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Biomedical subjects

S N Huang

Publications and source records attributed to S N Huang.

At least 19 recordsLinked to original sources
PubMed2006

Supercritical carbon dioxide extract exhibits enhanced antioxidant and anti-inflammatory activities of Physalis peruviana.

Physalis peruviana L. (PP) is a medicinal herb widely used in folk medicine. In this study, supercritical carbon dioxide (SFE-CO2) method was employed to obtain three different PP extracts, namely SCEPP-0, SCEPP-4 and SCEPP-5. The total flavonoid and phenol concentrations, as well as antioxidant and anti-inflammatory activities of these extracts were analyzed and compared with aqueous and ethanolic PP extracts. Among all the extracts tested, SCEPP-5 demonstrated the highest total flavonoid (234.63+/-9.61 mg/g) and phenol (90.80+/-2.21 mg/g) contents. At concentrations 0.1-30 microg/ml, SCEPP-5 also demonstrated the strongest superoxide anion scavenging activity and xanthine oxidase inhibitory effect. At 30 microg/ml, SCEPP-5 significantly prevented lipopolysaccharide (LPS; 1 microg/ml)-induced cell cytotoxicity in murine macrophage (Raw 264.7) cells. At 10-50 microg/ml, it also significantly inhibited LPS-induced NO release and PGE2 formation in a dose-dependent pattern. SCEPP-5 at 30 microg/ml remarkably blocked the LPS induction of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Taken together, these results suggest that SCEPP-5, an extract of SFE-CO2, displayed the strongest antioxidant and anti-inflammatory activities as compared to other extracts. Its protection against LPS-induced inflammation could be through the inhibition of iNOS and COX-2 expression.

Animals↗
PubMed2006

Nonlinear adaptive control of interconnected systems using neural networks.

In this letter, we solve the problem of decentralized adaptive asymptotic tracking for a class of large scale systems with significant nonlinearities and uncertainties. Neural networks (NNs) are used as a control part to cancel the effect of the unknown nonlinearity. Semiglobal asymptotic stability results are obtained and the tracking error converges to zero.

Algorithms↗
PubMed2001

Riboflavin uptake in human trophoblast-derived BeWo cell monolayers: cellular translocation and regulatory mechanisms.

Riboflavin (vitamin B2) is essential for fetal development and must be acquired from maternal sources. The uptake mechanism of riboflavin and the major regulatory pathways involved were characterized in a model for the placental barrier, the human choriocarcinoma cell line, BeWo. Uptake of [3H]riboflavin was saturable (Kt = 1.32 +/- 0.68 nM, Jmax = 266.63 +/- 26.89 fmol/mg of protein/20 min), and was significantly reduced at low temperature and in the presence of metabolic inhibitors (azide, 2-deoxyglucose) or structural analogs. Ouabain, amiloride, sodium-free buffers, and medium with pH values ranging from 3 to 8 did not affect uptake of [3H]riboflavin. In contrast, substitution of chloride with other monovalent anions significantly inhibited its uptake. Induced differentiation of BeWo cells into syncytiotrophoblasts by forskolin or 8-bromo-cyclic adenosine monophosphate introduced a time-dependent decrease of riboflavin uptake. Preincubation with activators of cyclic nucleotide-dependent protein kinase pathways (3-isobutyl-1-methylxanthine and p-chlorophenylthio-cyclic guanosine monophosphate) and calmodulin antagonists (calmidazolium and W-13) resulted in a concentration-dependent reduction of [3H]riboflavin uptake, whereas specific modulators of protein kinase C pathways did not have significant effects. 3-Isobutyl-1-methylxanthine exerted its regulatory effect on riboflavin uptake via decreasing both Kt and Jmax of the riboflavin uptake process (Kt = 6.32 +/- 1.29 nM, Jmax = 135.57 +/- 10.42 fmol/mg of protein/20 min). In summary, we report the presence of high- affinity riboflavin transporter(s) on the microvillous membrane of BeWo cells that appears to be modulated by cellular cyclic nucleotide levels and calmodulin.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

Constitutive activation of nuclear factor kappaB in hepatocellular carcinoma.

