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Biomedical subjects

N Ouyang

Publications and source records attributed to N Ouyang.

14 recordsLinked to original sources
PubMed2006

Angiotensin type 1 and type 2 receptor blockade in chronic allograft nephropathy.

Angiotensin-II (Ang-II) type 1 (AT(1)) receptor blockers may delay the progression of chronic allograft nephropathy (CAN). However, neither the optimal time for initiating AT(1) receptor blockade in order to delay CAN potentially nor the role of Ang-II type 2 (AT(2)) receptors under AT(1) receptor blockade is known. Both AT receptors can regulate p53 expression and apoptosis. We investigated what time of initiation with AT(1) blockers most effectively delayed CAN as well as the role of the AT(2) receptor, and how angiotensin receptor blockade affected apoptosis and its regulating factors in this context in a rat model. Kidneys of Fisher (F344) rats were transplanted into Lewis rats. Animals were treated with AT(1) (candesartan) and/or AT(2) (PD123319) receptor antagonists, a calcium channel blocker, or vehicle (treatment periods: day -7 before to week 24 after transplantation (long term), week 12 to week 24 (late), day -7 to day +5 (early)) and observed the animals for 24 weeks. Reduction of proteinuria, grade of CAN, and number of apoptotic cells was most pronounced in animals receiving long-term AT(1) receptor blockade. A combined AT(1)/AT(2) blocker treatment reduced CAN similarly to AT(1) blocker treatment alone. The number of apoptotic cells and the level of p53 mRNA were significantly lower in long-term AT(1) blocker-treated animals. In summary, AT(1) receptor blockade delayed the progression of CAN, particularly in animals treated long term. Reduction of apoptosis could be related to these beneficial effects. The AT(2) receptor does not appear to play an important role in CAN.

Angiotensin Receptor Antagonists↗
PubMed2001

Soluble Fas ligand released by colon adenocarcinoma cells induces host lymphocyte apoptosis: an active mode of immune evasion in colon cancer.

Expression of membrane-bound Fas ligand (mFasL) on colon cancer cells serves as a potential mechanism to inhibit host immune function by inducing apoptosis of host lymphocytes. Membrane-bound FasL can be cleaved and released as a soluble mediator (sFasL), which may spread the apoptosis induction effect. Our study examined whether colon adenocarcinoma cells release sFasL, and induce apoptosis of host lymphocytes without direct cell-cell contact. In 12 consecutive patients with colon adenocarcinoma mFasL was identified in the tumours, sFasL was measured in the sera and apoptosis identified in tumour-infiltrating and peripheral blood lymphocytes. To analyse the function of sFasL, colon cancer cells were primarily cultured; sFasL was isolated from supernatants, measured, incubated with Fas-bearing Jurkat cells, and the resulting apoptosis was analysed. Serum levels of sFasL were significantly elevated in all colon cancer patients with mFasL expression in tumour tissues (n = 8). In these patients, the number of apoptotic lymphocytes was significantly increased within tumour and peripheral blood. Furthermore, sFasL was present in the corresponding supernatants and induced apoptosis of Jurkat cells in a dose-dependent manner. These findings suggest that mFasL-positive colon cancer cells release sFasL, and thus may induce apoptosis of host lymphocytes as a potential mechanism for immune evasion.

Adenocarcinoma↗
PubMed2001

Kupffer cells of cirrhotic rat livers sensitize colon cancer cells to Fas-mediated apoptosis.

Metastasis of colorectal carcinomas rarely occurs in cirrhotic livers. Our study investigated the influence of activated Kupffer cells from cirrhotic rat livers on hepatic colonization and FasR-mediated apoptosis of colon cancer cells. A rat colon cancer cell line, RCN-9, was used to inoculate rat livers. Treatment with conditioned media of Kupffer cells isolated from CCl(4)-induced cirrhotic rat livers (cirrhotic KCM) significantly reduced the incidence of hepatic colonization of RCN-9 cells. In vitro cytotoxicity of Kupffer cells and tumour infiltrating lymphocytes (TILs) on RCN-9 cells was evaluated using [(3)H]-release assay. RCN-9 cells were resistant to cytotoxicity mediated by cirrhotic Kupffer cells, but were sensitized to TIL-mediated killing after treatment with cirrhotic KCM. The specific killing induced by TILs was FasR-mediated, as it was inhibited by ZB4, an antagonistic anti-FasR antibody. In agreement, cirrhotic KCM increased recombinant Fas ligand-induced apoptosis of RCN-9 cells, and up-regulated FasR expression on RCN-9 cells as evaluated by RT-PCR and flow cytometry. These findings suggest that Kupffer cells in cirrhotic livers sensitize metastatic colon cancer cells to FasR-mediated apoptosis by up-regulating the receptors, which thus prepare them to be eliminated by infiltrating lymphocytes.

