Secretion of atrial natriuretic peptide in idiopathic giant atrium.
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Aged↗
Biomedical subjects
M Arima
Publications and source records attributed to M Arima.
Binding of BAZF and Bc16 to STAT6-binding DNA sequences.
BAZF, a family member of Bcl6, can function as a sequence-specific transcriptional repressor. We determined BAZF-binding DNA sequence. The consensus binding sequence (CBS) of BAZF is almost the same as those of Bcl6 previously described. Three nucleotides of T, G and A at position 6, 8, and 9 in the CBS (5'-ATTCCTAGAAAG-3') are important nucleotides for binding of both BAZF and Bcl6. Since a part (5'-TTC-CTA-GAA-3') of the CBS resembled the sequence motif (5'-TTC-(N3-4)-GAA-3') bound by STAT factors, BAZF and Bcl6 can bind to the CD23b-STAT6-binding sequence (5'-TTTC-TTA-GAAAT-3'), the immunoglobulin germline epsilon-STAT6-binding sequence (5'-CTTC-CCAA-GAAC-3'), and the IL4-STAT6-binding sequence (5'-TTTC-CCA-GAAAA-3') with weak affinity. However, a mutation of C nucleotide to T nucleotide in the IL4-STAT6-binding sequence (5'-TTTC-CTA-GAAAA-3') strongly increased the binding activity of BAZF and Bcl6. These results suggest that BAZF and Bcl6 can repress some of STAT-induced transcription by binding to DNA sequences recognized by STAT factors.
Animals↗
Interleukin (IL)-4/IL-9 and exogenous IL-16 induce IL-16 production by BEAS-2B cells, a bronchial epithelial cell line.
Previous studies have suggested that bronchial epithelial cells may perpetuate airway inflammation. We have reported that the bronchial epithelial cell line BEAS-2B can produce interleukin (IL)-16, a potent chemoattractant for CD4+ T cells. IL-16 is thought to regulate airway inflammation in asthmatics. Recent studies showed that IL-4 induces inflammatory cytokines in bronchial epithelial cells and that IL-9 is a candidate gene for development of asthma. The present study demonstrated that BEAS-2B cells produced specifically IL-16 by synergistic effects of IL-4 + IL-16, or IL-9 + IL-16, and that the synthesized IL-16 induced migration of CD4+ T cells. This study is a first report indicating that IL-16 production may be maintained by an autocrine machinery by epithelial cell-derived IL-16 with IL-4 and IL-9 in asthma.
Bronchi↗
A549 cells can express interleukin-16 and stimulate eosinophil chemotaxis.
Alveolar epithelial cells produce many types of chemokines such as regulated on activation, normal T cells expressed and secreted (RANTES), eotaxin induced by interleukin (IL)-1 beta, or tumor necrosis factor (TNF)-alpha and may contribute to allergic disease by recruiting eosinophils. However, identification of the eosinophil chemotacic activity (ECA) release from A549 cells, an alveolar type II cell line, has not yet been completed. Recently, IL-16 was also reported to be a potent chemotactic stimulus for CD4(+) T lymphocytes and eosinophils in asthma and other pulmonary diseases. To test the possibility that alveolar epithelial cells produce IL-16, we analyzed RNA and culture supernatant from A549 cells by reverse transcription/ polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The release of ECA from A549 cells was assessed using a blind-well chemotactic chamber. IL-16 release was increased in a concentration-dependent manner by stimulation with IL-1 beta or TNF-alpha. A549 cells also expressed IL-16 messenger RNA. The combination of IL-4 and IL-1 beta or TNF-alpha had an additive effect on IL-16 production. The release of ECA was induced by IL-1 beta or TNF-alpha in a dose-dependent manner. The combination of these cytokines had a greater effect than one alone. The blockade of eotaxin and IL-16 caused 70% inhibition of ECA, but anti-RANTES antibodies only caused 30% inhibition and anti-IL-8 antibodies failed to affect inhibition. These findings suggest a role for chemokines released by alveolar epithelial cells in the recruitment of eosinophils into the lung in pulmonary disorders such as asthma and interstitial lung diseases, and suggested that eotaxin and IL-16 are potent and effective eosinophil chemoattractants.