BACKGROUND: Nuclear factor kappaB (NF-kappaB) is a transcription factor that plays important roles in cell proliferation and in immunity against viral infections. NF-kappaB is a dimer of Rel proteins that is sequestered in the cytoplasm as an inactive form through interaction with an inhibitory kappaB (IkappaB) protein. When IkappaB is degraded, the NF-kappaB dimer will enter the nucleus to activate the target genes. Chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection may activate NF-kappaB and, thus, may modulate cell apoptosis and may be associated with oncogenesis. The role of NF-kappaB in hepatocellular carcinoma (HCC) has not yet been explored. METHODS: Immunohistochemical staining to search for active nuclear RelA and nuclear IkappaBalpha proteins were done on formalin fixed liver tissues from 65 patients with HCC and from 9 normal control participants. Nuclear extracts of fresh-frozen tumor and nontumor liver tissues from 37 patients with HCC and from 7 normal controls were tested for NF-kappaB-DNA binding activity by electrophoretic mobility shift assay. The RelA and IkappaBalpha protein expressions were studied by Western blot analysis. RESULTS: Nuclear NF-kappaB stainings were significantly more abundant in HBV-infected or HCV-infected tumors as well as nontumor parts of HCC compared with normal controls. Nuclear NF-kappaB DNA binding activity and nuclear RelA protein expression were greater in tumor tissue compared with nontumor tissue, whereas cytosolic IkappaBalphs protein expression was generally greater in nontumor tissue compared with tumor tissue. CONCLUSIONS: Constitutive activation of NF-kappaB was found more frequently in tumor tissue compared with nontumor tissue. It is possible that NF-kappaB overexpression accompanied by dysregulation of IkappaBalpha may play a role in the hepatocarcinogenesis of HBV or HCV infection.

Adult↗
PubMed2000

Activation of nuclear factor kappaB in hepatitis C virus infection: implications for pathogenesis and hepatocarcinogenesis.

The hepatitis C virus (HCV) core protein is a multifunctional protein. It may bind to the death domain of tumor necrosis factor receptor 1 (TNFR1) and to the cytoplasmic tail of lymphotoxin-beta receptor, implying that it may be involved in the apoptosis and anti-apoptosis signaling pathways. In vitro studies have been inconclusive regarding its ability to inhibit or enhance TNF-alpha-induced apoptosis. To address this issue, electrophoretic mobility shift assay (EMSA) and immunohistochemical studies were used to show the activation of nuclear factor kappaB (NF-kappaB) in HCV-infected liver tissues and in HCV core-transfected cells. The activation of NF-kappaB was correlated with the apoptosis assays. The results showed that NF-kappaB activation could be shown in HCV-infected livers and HCV core-transfected cells. The data of EMSA correlated with those of immunohistochemical studies, which revealed a higher frequency of NF-kappaB nuclear staining in HCV-infected than in normal livers. NF-kappaB activation conferred resistance to TNF-alpha-induced apoptosis in HCV core-transfected cells. Inhibition of NF-kappaB activation by pyrrolidine dithiocarbamate sensitized them to TNF-alpha-induced apoptosis. These findings suggest that HCV infection may cause anti-apoptosis by activation of NF-kappaB and implicate a mechanism by which HCV may evade the host's immune surveillance leading to viral persistence and possibly to hepatocarcinogenesis.

Adult↗
PubMed2000

Well-differentiated fetal adenocarcinoma of the lung.

We describe the case of a 43-year-old woman with a tumor shadow in the upper lobe of the left lung. The tumor was initially suspected to be a carcinoid tumor, following percutaneous needle biopsy. Subsequently, a left upper lobectomy was performed, and a well-differentiated fetal adenocarcinoma was diagnosed histologically. Unlike the biphasic epithelial and stromal features of pulmonary blastoma, it was composed solely of malignant glands of embryonal appearance.

Adenocarcinoma↗
PubMed2000

Involvement of a receptor-mediated component in cellular translocation of riboflavin.

This study addresses the transport mechanism of riboflavin (vitamin B(2)) across intestinal epithelium in the presence and absence of pharmacologically active compounds. A polarized transport process with a 6-fold higher basolateral (BL)-to-apical (AP) flux was observed in both a human intestinal cell model (Caco-2) and rat intestinal tissue. Riboflavin-specific translocation systems on both the AP and BL cell surfaces were saturable with affinity values close to most receptors (K(m): 9.72 +/- 0.85 and 4.06 +/- 0.03 nM, respectively). Pharmacological agents known to alter intracellular endocytic events were used to examine the potential involvement of receptor-mediated events. Nocodazole significantly inhibited AP uptake (58.4%), BL-to-AP riboflavin (56.7%) and fluorescein isothiocyanate-labeled transferrin (FITC-Tf) (31.8%) transport without affecting mannitol or cholic acid transport, whereas AP-to-BL riboflavin (252.8%) and FITC-Tf (145.1%) transport was increased. Brefeldin A significantly enhanced AP-to-BL riboflavin (37.1%) and bidirectional FITC-Tf transport (AP-to-BL: 13-fold; BL-to-AP: 5-fold). without affecting BL-to-AP riboflavin transport. Combined, these data suggest an essential role of microtubule-dependent movement and vesicular sorting component(s) in the bidirectional transport of riboflavin. Dissociation of riboflavin from the cell surface was pH-dependent with significantly higher substrate release at acidic pH, indicating the presence of riboflavin-specific cell surface receptors. In summary, our studies provide biochemical evidence of the involvement of a receptor-mediated mechanism in the cellular translocation of riboflavin.