Animals↗
PubMed2001

[Detection of neuroendocrine differentiation in NSCLC and its clinical significance].

OBJECTIVE: To study differentiation of neuroendocrine (NE) in non-small cell lung carcinoma (NSCLC) and its effect on the responsiveness to chemotherapy. METHODS: Neuron-specific enolase (NSE), chromogranin A (CgA) and synaptophysin (SYN) were detected in 42 cases of NSCLC by using Western blot and immunohistochemistry. Electron microscopy was also used to observe the ultrastructure of NE granule in above specimens. The relationship between the chemotherapeutic responsiveness and the differentiation of NE in carcinoma tissues was evaluated. RESULTS: (1) The positive rate of NE detected by Western blot is higher than that detected by immunohistochemistry and electron microscopy. (2) There is no relationship between the expression of NE and the type of lung carcinoma as well as the differentiated degree of carcinoma. (3) The positive rate of three markers detected by immunohistochemistry and Western blot methods in the group of responsive to chemotherapy is higher than that in non-responsive group (P < 0.05). CONCLUSIONS: There is a high rate of NE differentiation in NSCLC, of which NSE's rate is highest, SYN takes second place, and CgA's rate is lowest. Immunohistochemistry and Western blot method are both very useful for the diagnosis of NE differentiation in NSCLC. The sensitivity of Western blot is higher than immunohistochemistry. The differentiation of NE may be one of the factors effected the chemotherapy in NSCLC.

Aged↗
PubMed2001

[Tracheobronchopathia osteochondroplastica].

OBJECTIVE: To describe the clinical manifestations of tracheobronchopathia osteochondroplastica (TO). METHODS: X-ray film, CT-scanning, lung function, fibro-bronchoscopy and histological examination were performed in all 4 patients. Clinical features were analyzed with reviewing the reported literatures. RESULTS: From June 1999 to May 2000, 4 cases of TO (male/female: 2/2, age: 35 approximately 60 yrs) were found among the 1 125 cases of fibro-bronchoscopy, with the positive rate of 0.35%. TO was characterized by cartilaginous and /or osseous submucosal nodules in the trachea and the central bronchi. Symptoms included cough (3/4), hemoptysis (2/4), hoarseness (1/4), with one case of entirely symptom free. Radiography showed no use for the diagnosis. Multiple submucosal nodules and plaques that outgrew into the lumen of the trachea were revealed by CT-scanning in 3 of 4 cases. Pulmonary function testing showed normal in 3 patients and mild obstruction in 1 patient. The bronchoscopic appearance of TO presented with multiple whitish, hard nodules projecting into the tracheal lumen from anterior and lateral walls, with sparing of the posterior wall. Pathological examination showed island of bony tissue and cartilage in the submucosa with almost intact respiratory epithelium. The symptoms and mucosal hyperemia were improved in one patient treated with beclomethasone dipropionate and theophylline for 6 months. CONCLUSIONS: As an uncommon disease, TO is often misdiagnosed or underdiagnosed. Fibro-bronchoscopy and CT scan remain the main methods for the diagnosis of TO.

Adult↗
PubMed2000

Influence of alternatively and classically activated macrophages on fibrogenic activities of human fibroblasts.

Activated macrophages regulate fibrogenesis by providing cytokines and growth factors that modulate the proliferation and collagen synthesis of fibroblasts. However, macrophages can be activated in a classical pathway induced by LPS or IFN-gamma and an alternative pathway induced by IL-4 or glucocorticoid. Differently activated macrophages display distinct biological features. To clarify the difference between these two subsets of macrophages in the regulatory mechanisms controlling fibrogenesis, human peripheral blood monocytes were used as the source of macrophages and cocultivation of differently activated macrophages and a fibroblast cell line, WI-38, was performed. Alternatively activated macrophages increased the proliferation index and collagen synthesis of cocultivated WI-38 cells in comparison to untreated monocytes, while classically activated macrophages markedly reduced collagen production of cocultivated WI-38 cells. Additionally, mRNA expression and protein production of TGF-beta(1), PDGF-AA, and PDGF-BB were elevated in alternatively activated macrophages in parallel to their profibrogenic effects. In contrast, expression and production of TNF-alpha, as well as MMP-7, were enhanced in classically activated macrophages. These findings suggested that alternatively activated macrophages enhance fibrogenesis of fibroblasts by providing profibrogenic factors, while classically activated macrophages inhibit fibrogenesis of fibroblasts by releasing antifibrogenic or fibrolytic factors.

