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K Chida

Publications and source records attributed to K Chida.

At least 145 records · Page 8Linked to original sources
PubMed1995

[Clinical and immunological study of airway disease in collagen vascular disease].

We studied the clinical and immunological characteristics of patients with bronchiolar diseases associated with collagen vascular disease (15 patients with rheumatoid arthritis and 1 primary Sjögren's syndrome). Histological examinations showed that 9 patients had follicular bronchiolitis and 7 had bronchiolitis obliterans. Follicular bronchiolitis was characterized by hyperplasia of bronchus-associated lymphoid tissue, and immunohistochemical studies revealed that the pattern of distribution of T cells and B cells in bronchus-associated lymphoid tissue from patients with follicular bronchiolitis was similar to that in diffuse panbronchiolitis, which may be used as a representative model of chronic respiratory infection. In addition, bacterial cultures of sputum samples were positive in 44% of patients with follicular bronchiolitis and in 71% of patients with bronchiolitis obliterans. These results suggest that antigen stimulation is involved in the development of bronchiolar diseases associated with collagen vascular disease.

Aged↗
PubMed1994

Overproduction of a Ca(2+)-independent protein kinase C isozyme, nPKC epsilon, increases the secretion of prolactin from thyrotropin-releasing hormone-stimulated rat pituitary GH4C1 cells.

Rat pituitary GH4C1 cells express protein kinase C (PKC) transcripts for cPKC alpha, cPKC beta II, nPKC delta, nPKC epsilon, nPKC eta, and aPKC zeta, but not for cPKC gamma or nPKC theta. Of the transcripts produced, the nPKC epsilon isoform is the most abundant. Transfection of GH4C1 cells with an expression plasmid containing nPKC epsilon cDNA leads to the transient overexpression of cellular nPKC epsilon and confers enhanced phorbol ester binding activity. Transient expression of an inactive point mutant (nPKC epsilon K-->R) of nPKC epsilon, where Lys436 at the putative ATP-binding site is replaced with Arg, also confers elevated binding activity. However, only overproduction of the wild type in transfected cells increases the basal levels and stimulates the secretion of prolactin (PRL) by 12-O-tetradecanoylphorbol-13-acetate or thyrotropin-releasing hormone (TRH). In stable clones overexpressing nPKC epsilon, immunocytofluorescence and immunoblot experiments indicated that TRH causes the rapid translocation and down-regulation of an appreciable fraction of nPKC epsilon. Both the basal and TRH-stimulated levels of PRL secretion are clearly correlated with the expression level of nPKC epsilon but not with the TRH receptor densities in these clones. The dose dependence of TRH-stimulated secretion were similar in all cells overexpressing cPKC alpha, cPKC beta II, nPKC epsilon, and nPKC delta, but the enhancement of PRL secretion was specific for the overproduction of nPKC epsilon, no effect was found when other isozymes were overproduced. These findings clearly demonstrate that the expression level of nPKC epsilon in GH4C1 cells is rate-limiting for basal and TRH-stimulated PRL secretion, and they provide the first direct evidence that nPKC epsilon plays a key role in hormonal secretory processes.

Animals↗
PubMed1994

Phospholipid analysis of alveolar macrophages and bronchoalveolar lavage fluid following bleomycin administration to rabbits.

Changes in the lipid metabolism of the lung during pulmonary injury were investigated by quantitative and qualitative analysis of phospholipids in pulmonary surfactant and alveolar macrophages (AM) obtained from rabbits that had been given a single transtracheal injection of bleomycin hydrochloride (BLM) 0, 7, 14, 21, and 28 days previously. BLM treatment increased the phospholipid content of both bronchoalveolar lavage (BAL) supernatant fluids and BAL cells. Furthermore, the proportion of phosphatidylcholine (PC) showed an increase in BAL cells during the development of pulmonary injury, and BLM treatment appeared to cause transformation of AM to foamy AM. Lipid analyses of the foamy AM revealed that their phospholipid content was increased, and that the percentage of PC with palmitic acid was elevated. Thus it appears that accumulation of phospholipids derived from pulmonary surfactant contributes to the increase in phospholipids and PC in BAL cells. These findings indicate that BLM treatment produces an alteration in the amount and composition of AM phospholipids, and also in BAL supernatant fluids.

Animals↗
PubMed1994

The eta isoform of protein kinase C is localized on rough endoplasmic reticulum.

The eta isoform of protein kinase C, isolated from a cDNA library of mouse skin, has unique tissue and cellular distributions. It is predominantly expressed in epithelia of the skin, digestive tract, and respiratory tract in close association with epithelial differentiation. We report here that this isoform is localized on the rough endoplasmic reticulum in transiently expressing COS1 cells and constitutively expressing keratinocytes. By the use of polyclonal antibodies raised against peptides of the diverse D1 and D2/D3 regions, we found that immunofluorescent signals were strongest in the cytoplasm around the nucleus and became weaker toward the peripheral cytoplasm. Under immunoelectron microscopic examination, electron-dense signals were located on the rough endoplasmic reticulum and on the outer nuclear membrane which is continuous with the endoplasmic reticulum membrane. However, no signals were detected in the nucleus, inner nuclear membrane, smooth endoplasmic reticulum, Golgi apparatus, mitochondria, or plasma membrane. Treatment of the cells in situ with detergents suggested association of the isoform of protein kinase C with intracellular structures. By immunoblotting, a distinct single band with an M(r) of 80,000 was detected in whole-cell lysate and in rough microsomal and crude nuclear fractions, all of which contain outer nuclear membrane and/or rough endoplasmic reticulum. We further demonstrated the absence of a nuclear localization signal in the pseudosubstrate sequence. The present observation is not consistent with the report of Greif et al. (H. Greif, J. Ben-Chaim, T. Shimon, E. Bechor, H. Eldar, and E. Livneh, Mol. Cell. Biol. 12:1304-1311, 1992).