Biological Transport↗
PubMed1999

Development of a PCR assay for diagnosis of Pneumocystis carinii pneumonia based on amplification of the multicopy major surface glycoprotein gene family.

We have evaluated a PCR technique using primers based on Pneumocystis carinii major surface glycoprotein (MSG) genes, a multicopy gene family, for utility in detection of P. carinii in BAL and oropharyngeal samples obtained from immunosuppressed patients. These primers were able to detect P. carinii DNA in as little as 16 fg of genomic DNA. PCR using MSG primers detected P. carinii DNA in 7 smear-positive BAL samples (100% sensitivity), and found no P. carinii DNA in 12 smear-negative BAL samples (100% specificity). Mitochondrial ribosomal RNA (mrRNA) primers, commonly used in PCR studies of PCP, detected P. carinii in six of seven positive samples (85.7% sensitivity) and none of 12 were negative samples (100% specificity). Diagnosis of PCP by amplification of 81 oropharyngeal samples using MSG primers had a 50% sensitivity (4/8) and 96% specificity (70/73). PCR with mrRNA primers was 37.5% sensitive (3/8) and 100% specific (73/73). All three false-positive MSG results showed a very low intensity on Southern hybridization. PCR using MSG gene primers should prove valuable in the diagnosis of PCP.

Fungal Proteins↗
PubMed1999

Identification and characterization of novel variant major surface glycoprotein gene families in rat Pneumocystis carinii.

The major surface glycoprotein (MSG) is an abundant, immunodominant protein on the surface of the opportunistic pathogen Pneumocystis carinii. The current study identified two novel variant MSG (vMSG) gene families in rat P. carinii that are closely related to but distinct from MSG. These gene families encode proteins of approximately 90 kDa (v1MSG) and approximately 115 kDa (v2MSG). Compared with MSG, v1MSG is characterized by a deletion near the carboxyl terminus. The predicted v1MSG and v2MSG proteins are highly homologous to MSG at the carboxyl, but not the amino, terminus. Like MSG, they are cysteine-rich. Approximately 10% of the apparent molecular weight is due to N-linked glycosylation. Southern blotting studies demonstrated that, like MSG, v1MSG and v2MSG are the products of multicopy gene families. However, unlike MSG, each vMSG gene encodes a signal peptide, suggesting that the regulation of vMSG is different from that of MSG.

5' Untranslated Regions↗
PubMed1997

Histopathology and pathobiology of hepatotropic virus-induced liver injury.

The present report concerns current knowledge regarding immunopathogenesis that can be applied in the interpretation of histopathological changes in acute and chronic viral hepatitis. The histopathological features of viral hepatitis have not been changed and light microscopic examination remains essential for making a diagnosis and classification of chronic hepatitis and for the provision of objective parameters on grading and staging. However, new understanding and knowledge of viral pathogenesis, host immune responses, the biological behaviour of the causative viral agents and, in particular, viral interference in multiple hepatotropic viral infections must be taken into consideration in the interpretation of histopathological and immunopathological findings of liver tissues. This report also presents some histopathological analyses on multiple hepatotropic viral infections. It can be concluded that the diagnostic histological criteria for acute hepatitis remain applicable in such settings. However, the cause of acute flare up in chronic hepatitis could not be determined without clinical, virological and serological information. Routine histopathology cannot distinguish a new infection from an acute exacerbation due to a high level of viral replication or mutant virus. A repertoire of immunocytochemical stainings for viral antigens is helpful, but caution must be exercised in suggesting a specific viral aetiology due to the fact that suppression of pre-existing viral antigens can be pronounced when the new or concurrent infection is hepatitis C virus related.

Animals↗
PubMed1997

T cell mechanisms in the immunopathogenesis of viral hepatitis B and C.