Base Sequence↗
Recurrence of myocarditis presenting as pacing and sensing failure after implantation of a permanent pacemaker at first onset.
A 31-year-old woman was admitted to hospital with loss of consciousness and generalized convulsions. Electrocardiography (ECG) showed complete atrioventricular block (AV block) with a pulse rate of 30 beats/min. Endomyocardial biopsy from the right ventricle showed massive necrosis and degeneration of myocardial cells with extensive infiltration of lymphocytes into the interstitial space. These pathological findings suggested fulminant myocarditis. Following glucocorticoid therapy, the patient became asymptomatic, but the AV block did not resolve completely and a bifocal pacemaker was implanted. However, similar symptoms recurred 7 years later. An ECG showed pacing and sensing failure linked to an increase in the pacing threshold and a decrease in the sensing threshold. Endomyocardial biopsy from the right ventricle again showed interstitial infiltration with lymphocytes and eosinophils. After glucocorticoid therapy, she became asymptomatic once more, and the improvement in the pacing and sensing failure, and cardiomegaly, was satisfactory. This patient represents a very rare case of recurrence of acute myocarditis without progression, as much as 7 years after its first occurrence. Glucocorticoid therapy was still effective in treating the recurrent myocarditis presenting with pacing and sensing failure.
Acute Disease↗
Serum p53 antibody is a useful tumor marker in superficial esophageal squamous cell carcinoma.
BACKGROUND: Patients with superficial (mucosal or submucosal) esophageal carcinoma (SEC) have significantly better survival rates than patients with advanced carcinoma. Some patients with advanced esophageal carcinoma have been reported to test positive for serum p53 antibodies (Abs). Because very few patients with superficial carcinoma have been examined, the aim of this study was to evaluate the clinical significance of serum p53-Abs in patients with superficial esophageal squamous cell carcinoma (SESCC). METHODS: Thirty-five consecutive patients with SESCC were studied for serum p53-Abs by enzyme-linked immunoabsorbent assay before and after treatment. The clinicopathologic features of p53 seropositive and p53 negative patients were compared. The relation between the presence of serum p53-Abs and p53 immunoreactivity of the resected specimens was examined. Three tumor markers (squamous cell carcinoma antigen [SCC-Ag], CYFRA21-1, and carcinoembryonic antigen [CEA]) were assessed to compare their sensitivities with serum p53-Abs. RESULTS: Fourteen of 35 patients (40%) were p53 seropositive. Relatively few patients tested positive for the other tumor markers: CEA, 11.4%; SCC-Ag, 14.3%; CYFRA21-1, 5.7%. There were no significant correlations between clinicopathologic features and p53 seropositivity except for tumor location. A strong correlation between p53 immunostaining and the presence of serum p53-Abs was observed (P = 0.003). Of the 14 patients with seropositive results, 12 turned seronegative after resection, and the other 2 experienced disease recurrence. CONCLUSIONS: Surveillance of serum p53-Abs is superior to the three tumor markers for detecting SESCC. This serum marker is also useful for the detection of p53 protein overexpression and for the monitoring of residual tumor cells.
Aged↗
Surfactant protein A exhibits inhibitory effect on eosinophils IL-8 production.