Amino Acid Sequence↗
PubMed1994

Rare case with metastatic involvement of hypothalamo-pituitary and pineal body presenting as hypopituitarism and diabetes insipidus.

An unusual case with metastatic spread of a small oat cell lung carcinoma to the hypothalamo-pituitary region and pineal body presenting as pituitary insufficiency is reported. Computed tomographic scan revealed an isodense mass in the hypothalamo-pituitary region and pineal body that was strongly enhanced by contrast medium. Magnetic resonance imaging demonstrated a downward displacement of the posterior lobe of the pituitary by the hypothalamo-pituitary mass. Dynamic assessment of hypothalamo-pituitary function showed hypopituitarism and diabetes insipidus; partial recovery was observed with the improvement in the carcinoma by chemotherapy. The brain was subsequently irradiated. The patient survived 10 months.

Aged↗
PubMed1994

Guillain-Barré syndrome following fulminant viral hepatitis A.

Guillain-Barré syndrome (GBS) developed soon after the onset of acute viral hepatitis A (HA) in a 62-year-old man. GBS associated with HA is extremely rare, even though HA is common. In a review of case reports the clinical features of GBS following HA could be summarized as follows: 1) Most of the patients are men. 2) GBS develops within 14 days after the onset of HA. 3) Facial nerve palsy is frequently present. 4) Proprioception is likely impaired in addition to superficial sensation. 5) The outcome of neuropathic symptoms is uniformly good, regardless of the degree of liver dysfunction as evaluated on the basis of alanine aminotransferase levels. These findings indicate that GBS following HA essentially does not differ from typical GBS.

Acute Disease↗
PubMed1994

[A case of aspirin-induced cough without bronchoconstriction. A new type of aspirin hypersensitivity].

A 54-year-old woman was admitted to our hospital because of an asthmatic attack. Her first asthma attack occurred when she was 53 years old. It was followed by a flu-like infection, and was preceded for one year perennial rhinitis and loss of the sense of smell. Symptoms were perennial, and unrelated to the seasons. Because these clinical findings resembled those of aspirin-induced asthma (AIA), an aspirin-DL-lysine i.v. challenge test was done. Cough, perspiration, and flushing was provoked within 15 min after aspirin-DL-lysine injection, but FEV1 did not change. Respiratory sounds were normal and no wheezing was audible. Other cyclooxygenase inhibitors (ketoprofen, sulpyrine and acetaminophen) provoked the same symptoms. Successively increasing doses of injected aspirin-DL-lysine resulted in complete tolerance to this stimulus. We propose that aspirin-induced cough without bronchoconstriction is a new type of aspirin hypersensitivity.

Aspirin↗
PubMed1994

Cholesterol sulfate, a novel activator for the eta isoform of protein kinase C.

Activity of protein kinase C depends on the interaction with polar head-groups of two membrane lipids, i.e., phosphatidylserine and diacylglycerol. In the present study, we demonstrated a novel activation mechanism of the eta isoform of protein kinase C (nPKC eta), which is predominantly expressed in epithelial tissues in close association with epithelial differentiation. We found that the nPKC eta was activated by cholesterol sulfate, a metabolite of cholesterol formed during squamous differentiation. This activation was greater than that by phosphatidylserine plus phorbol ester; the Vmax for the activation by cholesterol sulfate was 3.6 times that by phosphatidylserine plus phorbol ester, while Kms were almost equal. In the presence of cholesterol sulfate, phorbol ester only weakly enhanced the activity of nPKC eta. Activation of nPKC eta by cholesterol sulfate was further demonstrated by autophosphorylation of the kinase molecule. However, the alpha and delta isoforms of protein kinase C were not activated by cholesterol sulfate. The present observation affords a new insight into a signal transduction pathway of squamous differentiation.

Amino Acid Sequence↗
PubMed1994

[The significance of biochemical data of patients with sarcoidosis].

The clinical laboratory has a significant role in sarcoidosis. We summarized the biochemical data of laboratory tests in serum of patients with sarcoidosis. To clarify their importance, we put emphasis on the following aspects, including: 1. The data reflecting pathophysiology of sarcoidosis, such as angiotensin converting enzyme, lysozyme, adenosine deaminase, beta 2-microglobulin and intercellular adhesion molecule-1, 2. The data resulting from organ involvement, such as amylase, LDH, and Ca, 3. The data serving as an indicator of disease activity, 4. The data related to prognostic outcome, Keeping these differences in mind helps us make the best use of the clinical data of sarcoidosis.

Adenosine Deaminase↗
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↗