Considerable evidence suggests that immune mechanisms are involved in the pathogenesis of both hepatitis B and C. Both CD4+ and CD8+ T cell responses to viral antigens are important mechanisms that may be responsible for the hepatocyte damage in hepatitis B and C. CD4+ T cell proliferative responses to hepatitis B core antigen (HBcAg) in terms of stimulation index are correlated with hepatitis activity. These responses can be demonstrated in both adult and paediatric patients, and are more vigorous in patients with acute self-limited hepatitis B than in patients with chronic hepatitis B. Patients with hepatitis C also had a significant CD4+ T cell response to hepatitis C virus (HCV) antigens. These responses are also vigorous in acute hepatitis C with recovery than in those cases that evolve to chronic hepatitis C. In terms of human leucocyte antigen (HLA) class I-restricted, CD8+ cytotoxic T lymphocyte (CTL) response, antigenic peptides derived from HBcAg, hepatitis B surface antigen (HBsAg), and polymerase have been demonstrated as the targets for CTL recognition in hepatitis B patients. Multiple CTL epitopes within both HBsAg and HBcAg can be detected by sensitizing target cells with synthetic peptides. Similar to hepatitis B virus (HBV) infection, multispecific, HCV-specific CTL responses can coexist with an extensive quasispecies of viral variants. The mechanisms of viral persistence in both hepatitis B and C are not yet clarified.

Epitopes↗
PubMed1996

Heat shock pretreatment prevents hydrogen peroxide injury of pulmonary endothelial cells and macrophages in culture.

The purpose of the present study was to determine whether heat shock pretreatment would protect pulmonary endothelial cells and alveolar macrophages against hydrogen peroxide (H2O2)-induced injury. The bovine pulmonary artery endothelial cells (BPAECs) heat-shocked (42 degrees C for 2 h) prior to exposure to H2O2 (1 mmol/L for 45 min) showed significant decrease in H2O2-mediated increment of release of lactate dehydrogenase and production of thiobarbituric acid-reactive substances, and obvious alleviation in H2O2-induced decrease in activities of catalase and superoxide dismutase. Heat-shocked (42 degrees C for 2 h) rat pulmonary alveolar macrophages (PAMs) also obtained acquired resistance to injury by subsequent exposure of 1, 2, or 3 mmol/L H2O2 for 45 min. Simultaneously with this acquired oxidative resistance, Northern blot analysis showed that heat-shocked BPAECs and PAMs, contained an increased level of mRNA coding for the inducible form of heat shock protein 70 (HSP70), and Western blot analysis indicated that there were increased expression of HSP70. Inhibition of protein synthesis by cycloheximide (25 micrograms/mL) and inhibition of RNA synthesis by actinomycin D (5 micrograms/mL) prevented the cytoprotection against H2O2. These results are consistent with the hypothesis that heat shock pretreatment would protect pulmonary endothelial cells and alveolar macrophages against H2O2-induced injury, and possibly that HSPs play a role in this cytoprotection.

Animals↗
PubMed1995

Massive programmed cell death in intestinal epithelial cells induced by three-dimensional growth conditions: suppression by mutant c-H-ras oncogene expression.

Deregulation of molecular pathways controlling cell survival and death, including programmed cell death, are thought to be important factors in tumor formation, disease progression, and response to therapy. Studies devoted to analyzing the role of programmed cell death in cancer have been carried out primarily using conventional monolayer cell culture systems. However the majority of cancers grow as three-dimensional solid tumors. Because gene expression, and possibly function, can be significantly altered under such conditions, we decided to analyze the control and characteristics of cell death using a compatible three-dimensional tissue culture system (multicellular spheroids) and compare the results obtained to those using two-dimensional monolayer cell culture. To do so we selected for study an immortalized, but nontumorigenic line of rat intestinal epithelial cells, called IEC-18, and several tumorigenic variants of IEC-18 obtained by transfection with a mutant (activated) c-H-ras oncogene. The rationale for choosing these cell lines was based in part on the fact that intestinal epithelial cells grow in vivo in a monolayer-like manner and form solid tumors only after sustaining certain genetic mutations, including those involving the ras gene family. We found that the IEC-18 cells, which grow readily and survive in monolayer cell culture, undergo massive cell death within 48-72 h when cultured as multicellular spheroids on a nonadhesive surface. This process was accompanied by a number of features associated with programmed cell death including chromatin condensation (Hoechst 33258 staining) apoptotic morphology, DNA degradation, and a virtual complete loss of colony forming (clonogenic) ability in the absence of apparent membrane damage as well as accumulation of lipid containing vacuoles in the cytoplasm. Moreover, enforced over-expression of a transfected bcl-2 gene could prevent this cell death process from taking place. In marked contrast, three different stably transfected ras clones of IEC-18 survived when grown as multicellular spheroids. In addition, an IEC cell line (called clone 25) carrying its mutant transfected ras under a glucocorticoid inducible promoter survived in three-dimensional culture only when the cells were exposed to dexamethasone. If exposure to dexamethasone was delayed for as long as 48 h the cells nevertheless survived, whereas the cells became irreversibly committed to programmed cell death (PCD) if exposed to dexamethasone after 72 h. These results suggest that intestinal epithelial cells may be programmed to activate a PCD pathway upon detachment from a physiologic two-dimensional monolayer configuration, and that this process of adhesion regulated programmed cell death (ARPCD) can be substantially suppressed by expression of a mutant ras oncogene.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Strong, sustained hepatocellular proliferation precedes hepatocarcinogenesis in hepatitis B surface antigen transgenic mice.

