Biomedical subjects

Ying Huang

Publications and source records attributed to Ying Huang.

At least 163 records · Page 9Linked to original sources

PubMed2004

Nocardia pigrifrangens sp. nov., a novel actinomycete isolated from a contaminated agar plate.

A polyphasic study was undertaken to establish the taxonomic position of an actinomycete strain isolated from a contaminated agar plate. The strain, designated 7031T, had morphological and chemotaxonomic properties typical of the genus Nocardia. An almost-complete 16S rRNA gene sequence determined for the strain was aligned with available sequences for nocardiae, and phylogenetic trees were inferred using three tree-generating algorithms. Strain 7031T clustered with the type strains of Nocardia carnea and Nocardia flavorosea, showing low 16S rRNA gene sequence similarities to these species (97.2 and 97.5 %, respectively). The strain was also distinguished from the closest species by a range of phenotypic properties. It is proposed that the strain be recognized as a novel species of Nocardia, Nocardia pigrifrangens sp. nov., the type strain of which is 7031T (= AS 4.1808T = JCM 11884T).

Bacterial Typing Techniques↗

PubMed2004

Streptomyces glauciniger sp. nov., a novel mesophilic streptomycete isolated from soil in south China.

A polyphasic study was undertaken to establish the taxonomic status of a soil isolate. The organism, strain FXJ14(T), was found to have chemical and morphological properties characteristic of streptomycetes. Phylogenetic analyses based on an almost complete 16S rRNA gene sequence of the strain and on the 120 nt variable gamma-region of the 16S rRNA molecule showed that it formed a distinct phyletic line within the range of variation encompassed by the genus Streptomyces. The sharp separation of the organism from representatives of the genus Streptomyces was strengthened by the fact that its BOX-PCR and RFLP of 16S rDNA-ITS fingerprints differed from those of over 450 recognized Streptomyces species. The isolate also had a profile of phenotypic properties that readily distinguished it from the genotypically close type strains. It is evident from the combination of genotypic and phenotypic data that strain FXJ14(T) (=AS 4.1858(T)=JCM 12278(T)=LMG 22082(T)) should be classified as the type strain of a novel species of the genus Streptomyces, for which the name Streptomyces glauciniger sp. nov. is proposed.

Bacterial Typing Techniques↗

PubMed2004

Death receptors as targets of cancer therapeutics.

To date six bona fide death receptors (DRs) have been discovered and include tumor necrosis factor receptor 1 (TNF-R1), Fas, DR3, DR4, DR5 and DR6. Each receptor contains an extracellular region and an intracellular region; the intracellular region harbors a death domain that is critical for transduction of apoptotic signals. These death receptors are activated by their respective ligands. For example, TNFalpha activates TNF-R1 while FasL and TL1A activate Fas and DR3 respectively. TNF-related apoptosis inducing ligand (TRAIL), also known as Apo2L, activates DR4 and DR5. The ligand for DR6 has yet to be identified. These death receptors are also believed to be activated in a ligand-independent manner. A large body of recent evidence suggests that death receptors could be utilized as key molecular targets to develop novel therapeutics. This review discusses the pros and cons of targeting death receptors in the development of novel cancer therapeutic agents.

Animals↗

PubMed2004

Growth factor signaling and resistance to cancer chemotherapy.

Multiple mechanisms contribute to chemoresistance, eventually leading to failure of cancer chemotherapy. Deregulated growth factor signaling pathways promote cell proliferation and render cancer cells resistant to apoptosis, a common mechanism of chemoresistance. Therefore, inhibitors of growth factor signaling, including antibodies and small molecules, are promising drug candidates for chemotherapy, either given alone or as adjuvants to overcome general drug resistance. While dramatic responses have been attained in some cases, innate or acquired resistance to these novel anticancer drugs is common and limits broad applicability. Treatment failure may arise from complexity of growth factor signaling, with numerous parallel pathways and diverse downstream events. This review discusses the use of pharmacogenomics, assessing multiple growth factor signaling pathways and complex chemoresistance mechanisms. Monitoring expression profiles and activating mutations in growth factor receptors holds promise for the design of individualized therapy with a combination of drugs.

Drug Resistance, Neoplasm↗

PubMed2004

[Comparison of three methods for quantitative analysis of LPO in different biological samples].

OBJECTIVE: To explore the optimized methods for detecting lipid peroxide (LPO) in biological samples and the reference value of LPO in human plasma. METHODS: Three most commonly adopted methods were used for detecting LPO in different biological samples simultaneously, and then their linearity, accuracy, precision, stability and detecting efficiency were compared. The methods were FOX assay, Modified iodometric assay and TBARS assay. The standard curve (linearity evaluation), rate of sample recovery (accuracy evaluation), reproducibility (precision evaluation), stability of reading number (stability evaluation), as well as the detected values of LPO in different sample systems by three methods simultaneously (detecting efficiency) were evaluated. The sample systems were: isolated low-density lipoprotein (LDL), supernatant of cell culture, and human plasma. RESULTS: When applied to detecting LPO in the isolated LDL sample system, FOX assay was found to have the most sensitive detecting efficiency, good accuracy and precision. When applied to detecting LPO in the supernatant of cell culture and human plasma sample systems, the Modified iodometric assay and TBARS assay showed better function than FOX assay; the rate of sample recovery of FOX assay 61.92% +/- 2.92% was obviously lower as compared with 99.00% +/- 2.65% of modified iodometric assay and 101.63% +/- 12.00% of TBARS assay; and the reproducibility of FOX assay 19.15% was also lower as compared with 4.36% of Modified iodometric assay and 3.14% of TBARS assay. The three methods all showed fine linearity and stability. The values of LPO concentration in normal human plasma were (14.189 +/- 4.889) mumol/L by Modified iodometric assay and (0.936 +/- 0.462) mumol/L by TBARS assay; these values were close to those in other reports. CONCLUSION: FOX assay was found to be most sensitive in the three methods for measurement of LPO in a relative pure sample system (such as isolated LDL). In complex sample system, however, the Modified iodometric assay and TBARS assay showed better function. The authors suggest that suitable method be chosen according to the nature of sample, that more than one method be chosen for plasma LPO assay in the same planned analysis, and that Modified iodometric assay and TBARS assay be worth the first choice.

