was admitted to our hospital because of cough and fever. Coarse crackles were audible over her left chest. A chest X-ray obtained on May 5, 1989, showed consolidation in the left S10 and a nodule in the right S1. Clinical symptoms improved during the course of hospitalization. Neither antibody titers against mycoplasma and chlamydia nor viral titers were elevated in paired sera. BALF findings of the left B10 showed increased numbers of eosinophils and lymphocytes. We diagnosed this case as eosinophilic pneumonia (EP). Environmental provocation testing was carried out in her home and yielded a positive result. After clearing of the house, she was able to return and has since experienced no relapses. We suspect that environmental conditions influence the pathogenesis of EP.

Adult↗
PubMed1993

Hyperphosphorylation of keratins by treatment with okadaic acid of BALB/MK-2 mouse keratinocytes.

Protein hyper- or hypophosphorylation induced by okadaic acid (OA) treatment was examined using quiescent cultures of the BALB/MK-2 mouse epidermal keratinocytes. Treatment with OA enhanced the phosphorylation of five proteins with molecular weights of 65,000, 55,000, 50,000, 28,000 and 15,000 (p65, p55, p50, p28, and p15, respectively) and decreased that of two proteins with molecular weights of 22,000 and 20,000 (p22 and p20, respectively). The two major phosphorylated proteins, p65 and p55, were identified as type II and type I keratins, respectively, by immunoblotting and immunoprecipitation with keratin specific antibodies. Serine was the only phosphoamino acid residue in hydrolysates of the 32P-labeled keratins purified from OA-treated cells. Two-dimensional tryptic peptide maps of the phosphorylated keratins showed that the hyperphosphorylation was largely due to phosphorylation at several additional sites in both keratins. The hyperphosphorylation of keratins induced by OA treatment resulted in a drastic change in their solubility. This change closely correlated with reorganization of the keratin filament network, which finally collapsed into large perinuclear aggregates. Concomitantly the cells changed from a typical epithelial shape to a round shape. Of several protein kinase inhibitors tested, only staurosporine interfered with this OA-induced morphological change and reorganization of the keratin network.

Animals↗
PubMed1993

Rapid phosphorylation of 28-kDa heat-shock protein by treatment with okadaic acid and phorbol ester of BALB/MK-2 mouse keratinocytes.

Protein phosphorylation by okadaic acid and 12-O-tetradecanoylphorbol-13-acetate (TPA) was examined using quiescent cultures of BALB/MK-2, a cell line derived from mouse epidermal keratinocytes. Treatment with okadaic acid caused rapid phosphorylation of five proteins with molecular masses of 65, 55, 50, 28 and 15 kDa (p65, p55, p50, p28, p15, respectively) while TPA caused rapid phosphorylation of five proteins with molecular masses of 80, 70, 40, 34 and 28 kDa (p80, p70, p40, p34, p28, respectively). In the present study, we examined p28, a common target protein of okadaic acid and TPA. The phosphorylation of p28 increased depending on time of exposure and doses of okadaic acid and TPA. Combined treatment with okadaic acid and TPA resulted in an additive effect. Its position on two-dimensional gel electrophoresis suggested that p28 is the 28-kDa heat-shock protein (HSP28). This possibility was confirmed by migration of p28 with HSP28 and comparative peptide mapping of the two proteins. The phosphoamino-acid residue of phosphorylated HSP28 was serine. In two-dimensional tryptic peptide maps, the same peptides were phosphorylated after treatment with both okadaic acid and TPA.

Animals↗
PubMed1993

Pharmacokinetics of flosequinan in elderly patients with chronic congestive heart failure.

We have investigated the pharmacokinetics of the direct vasodilator flosequinan in elderly patients with congestive heart failure. Eight patients received a single dose of 50 mg, and 8 patients received once-daily treatment with 25 mg for two weeks. In the single dose study, the tmax of flosequinan was 2.5 h, Cmax was 1.17 microgram.ml-1 and t1/2 was 5.63 h. The tmax of the metabolite BTS 53554 was 20.3 h, Cmax was 1.44 microgram.ml-1 and t1/2 was 62.0 h. BTS 53554 accumulated gradually in the 14-day repeated dose study and steady-state was reached after approximately 2 weeks. Flosequinan was not found to accumulate. Adverse reactions were not observed in either the single or repeated dose study. It is advisable to consider renal function and body weight when flosequinan is to be administered to elderly patients with congestive heart failure. The initial dose should be 25 mg.