Eosinophils are believed to be one of the important sources of cytokines such as IL-8 at the site of allergic inflammation. It has been demonstrated that pulmonary surfactant protein A (SP-A) plays a potential role in modifying inflammation and the immune function. To verify the regulating effect of SP-A on eosinophil cytokine generation, we studied the effect of SP-A by determining of IL-8 production and expression stimulated with sIgA or PMA. SP-A purified from surfactant recovered from patients with alveolar proteinosis was added to eosinophils isolated by the negative selection method with immunomagnetic beads, and cultured for 24 h. The concentrations of IL-8 in the cell-free supernatants and cell lysates were then measured by ELISA. We also used a semiquantitative reverse transcriptase-polymerase chain reaction assay to detect the effect of SP-A on IL-8 mRNA expression. SP-A inhibited the secretion of IL-8 in a dose-dependent fashion. Suppression of IL-8 production by SP-A was significantly inhibited by SP-A antibody (PE10). SP-A also attenuated expression of IL-8 mRNA in eosinophils. These results indicate that SP-A might have the potential role to modify allergic inflammation by inhibiting IL-8 expression and production from eosinophils.
Antibodies↗
A feasibility study of chemosensitivity assay by adhesive tumor cell culture system using biopsy specimens for gastric cancer.
BACKGROUND AND OBJECTIVES: The adhesive tumor cell culture system (ATCCS) is known to produce high colony-forming efficiency. We, therefore, studied the feasibility of ATCCS for gastric cancer by use of biopsy specimens and the relationship between the results of ATCCS and histological effects of anticancer drugs. METHODS: Tumor specimens extracted by gastroendoscopic biopsy were sufficient for obtaining the result of sensitivity to at least one drug in 24 out of 30 (80%) patients. Twenty patients were administered 5-fluorouracil (5-FU) for 14 days prior to surgery, and the results of ATCCS were compared with histological changes of the resected specimens. RESULTS: The histological response rate was found to be 100% (4/4) when the 90% inhibition concentration (IC90) of 5-FU was less than 0.24 microg/ml (sensitive) and was 0% (0/3) when IC90 was greater than 0.40 microg/ml (resistant). CONCLUSIONS: Although lacking in statistical significance, the results suggest that the drug to which the tumor revealed sensitivity in the ATCCS would produce histological effects and the drug to which the tumor was resistant would have no histological effect.
Aged↗
Clinical benefits of steroid therapy on surgical stress in patients with esophageal cancer.
BACKGROUND: Despite improvements in surgical techniques and perioperative care, severe complications lead to long hospital stays for some esophageal cancer patients. The purpose of this study was to evaluate the safety and effectiveness of perioperative steroid therapy on the postoperative clinical course. METHODS: Fifty-seven patients operated for esophageal cancer in 1997 and 1998 were treated with perioperative steroid therapy. Fifty consecutive patients operated in 1995 and 1996 served as a control group. In the steroid group, each patient was given 250 mg of methylprednisolone intravenously before operation followed by 125 mg on postoperative days 1 and 2. Serum interleukin-6, polymorphonuclear cell elastase, and C-reactive protein levels, and the postoperative clinical course were compared between the groups. RESULTS: Morbidity rates including hyperbilirubinemia, anastomotic leakage, and liver dysfunction were significantly lower in the steroid group than in the control group. Days until extubation and hospital stay were significantly shorter for the steroid group. Inflammatory mediators, body temperature, heart rate, and respiratory index after the surgical procedure were significantly lower in the steroid group. Adverse effects possibly caused by steroid therapy were not observed. CONCLUSIONS: Perioperative steroid therapy was safe and effective for the inhibition of inflammatory mediators and the improvement of the postoperative clinical course of patients with esophageal cancer.
Acute-Phase Proteins↗
Isolated coronary ostial stenosis associated with coronary vasospasm.
A 50-year-old woman was brought to the emergency room in a preshock condition. An emergency coronary angiogram revealed 90% ostial stenosis of the left coronary artery with delayed distal filling. After intracoronary nitrate, the degree of stenosis was reduced to 75%; no other coronary lesions were evident. The patient was found to have hyperthyroidism and she became euthyroid after a 2-month regimen of methimazole. A follow-up coronary angiogram showed that the left coronary artery had 50% ostial stenosis without delayed distal filling. At the same time, an aortogram showed complete occlusion of the right subclavian artery in its proximal site, a slight dilatation of the truncus brachiocephalic artery, and a diffuse wall irregularity of the abdominal aorta, suggestive of Takayasu's arteritis.
