The effect of celecoxib in traumatic heterotopic ossification around temporomandibular joint in mice.

OBJECTIVE: In this study, the role of inflammation in traumatic heterotopic ossification around temporomandibular joint (THO-TMJ), as well as the preventive and treatment effect of celecoxib in THO-TMJ both in vivo and in vitro were explored. DESIGN: A surgically-induced THO-TMJ mouse model and a co-culture model of ATDC-5 or MC3T3-E1 and RAW-264.7 cells were used in this study for in vivo and in vitro research. RESULTS: A series of inflammatory factors, such as CD3, CD68, CD20, IL-10, IL-6 and TNF-α, were activated 48 h after trauma in a THO-TMJ model. Local trauma initiated systemic inflammatory responses as well as T cell- and macrophage-mediated local inflammatory responses around TMJ. In addition, expression of COX-2 was significantly elevated. The findings also showed that local injection of celecoxib could effectively alleviate the inflammatory response around TMJ at the early stage of trauma and inhibit the formation of THO-TMJ in vivo. Meanwhile, celecoxib could inhibit chondrogenic differentiation of ATDC-5 and osteogenic differentiation of MC3T3-E1 under inflammatory condition in vitro. Furthermore, celecoxib could inhibit the expression of Bmpr1b in the injured condylar cartilage at the initiation stage of THO-TMJ, which implied that Bmpr1b expressed by the residual condylar cartilage might be related to the pathogenesis of THO-TMJ. CONCLUSIONS: Inflammation played a crucial role in the pathogenesis of THO-TMJ, and anti-inflammation might be a possible choice to inhibit THO-TMJ, which provided scientific clues for the mechanisms, pharmacotherapy and molecular intervention of THO-TMJ.

[Expression and prognosis effect of methylation-regulated SLIT3 and SPARCL1 genes in smoking-related lung adenocarcinoma].

Objective: To investigate the expression and prognosis effect of methylation-regulated SLIT3 and SPRCL1 genes in smoking-related lung adenocarcinoma. Methods: The expression levels of SLIT3 and SPARCL1 in cigarette smoke-induced malignant transformed cell (S30) and lung adenocarcinoma (LUAD) cell lines were measured by real-time fluorescence quantitative PCR (qPCR). Datasets of mRNA expression, DNA methylation and patient information data were obtained from The Cancer Genome Altas (TCGA) database. The mRNA expression levels of SLIT3 and SPARCL1 were validated in LUAD tissues. The 10-year survival curve of LUAD patients with different smoking history was plotted, and the correlation between mRNA expression level and DNA methylation level of LUAD patients was further analyzed. S30 cells were treated with 5-azacytidine (5-aza), an inhibitor of DNA methyltransferase, to analyze the methylation regulatory mechanism of SLIT3 and SPRCL1. Results: The qPCR results showed the significant down-regulation of SLIT3 and SPARCL1 in S30 cell and four LUAD cell lines (SLIT3: 0.493±0.134 and 0.041±0.014, 0.161±0.023, 0.277±0.055, 0.035±0.005; SPARCL1: 0.507±0.131 and 0.453±0.045, 0.420±0.040, 0.153±0.035, 0.430±0.050; all P<0.01). Bioinformatics analysis showed that SLIT3 and SPARCL1 were low expressed in LUAD tissue (8.12±1.58 vs 10.84±0.69 and 11.46±1.06 vs 13.57±0.67; both P<0.001) compared with adjacent peritumoral tissues, and expression levels of SLIT3 and SPARCL1 were significantly correlated with smoking history (both P<0.001). Non-smoker with high expression of SLIT3 and SPARCL1 was associated with better prognosis among LUAD patients. There was a significant negative correlation between promoter methylation and mRNA expression level of the two genes (r=-0.208, -0.574; both P<0.001). 5-aza treatment significantly up-regulated the expression levels of SLIT3 and SPARCL1 genes in S30 cells (2.137±0.281, 3.657±0.882; both P<0.01). Conclusion: SLIT3 and SPARCL1 can be regulated by DNA methylation and down-regulated in LUAD tissue, which has important prognostic significance on the smoking-induced LUAD patients.

Case Report Identification of a novel SLC45A2 mutation in albinism by targeted next-generation sequencing.

Albinism is a diverse group of hypopigmentary disorders caused by multiple-genetic defects. The genetic diagnosis of patients affected with albinism by Sanger sequencing is often complex, expensive, and time-consuming. In this study, we performed targeted next-generation sequencing to screen for 16 genes in a patient with albinism, and identified 21 genetic variants, including 19 known single nucleotide polymorphisms, one novel missense mutation (c.1456 G>A), and one disease-causing mutation (c.478 G>C). The novel mutation was not observed in 100 controls, and was predicted to be a damaging mutation by SIFT and Polyphen. Thus, we identified a novel mutation in SLC45A2 in a Chinese family, expanding the mutational spectrum of albinism. Our results also demonstrate that targeted next-generation sequencing is an effective genetic test for albinism.