Aged↗
PubMed1993

A bronchofibroscopic analysis of the bronchial mucosa using a dye-scattering method for the detection of bronchial lesions.

A study was undertaken to evaluate the usefulness of a dye-scattering method for the analysis of bronchial lesions. After methylene blue was introduced through a cannula, the bronchial staining intensities seen by bronchofibroscopy were later compared with the histologic findings in 74 biopsied specimens of lesions taken from 20 patients with lung cancer and from 6 patients with bronchiectasis, 2 with a rheumatoid lung, and 2 with sarcoidosis. It was found that 86% (25 of 29) of the specimens that stained positively were malignant. Further, 4 specimens that manifested a false positive response to staining were either too small to be inspected histologically or showed necrosis. Of 27 specimens that were negative to staining, 89% (24 of 27) were revealed to be nonmalignant lesions. In this latter group the response of 3 specimens was false negative on histologic inspection, 2 showing cancer cells without surface infiltration. We thus conclude that this dye-scattering method is of great use in enabling the differentiation of nonmalignant mucosa from neoplastic lesions and the preoperative determination of the stage of a tumor.

Bronchi↗
PubMed1993

Dominantly inherited cytoplasmic body myopathy in a Japanese kindred.

An autosomal dominant progressive myopathy with diffuse cytoplasmic bodies (CBs) is described. In four successive generations, 12 patients suffered from weakness and atrophy of muscles in the distal extremities, neck, thorax and shoulder girdles. The mean age at onset was 42 years old, and the patients became disabled after 5 to 10 years due to chronic respiratory failure. The level of serum creatine kinase was normal or slightly elevated. An electromyogram showed a predominant myopathic change with a slight neurogenic change. Autopsy of 2 cases revealed numerous CBs in the skeletal muscles. Smooth and cardiac muscles were also affected. CBs were present predominantly in type I fibers in skeletal muscles. Males were more frequently affected than females (2:1). An electron microscopic examination showed dense central cores of myofilaments surrounded by radiating filaments. Characteristics of clinical course and histopathological findings in a new kindred are discussed in this rare disease.

Adult↗
PubMed1993

Immunohistochemical detection of alkaline phosphatase in formalin-fixed and paraffin-embedded rat liver.

Alkaline phosphatase (ALP) in rat liver was detected by means of immunohistochemical techniques in ordinary histologic specimens which were fixed with formalin and embedded in paraffin. The specimens were incubated in anti-ALP antibody at room temperature for a longer time, 3hr, than ordinary incubation time. Antigen detection sensitivity and contrast of reaction product of the immunogold silver staining were superior to those of the peroxidase-labeled antibody method. In rat livers which were partially hepatectomized 24 hr before, the more abundant enzyme localized around enlarged bile canalicular spaces.

Alkaline Phosphatase↗
PubMed1993

Immunohistochemical detection of alkaline phosphatase in formalin-fixed and paraffin-embedded rat organs by means of avidin-biotin peroxidase complex method.

The author attempted the detection of alkaline phosphatase (ALP) protein in various rat organs, which were fixed with formalin and embedded in paraffin, by means of the avidin-biotin peroxidase complex (ABC) method. Reaction products were detected after a usual incubation time of 30 min at room temperature in anti-ALP antibody. Positive reactions were observed in the kidney and liver but not in the small intestine, and this indicates that the antibody used in the present study reacts only with the tissue-nonspecific type of ALP.

Alkaline Phosphatase↗
PubMed1993

[An elderly case of supernormal conduction in the posterior division of the left bundle branch].