Coronary Disease↗
[X-ray and endoscopic diagnosis of esophageal achalasia].
We evaluated diagnostic X-ray and endoscopic examination findings in 486 patients with esophageal achalasia. Concerning the association between the duration of disease and the X-ray dilatation type, the duration was 1-4 years in more than 50% of patients with the Sp type, a mean of 8.5 years in those with the F type, and frequently more than 10 years in those with the S type. Endoscopy is generally used to determine the presence or absence of abnormal movement. In achalasia, the endoscope can be inserted into the stomach despite resistance at the stenotic site, and the mucosal surface is normal. Squamous cell carcinoma as a complication was observed in 21 patients (4.3%). The carcinoma complication rate was higher with a longer duration of disease and a longer observation period. The mean total course including the postoperative course was 27 years. Long-term and periodic X-ray and endoscopic observation of the disease course is important, and iodine staining is indispensable for early detection of esophageal cancer.
Adolescent↗
[Significance of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) activity in breast cancer tissue].
TS, DPD, uridine phosphorylase and thymidine phosphorylase are enzymes involved in the metabolism of the anticancer drug pyrimidine fluoride. In this study, levels of these enzymes were measured in 47 women with primary breast cancer. These enzyme levels were then compared to levels determined from breast cancer patients who received either preoperative chemotherapy or nothing, in order to determine whether they might predict clinical outcome. The TS inhibition rate was significantly higher (p < 0.05) in patients receiving preoperative chemotherapy (20.4 +/- 13.3%) than in the untreated group (11.4 +/- 9.8%). No other significant differences in activity were noted between the treated and untreated groups for any of the other enzymes studied. The activity of each enzyme at the tumor site and the tumor/normal (T/N) ratio were also compared between patients with and without recurrence. The TS inhibition rate at the tumor site was lower in recurring cases than in non-recurring cases, and the T/N ratio tended to be higher for DPD in patients with recurrences. These findings indicate that the TS inhibition rate and DPD activity may be useful predictors for early recurrence of breast cancer following surgery.
Antineoplastic Combined Chemotherapy Protocols↗
Impact of circulating p53 autoantibody monitoring after endoscopic resection in mucosal gastric cancer.
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Aged↗
[Sudden death in persons with mental retardation--the questionnaire survey in nationwide residential facilities for intellectual disability].
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Adult↗
The role of Bcl6 in mature cardiac myocytes.
OBJECTIVE: The Bcl6 gene encodes a sequence-specific transcriptional repressor and is ubiquitously expressed in adult murine tissues including heart muscle. The objective of this study was to examine the role of Bcl6 in cardiac myocytes. METHOD: We developed Bcl6-deficient (Bcl6-/-) mice and histologically examined hearts from these mice. RESULTS: Massive myocarditis with eosinophilic infiltration occurred in Bcl6-/- mice after 4-6 weeks of age. Since expression of the Bcl6 gene was induced in normal cardiac myocytes after 2 weeks of age and thereafter detected through adulthood, loss of Bcl6 in mature cardiac myocytes may be related to the induction of eosinophilic myocarditis. To examine the effects of eosinophils from Bcl6-/- mice on normal hearts, bone marrow cells from Bcl6-/- mice were adoptively transferred into sublethally irradiated RAG1-deficient mice. Although massive eosinophilic infiltration was detected in conjunctivas and spleens from the chimeric mice, myocarditis was never observed. Electron microscopic analysis of cardiac myocytes from Bcl6-/- mice revealed a spectrum of degenerative changes prior to eosinophilic infiltration. CONCLUSION: Bcl6 maynot be essential for the maturation of cardiac myocytes but may play a role in protecting mature cardiac myocytes from eosinophilic inflammation.
Adoptive Transfer↗
Eosinophilic myocarditis associated with dense deposits of eosinophil cationic protein (ECP) in endomyocardium with high serum ECP.