Mechanical Strain Promotes Osteogenesis of BMSCs from Ovariectomized Rats via the ERK1/2 but not p38 or JNK-MAPK Signaling Pathways.

Osteoporosis has become a world-wide health problem. As a promising intervention, mechanical strain is considered to be an important factor in bone remodeling. However, the underlying mechanisms are still not clarified clearly. In the present study, we aim to investigate the possible mechanism by which mechanical stimulation induces osteogenic differentiation of bone mesenchymal stem cells (BMSCs) from ovariectomized rats (OVX BMSCs). The results demonstrated that intermittent mechanical strain (IMS) promoted osteogenic differentiation of OVX BMSCs by activating Runt-related transcription factor 2 (Runx2). When the extracellular regulated kinase1/2-mitogen activated protein kinases (ERK1/2-MAPK) signaling pathway was blocked, the osteogenenic effects of IMS were diminished; while blocking of the p38-MAPK signaling pathway had little effect on subsequent osteogenic events. In addition, the phosphorylation level of JNK was not affected by IMS. Our results indicated that strain-induced osteogenic differentiation of OVX BMSCs may take effect via ERK1/2-MAPK not p38 or c-Jun N-terminal (JNK)-MAPK signaling pathway. These findings may have implications for physical treatment of osteoporosis in vitro.

The metabolism and pharmacokinetics of phospho-sulindac (OXT-328) and the effect of difluoromethylornithine.

BACKGROUND AND PURPOSE: Phospho-sulindac (PS; OXT-328) prevents colon cancer in mice, especially when combined with difluoromethylornithine (DFMO). Here, we explored its metabolism and pharmacokinetics. EXPERIMENTAL APPROACH: PS metabolism was studied in cultured cells, liver microsomes and cytosol, intestinal microsomes and in mice. Pharmacokinetics and biodistribution of PS were studied in mice. KEY RESULTS: PS undergoes reduction and oxidation yielding PS sulphide and PS sulphone; is hydrolysed releasing sulindac, which generates sulindac sulphide (SSide) and sulindac sulphone (SSone), all of which are glucuronidated. Liver and intestinal microsomes metabolized PS extensively but cultured cells converted only 10% of it to PS sulphide and PS sulphone. In mice, oral PS is rapidly absorbed, metabolized and distributed to the blood and other tissues. PS survives only partially intact in blood; of its three major metabolites (sulindac, SSide and SSone), sulindac has the highest C(max) and SSone the highest t(1/2) ; their AUC(0-24h) are similar. Compared with conventional sulindac, PS generated more SSone but less SSide, which may contribute to the safety of PS. In the gastroduodenal wall of mice, 71% of PS was intact; sulindac, SSide and SSone together accounted for <30% of the total. This finding may explain the lack of gastrointestinal toxicity by PS. DFMO had no effect on PS metabolism but significantly reduced drug level in mouse plasma and other tissues. CONCLUSIONS AND IMPLICATIONS: Our findings establish the metabolism of PS define its pharmacokinetics and biodistribution, describe its interactions with DFMO and largely explain its gastrointestinal safety.

The novel phospho-non-steroidal anti-inflammatory drugs, OXT-328, MDC-22 and MDC-917, inhibit adjuvant-induced arthritis in rats.

BACKGROUND AND PURPOSE: The use of non-steroidal anti-inflammatory drugs (NSAIDs) in the treatment of rheumatoid arthritis (RA) is limited by their toxicity. We evaluated the anti-inflammatory efficacy and safety of three novel modified NSAIDs, phospho-aspirin, phospho-ibuprofen and phospho-sulindac. EXPERIMENTAL APPROACH: We determined the anti-inflammatory effects and gastrointestinal safety of the phospho-NSAIDs in the rat adjuvant arthritis model and studied their mechanism of action in cultured cells, Cytokines were measured with elisa and activation of nuclear factor-κB (NF-κB) by immunohistochemistry. KEY RESULTS: All three phospho-NSAIDs showed less gastrointestinal toxicity than their parent compounds and demonstrated strong anti-inflammatory effects, essentially reversing joint inflammation and oedema. They have a broad but not uniform effect on the expression of relevant cytokines, in general decreasing IL-6 and IL-1ß and increasing IL-10 levels in rat plasma and cultured cells. Phospho-sulindac and phospho-ibuprofen but not phospho-aspirin suppressed PGE(2) production in vitro, whereas phospho-aspirin (in contrast to aspirin) showed the same effect in vivo. In joint tissues, phospho-aspirin inhibited NF-κB activation, and suppressed inflammation and bone resorption. Phospho-aspirin also inhibited Jurkat T cell proliferation. In general, phospho-aspirin had greater efficacy but different effects upon inflammatory mediators compared with aspirin. The chemical modification of the parent NSAIDs seems crucial for their safety and efficacy. CONCLUSIONS AND IMPLICATIONS: Phospho-aspirin, phospho-ibuprofen and phospho-sulindac were safer than their parent NSAIDs, were highly effective in rat adjuvant arthritis and inhibited many key mediators in the pathophysiology of RA. These novel compounds are promising candidate drugs for the treatment of RA and merit further evaluation.