An electrophysiologic study was performed in a 95-year-old man with bifascicular block (right bundle branch block and left anterior hemiblock). During sinus rhythm (AA interval = 980 ms), every sinus beat was conducted to the ventricle. The AH interval was 130 ms and HV interval was 50 ms. A programmed premature atrial stimulation was performed after 8 paced beats at a slightly shorter cycle length than the sinus cycle length (900 ms). As the atrial coupling interval was shortened, the H1H2 interval also shortened. At an H1H2 interval of 680 ms the premature atrial beat was blocked distal to the recording site of the His potential. The block persisted up to an H1H2 interval of 560 ms. AV conduction resumed paradoxically when the H1H2 interval was further shortened to intervals lasting 540-490 ms. During this period the H2V2 interval was 50 ms. At still shorter H1H2 intervals, H2 was again blocked. The H2V2 intervals during this phase of improved conduction were unchanged compared with those of other conducted beats. Therefore normalization due to the gap phenomenon could be ruled out, and the improved conduction could be explained by a phenomenon of supernormal conduction in the posterior division of left bundle branch.

Aged↗
PubMed1993

[Long-term follow-up study after permanent pacemaker implantation in patients aged 60 years or over with sick sinus syndrome].

Ninety-five patients aged 60 years or over with a permanent pacemaker implanted for sick sinus syndrome were divided into two groups: 32 patients with physiological pacing (group P) and 63 patients with ventricular pacing (group V). The mean follow-up period was 45.0 +/- 36.6 months in group P and 50.3 +/- 37.8 months in group V. Paroxysmal atrial fibrillation (Af) occurred in 28% of group P and 71% of group V (p < 0.05). The incidence of stable Af was also lower in group P than in group V (9% vs. 30%, p < 0.05). None of group P with only bradyarrhythmia had stable Af. However, 6 of 21 patients (29%) in group V with bradyarrhythmia showed stable Af. There was no significant difference in stable Af between group P with bradycardia-tachycardia syndrome (BTS) and group V with BTS (19% vs. 31%). A lower incidence of embolic events was also observed in group P (3% vs. 25%, p < 0.05). Nine of 16 patients with embolic events in group V died of complications following embolism (8 patients; cerebral embolism, one patients: renal and superior mesenteric arterial embolism). The survival rates at 5 and 10 years were 80% and 69%, respectively, for group P and 56% and 33% for group V (p < 0.01). Thus, with regard to permanent pacing for patients with sick sinus syndrome, physiological pacing should be selected for control of morbidity and total mortality.

Aged↗
PubMed1993

[A study of interstitial pneumonia associated with collagen vascular disease--comparison with the data of idiopathic pulmonary fibrosis].

To clarify the pathogenesis of idiopathic interstitial pneumonia (IIP), we compared the data of interstitial pneumonia (IP) associated with collagen vascular disease (CVD) with those of idiopathic pulmonary fibrosis (IPF). These disorders are found to have similar clinical, radiographic, and morphological findings, and lung function. However, the in vitro behavior of fibroblasts from CVD-IP and IPF, and the detection of soluble ICAM-1 were different. Further, in the T cell receptor repertoire, the predominance of different genes was found in bronchoalveolar lavage cells from CVD and IPF. These differences could partly explain the variability of IP pattern seen in CVD. In summary, our results indicate the possibility that CVD-IF and IPF result from different mechanisms although they share the same spectrum of pulmonary changes.

Collagen Diseases↗
PubMed1993

[Acute exacerbation following bronchoalveolar lavage in idiopathic interstitial pneumonia].

We report two cases of idiopathic interstitial pneumonia (IIP) with acute deterioration after bronchoalveolar lavage (BAL). Case 1 was a 54-year-old woman, and case 2 was a 75-year-old man. Both were diagnosed as having IIP, and hospitalized with complaints of high fever and dyspnea. After BAL, the degree of dyspnea increased. White blood cell count and lactate dehydrogenase were elevated, and PaO2 was decreased. Chest X-ray revealed consolidation of the upper lung fields and reticulo-granular shadows spreading through both lungs. BAL fluid examination showed an elevated neutrophil fraction (case 1: 6.5%, case 2: 35.2%), suggesting respiratory tract infection although bacteria could not be detected. Case 1 died of respiratory failure despite corticosteroid therapy. Autopsy revealed diffuse alveolar damage with focal pneumonia in the right S6 corresponding to the upper lobe consolidation. Case 2 improved after antibiotic therapy. These findings suggest that aspiration of infected fluid during BAL can cause acute exacerbation of IIP. It is important to recognize that the BAL procedure can induce an acute exacerbation of IIP.

Acute Disease↗