A case of eosinophilic myocarditis following high serum levels of eosinophil cationic protein (ECP) is described. A 27 year old woman was admitted with New York Heart Association (NYHA) class III congestive heart failure. A haematological study showed hypereosinophilia with degranulation and vacuoles; the total eosinophil count was 7980/ml and the ECP serum concentration was noticeably high at 150 ng/ml. Endomyocardial biopsy from the right ventricle showed infiltration of eosinophils and dense deposits of ECP in the endocardium as well as the myocardium. Steroid treatment returned the total eosinophil count and serum ECP to normal, with satisfactory improvement in clinical features. Eosinophilia may cause cardiac damage, and this report confirms that eosinophil degranulation is toxic. Thus, serum ECP seems to be a reliable indicator for diagnosis and for determining treatment parameters of eosinophilic myocarditis.
Adult↗
Expression of interleukin-16 by human epithelial cells. Inhibition by dexamethasone.
Production of chemoattractants by bronchial epithelial cells may contribute to the local accumulation of inflammatory cells in patients with bronchial asthma and other pulmonary diseases. Recently, interleukin (IL)-16 (lymphocyte chemoattractant factor) was reported to be a potent chemotactic stimulus for CD4(+) T lymphocytes and eosinophils, the types of leukocyte found in the proximity of bronchial epithelium in asthmatic individuals. To test the possibility that bronchial epithelial cells produce IL-16, we analyzed RNA and culture supernatants from the human bronchial epithelial cell line BEAS-2B, using reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. BEAS-2B constitutively expressed IL-16 messenger RNA (mRNA) and protein; IL-16 expression was significantly upregulated in a concentration-dependent manner within 24 h by stimulation with histamine, IL-1beta, or tumor necrosis factor (TNF)-alpha whereas interferon-gamma did not significantly increase IL-16. Findings in BEAS-2B cells were confirmed in primary bronchial epithelial cells. Using TA cloning, IL-16 was cloned from BEAS-2B airway epithelial cells. Sequence analysis confirmed its near identity with lymphocyte-derived IL-16. The combination of IL-1beta and TNF-alpha had an additive effect on IL-16 expression. This combination of cytokines also had a priming effect on histamine-induced IL-16 mRNA expression, which was observed within 24 h and which increased to at least 48 h after stimulation. The IL-16 expression induced by histamine and combined cytokines was significantly inhibited by pretreatment with the protein synthesis inhibitor cycloheximide (10 microg/ml). Pretreatment with dexamethasone also significantly suppressed the expression of IL-16, in a concentration-dependent manner. Sputum samples from asthmatic subjects were found to have higher levels of IL-16 than were samples from subjects with other pulmonary inflammatory diseases. These findings suggest that bronchial epithelial cells have the capacity to produce IL-16 after stimulation with histamine, IL-1beta, and TNF-alpha, and raise the possibility that epithelium-derived IL-16 may play a role in recruitment of eosinophils and CD4(+) T lymphocytes in the airways. Downregulation of IL-16 expression by dexamethasone suggests that glucocorticoids may inhibit airway inflammation partly by suppressing the synthesis of inflammatory cytokines including IL-16.
Adult↗
Clinical manifestation and survival of patients with idiopathic bilateral atrial dilatation.
We studied the histories of eight patients who lacked clear evidence of cardiac abnormalities other than marked bilateral atrial dilatation and atrial fibrillation, which have rarely been discussed in the literature. From the time of their first visit to our hospital, the patients' chest radiographs and electrocardiograms showed markedly enlarged cardiac silhouettes and atrial fibrillation, respectively. Each patient's echocardiogram showed a marked bilateral atrial dilatation with almost normal wall motion of both ventricles. In one patient, inflammatory change was demonstrated by cardiac catheterization and endomyocardial biopsy from the right ventricle. Seven of our eight cases were elderly women. Over a long period after the diagnosis of cardiomegaly or arrhythmia, diuretics or digitalis offered good results in the treatment of edema and congestion in these patients. In view of the clinical courses included in the present study, we conclude that this disorder has a good prognosis.
Aged↗