Pregnane X receptor suppresses proliferation and tumourigenicity of colon cancer cells.

BACKGROUND: Pregnane X receptor (PXR) is a nuclear receptor that regulates the metabolism and disposition of various xenobiotics and endobioitics. We investigated a novel PXR function in regulating colon tumourigenesis in this study. METHODS: Histochemistry, transfection, cell proliferation assay, anchorage-alpha-dependent assay, xenograft, immunohistochemistry, immunofluorescence flow cytometry. RESULTS: Using histochemistry analysis, we found that PXR expressions were lost or greatly diminished in many colon tumours. Ectopic expression of human PXR through stable transfection of PXR into colon cancer cell line HT29 significantly inhibited cell proliferation as determined by cell proliferation assay and anchorage-independent assay. Pregnane X receptor suppressed significantly HT29 xenograft tumour growth in nude mice compared with control (310+/-6.2 vs 120+/-6 mg, P<0.01). Immunohistochemistry and immunofluorescence analysis of Ki-67 on excised xenograft tumour tissues showed that PXR inhibited cancer cell proliferation. Furthermore, expressions of PXR and Ki-67 were mutually exclusive. The flow cytometry analysis indicated that PXR caused G(0)/G(1) cell-cycle arrest. p21(WAF1/CIP1) expression was markedly elevated whereas E2F1 expression was inhibited by PXR. CONCLUSION: PXR inhibits the proliferation and tumourigenicity of colon cancer cells by controlling cell cycle at G(0)/G(1) cell phase by regulating p21(WAF1/CIP1) and E2F/Rb pathways.

Lupus nephritis reoccurs following transplantation in the lupus prone mouse.

The incidence and pathomechanism of recurrent lupus nephritis (RLN) after transplantation is not clearly understood. Burning out of the autoimmune process or local immunoregulatory mechanisms in the kidney may be responsible for the low incidence of recurrence. These mechanisms cannot be investigated in human subjects, due to post-transplant immunosuppression. To investigate the pathomechanisms of RLN, male and female kidneys were transplanted from FAS deficient lupus prone (LPR) or control (FAS intact) MRL mice into either LPR or MRL recipients. Urinary protein and blood urea were assessed. Double negative (DN) lymphocyte proliferation was determined by flow cytometry. Two months after transplantation inflammatory infiltration of the glomerular, vascular and interstitial compartments were determined. Renal function as demonstrated by blood urea levels was normal in MRL recipients, but elevated in LPR recipients, independent of the donor strain. Paralleling functional results, inflammatory infiltration was mild or absent in MRL recipients of MRL grafts, and mild to moderate in MRL recipients of LPR grafts, suggesting that kidney removal from the autoimmune (LPR) environment significantly reduced inflammation. Graft infiltration was most severe in LPR recipients: grafts were similarly inflamed independent of the donor. All LPR recipients had significantly less CD4+ Th cells versus MRL mice. Transplantation of LPR grafts into MRL recipients reduced CD4+ Th cell percentage, accompanied by a slight induction of lupus autoantibody production. Our results demonstrate that lupus nephritis is not kidney specific in the LPR model with recurrence after transplantation in the absence of immunosuppression.

Histopathology and the detection of avian bornavirus in the nervous system of birds diagnosed with proventricular dilatation disease.

Avian bornavirus (ABV) is currently considered a probable etiologic agent of proventricular dilatation disease (PDD) of psittacines. We tested 24 stored avian brain samples, processed for histopathology and retained following their submission for necropsy or histopathology to the Schubot Exotic Bird Center diagnostic laboratory in 1992. Thirteen of these samples were from birds diagnosed at that time as suffering from PDD. The remaining 11 samples were diagnosed as suffering from diseases other than PDD. Immunohistochemistry was performed using an antiserum directed against the ABV nucleoprotein (N-protein). Stained slides were read by an investigator unaware of their prior histopathology results. Cells containing ABV N-protein were present in the nervous tissues of all 13 PDD cases. One bird not previously diagnosed with PDD also had ABV N-protein in its brain. A review of this bird's necropsy report indicated that it was, most probably, also suffering from PDD. The remaining 10 non-PDD birds had no detectable N-protein in their brains. The N-protein was present in the cerebrum, cerebellum and spinal cord. These findings support other studies that indicate that ABV is an etiological agent of PDD.

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.

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.

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.

[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.

[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.

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.

[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.

[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.

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.