Hepatocyte turnover rates were studied in two lineages of transgenic mice that overproduce the hepatitis B virus (HBV) large envelope protein and retain filamentous hepatitis B surface antigen (HBsAg) particles in the endoplasmic reticulum, resulting in the formation of ground glass hepatocytes. The high producer lineage (50-4) develops a necroinflammatory liver disease that progresses to hepatocellular carcinoma (HCC), whereas the low producer lineage (107-5) displays no histopathologic changes other than ground glass hepatocytes. Bromodeoxyuridine (BrdU)-labeling studies of S-phase hepatocytes provide quantitative evidence for a strong, sustained proliferative response in the hepatocytes in lineage 50-4 that occurs after the onset of hepatocellular injury but long before the development of liver cell tumors. In contrast, the level of hepatocellular proliferation in lineage 107-5 is the same as nontransgenic controls. The findings support the concept that sustained hepatocellular proliferation plays an important role in the development of hepatocellular carcinoma (HCC).

Animals↗
PubMed1994

Class I-restricted cytotoxic T lymphocytes are directly cytopathic for their target cells in vivo.

Although CD8-positive, class I-restricted CTL play a critical role in viral clearance and immunopathology in many model systems, they have not been shown to directly kill their target cells in vivo at the single cell level. Using a hepatitis B surface Ag transgenic mouse model of class I-restricted, CTL-mediated liver disease, we now demonstrate that CD8-positive, Ld-restricted hepatitis B surface Ag-specific CTL bind and kill their target cells in vivo by triggering them to undergo degenerative cytologic changes compatible with apoptosis. Unexpectedly, the data also indicate that the pathologic consequences of this direct, Ag-specific CTL effect are much less severe than the cytodestructive, Ag-nonspecific inflammatory response that they induce when they are activated by Ag recognition.

Animals↗
PubMed1994

Expression of the hepatitis delta virus large and small antigens in transgenic mice.

Simultaneous infection with hepatitis delta virus (HDV) and hepatitis B virus (HBV) in humans is often associated with severe viral liver disease including fulminant hepatitis. Since HBV is thought to be noncytopathic to the hepatocyte, the enhanced disease severity observed during dual infection has been attributed to either simultaneous immune responses against the two viruses or direct cytotoxic effects of HDV products on the hepatocyte or both. To examine these alternate possibilities, we produced transgenic mice that express the small and large delta antigens (HDAg) in hepatocyte nuclei at levels equal to those observed during natural HDV infection. No biological or histopathological evidence of liver disease was detectable during 18 months of observation, suggesting that neither the large nor small form of HDAg is directly cytopathic to the hepatocyte in vivo.

Alanine Transaminase↗
PubMed1994

[Relation of HSP70 gene and spontaneously hypertension in rats].

The level of heat shock protein 70 messenger RNA was examined in aortic smooth muscle cells (ASMC) and hepatic tissue of Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The restriction fragment length polymorphism (RFLP) was also analysed in hepatic DNA. It was demonstrated that the basic level of heat shock protein 70 messenger RNA in ASMC and hepatic tissue of SHR were lower than that of the WKY rats. The extent of heat shock protein 70 messenger RNA accumulated in ASMC was higher in SHR than in WKY rats when the cells were heated by immersing the culture bottles in 42 degrees C water bath for 15 min and allowed to recover at 37 degrees C for 2 h. In contrast with WKY rats, the Bam HI restricted bepatic DNA showed that a fragment about 5.6 kb was lost in heat shock protein 70 gene from hepatic DNA of SHR. The results suggest that the ASMC of SHR is more sensitive to heat stress than that of WKY rats and the changes of heat shock protein gene sequence may be related to genetic hypertension.

Animals↗