Cell Division↗
PubMed2000

[Bcl-2 antisense oligodeoxyribonucleotide increases apoptosis of lung carcinoma cells induced by cisplatin].

OBJECTIVE: To study the effect of antisense oligodeoxyribonucleotide (ODN) to apoptotic suppress gene bcl-2 on apoptosis of lung carcinoma cells induced by cisplatin. METHODS: The lung carcinoma cells expressing bcl-2 were chosen to participate in this experiment. Cultured cells were divided into 7 groups: ODN, nonsense, ODN + cisplatin, nonsense + cisplatin, cisplatin, lipofectin and control. Bcl-2 antisense or nonsense mixed with lipofectin was added into above corresponding cultured cells. After cultured for 6 hours, cisplatin was added into corresponding groups. The cells were cultured again for 16 hours. And then, the cells were smeared on slides. Apoptotic cells were labeled with TdT-mediated dUTP nick end labeling (TUNEL) method on cell smears. Apoptotic index (AI) was counted to show the percentage of apoptotic cancer cells. The immunocytochemistry was used to detect the expression of bcl-2 in carcinoma cells. RESULTS: The bcl-2 expression of cancer cell in ODN group was significantly decreased compared to the control and nonsense groups. The AI of ODN + cisplatin group was 16.4 +/- 1.7, cisplatin group 4.1 +/- 0.8, antisense group 5.9 +/- 0.2, nonsense group 3.3 +/- 0.7, nonsense + cisplatin 7.6 +/- 1.1, lipofectin 5.1 +/- 0.9, control group 3.6 +/- 0.6. The AI of antisense + cisplatin group was significantly higher than that of other groups. CONCLUSION: Antisense oligodeoxyribonucleotide to bcl-2 can inhibit significantly the expression of bcl-2 of lung cancer cells and increase apoptosis of cancer cells induced by cisplatin.

Antineoplastic Agents↗
PubMed2000

[NF-kappa B activation and the inhibitory effect of dexamethasone in experimental asthmatic guinea pigs].

OBJECTIVE: To investigate the role of NF-kappa B in pathogenesis of asthma. METHODS: Electrophoresis mobility shift assay and supershift assay were used to analyze the expression of NF-kappa B activation and its components. RESULTS: Nuclear extracts prepared from the thoracic blood mononuclear cells and the whole lung tissue, respectively in OVA-sensitized and challenged guinea pigs, both displayed stronger DNA-binding activity at 2 h timepoint (244.1 +/- 2.4; 176.0 +/- 4.0) comparing to the control (167.0 +/- 4.6; 67.3 +/- 2.5), and the activity peaked at 6 h timepoint (294.7 +/- 3.2; 282.3 +/- 6.8) and continued till 12 h timepoint (200.9 +/- 1.2; 110.8 +/- 1.0). The activated NF-kappa B contained p50. Dexamethasone suppressed the NF-kappa B activation (235.4 +/- 3.3; 104.6 +/- 8.4) in the nuclear extracts of the Blood mononuclear cells and the lung tissue, respectively. CONCLUSIONS: This result showed that NF-kappa B were possibly through transcriptionally regulating the expression of many important inflammatory proteins. The dexamethasone could inhibit the activation of NF-kappa B in the allergic model, possibly through which the antiinflammatory action was exerted.

Animals↗
PubMed1998

[Effects of dexamethasone on apoptosis of airway inflammatory cells in asthmatic guinea-pigs].

OBJECTIVE: Clearance of airway inflammatory cells is the key point of therapeutic effect in asthma. Apoptosis, a form of cell death, is thought to be critically important to promote the clearance of inflammatory cells and the resolution of inflammation. To investigate the effects of dexamethasone on apoptosis of airway inflammatory cells in asthma showed be very important. METHOD: Dexamethasone was used for the treatment of asthma model of guinea pigs set up by inhaling ovalbumin. Apoptotic cells were labelled with TdT-mediated dUTP nick end labeling(TUNEL) technique on formalin-fixed paraffin-embedded trachea and lung tissue sections. By way of immunohistochemistry, eosinophils were stained with EG2 antibody and T lymphocytes with CD3+, CD4+ and CD8+ antibodies on sections. RESULT: (1) The quantity of airway eosinophils and lymphocytes decreased in dexamethasone group, which could not be observed in the control one (P < 0.01). (2) Apoptotic index of lymphocytes was significantly elevated following dexamethasone treatment(P < 0.05). But no difference was found in the proportion of apoptotic eosinophils between these two groups. (3) The percentage of EG2 positive eosinophils and CD4+ positive lymphocytes decreased significantly following dexamethasone treatment. On the contrary, the number of CD8+ lymphocytes increased in dexamethasone group when compared with the control one (P < 0.05). CONCLUSION: (1) The quantity of airway eosinophils decreases following dexamethasone treatment in guinea-pigs asthma, and its mechanism may not be ascribed mainly to the apoptosis of eosinophils. (2) The number of lymphocytes, mainly CD4+, decreased following dexamethasone treatment in guinea-pig airways, and apoptosis may represent the mechanism that promotes the clearance of lymphocytes in asthma.

Animals↗
PubMed1997

Use of an artificial neural network to analyse an ECG with QS complex in V1-2 leads.

A feed-forward neural network with back-propagation algorithm is used to distinguish anterior wall myocardial infarction (AI) and non-infarction based on analysis of computerised electrocardiograms. Data used in the study are from 132 patients diagnosed as having AI by automated electrocardiograph analysis. Their ECGs show an abnormal Q-wave (or QS complex) or small R progression in leads V1 and V2. However, 66 of them are diagnosed as old AI from the history, physical examination, echocardiogram and other laboratory data, whereas the other 66 are not. The network is trained with the data from half of the AI and non-infarction patients; respectively. The diagnostic accuracy rate is then tested with the remaining 66 patients (33 infarction, 33 non-infarction) who have not been exposed to the network. The neural network correctly identifies 90.2% of the patients with AI and 93.3% of the patients without infarction. The neural network is capable of diagnosing anterior wall myocardial infarction better than a computer electrocardiograph.

Decision Trees↗
PubMed1997

[Expression of FGF-b and C-myc in rats lung tissue affected by hypoxia].

OBJECTIVE: To study FGF's roles in the reconstruction of vascular walls owing to chronic hypoxia. METHOD: 40 SD rats [corrected] were divided into different hypoxia groups and proceeded with various hypoxic intervals. Expression of FGF-b and transcription of c-myc mRNA of the rats [corrected] lung tissues were detected by immunohistochemical method and in situ hybridization. RESULTS: FGF-b increased obviously in the smooth muscle and advential tissue of pulmonary arteries after 14 days of hypoxia, whereas C-myc mRNA showed overexpression in rats [corrected] lung tissue from 7th to 21st day of hypoxia. CONCLUSION: (1) Hypoxia may lead to activation of C-myc oncogene and increase of FGF-b expression in lung tissue. (2) FGF-b and C-myc oncogene takes part in reconstruction of pulmonary arterial wall affected by chronic hypoxia.

Animals↗
PubMed1997

[Effects of chronic hypoxia on the expression of oncogene jun fos and myb mRNA in rat lung].

This paper is to investigate the expression of oncogene jun fos and myb mRNA in the lung of rats exposed to chronic hypoxia. 15 SD rats were put in low oxygen chamber (FiO2 = 0.1), 8 hrs daily for 1, 2 and 3 weeks. Five rats breathing room air served as control. Oncogene expression in lung tissue assessed by the use of in situ hybridization. The results showed that (1) there was a slight expression of jun mRNA but not fos and myb mRNA in the control normoxic rats' lung; (2) it was found that a less expression of jun mRNA in lung after 1 week hypoxia, but after 2 week hypoxia jun mRNA elevated again and significantly increased after 3 week hypoxia as compared with that in normoxia; (3) the oncogene myb mRNA expression showed significant increase in 1 and 2 week hypoxia and returned to normal status in 3 week hypoxia; (4) after 1 to 3 week hypoxia, a significant increased expression of fos mRNA was found as compared with that in normoxia. It is suggested hypoxia may induce increased expression of proto-oncogene jun myb and fos, which may be related to proliferation of pulmonary arterial smooth muscle cells and fibroblasts.

Animals↗
PubMedDate not supplied

Using a neural network to diagnose the hypertrophic portions of hypertrophic cardiomyopathy.

We studied the ability of a neural network to identify the hypertrophic cardiac regions in hypertrophic cardiomyopathy, with the network using electrocardiographic (ECG) information alone. Computer-based electrocardiography remains a fundamental diagnostic method for analysis of cardiac contour and rhythm. Almost all patients with hypertrophic cardiomyopathy have some abnormal findings on electrocardiography, but it is very difficult, even for an experienced cardiologist, to identify the hypertrophic regions on the basis of electrocardiography alone. Since neural networks are known to be better at pattern recognition than humans are, we tried using a neural network trained with ECG information to identify the hypertrophic regions in hypertrophic cardiomyopathy.

Algorithms↗