Clinical Chemistry Tests↗

PubMed2004

[Regulation for distribution of metastatic cervical lymph nodes of 512 cases of nasopharyngeal carcinoma].

BACKGROUND & OBJECTIVE: To identify the target volume of radiotherapy is more and more important. This study was designed to explore the regulation for the distribution of metastatic cervical lymph nodes of nasopharyngeal carcinoma (NPC) and to recommend the delineation of clinical target volume of the neck for three-dimensional conformal radiotherapy in NPC. METHODS: From Jan. 2003 to Jun. 2004, 512 of cases of NPC, histologically diagnosed, received enhanced transversal CT scan. The cervical node was divided into six levels (I-VI) plus retropharyngeal nodes according to RTOG guidelines proposed in 2003. RESULTS: Of 512 patients, 328 (64.1%) had cervical lymphadenopathy at presentation. Of the 328 neck positive cases, the node involvement was unilateral in 61.3% patient and bilateral in 38.7%. 328 (64.1%) cases showed enlargement of retropharyngeal node, and unilateral 50.9%, bilateral 49.1%. The involvement for levelIto level VI and retropharyngeal area in node-positive cases was 3.0%, 97.9%, 46.0%, 9.5%, 13.7%, 0% and 74.4%. Of the node-positive patient, the incidence of skip metastasis was from 4.6% to 6.5%. 25.3% of the node-positive cases showed involvement, which is beyond CTV for the neck of stage N0 recommended by RTOG. CONCLUSIONS: The cervical node involvement of NPC is spread orderly down the neck, and the incidence of skip metastasis is lower. Retropharyneal node was the first echo node to metastases of NPC. The retropharyngeal node, level II, and level III were the most frequently involved area. Level Ia and level VI were never involved. There are few cases with positive nodes beyond CTV for the neck of stage N0 recommended by RTOG. Our data is helpful for the delineation cervical target in the 3-D conformal radiotherapy of NPC.

Adolescent↗

PubMed2004

[Study on acute pancreatitis-associated lung injury induced by L-arginine in mice].

OBJECTIVE: To establish the model of acute pancreatitis (AP)-associated lung injury induced by L-arginine and study the role of TNF-alpha and ICAM-1 in the model mice. METHODS: For the establishment of the AP model, the mice were given the first injection (2 g/kg) of L-arginine intraperitoneally and then the second injection in the same way an hour later. At 12 h after the second injection, the animals' serum amylase activities were assayed by colorimetry, and the tumor necrosis factor-alpha (TNF-alpha) contents of their pancreatic tissue were determined by radioimmunoassay. At 24 h after the second injection, the histopathological changes in the animals' pancreatic and pulmonary tissues were observed. The pulmonary expression and cellular localization of intercellular adhesion molecule-1 (ICAM-1) were characterized by immunohistochemistry. RESULTS: The serum amylase activities, TNF-alpha content and ICAM-1 expression in lung tissue significantly increased in the AP group as compared with those in the control group. Histopathological examinations revealed that the acinar architecture was partially destroyed with necrosis, interstitial edema and inflammatory infiltration at 24 h after the second injection. CONCLUSION: TNF-alpha and ICAM-1 may play important roles in the mice with acute pancreatitis-associated lung injury.

Acute Disease↗

PubMed2003

Functional characterization of Narc 1, a novel proteinase related to proteinase K.

The NARC 1 gene encodes a novel proteinase K family proteinase. The domain structure of rat Narc 1 resembles that of the subtilisin-like proprotein convertases (SPCs), except that rNarc 1 lacks the canonical P-domain of SPCs, retaining only the RGD motif as part of what might be a cryptically functioning P-domain. Narc 1 undergoes autocatalytic intramolecular processing at the site LVFAQ/, resulting in the cleavage of its prosegment and the generation of an active proteinase with a broad alkaline pH optimum and no apparent calcium requirement for activity. Both primary and secondary structural determinants influence Narc 1 substrate recognition. Our functional characterization of Narc 1 reinforces the inference drawn from the analysis of its predicted structure that this enzyme is most closely related to representatives of the proteinase K family, but that it is also sufficiently different to warrant its possible classification in a separate sub-family.

Amino Acid Motifs↗

PubMed2003

Cloning and characterization of a novel gene PDRG that is differentially regulated by p53 and ultraviolet radiation.

We report the cloning and characterization of a novel p53 and DNA damage-regulated gene (PDRG). The human and mouse PDRG sequences are highly homologous and contain open reading frames of 133 amino acids each with molecular masses of 15.5 and 15.3 kDa, respectively. PDRG codes for a novel protein that does not show similarity to any known protein in the databases. Human PDRG is predominantly expressed in normal testis and exhibits reduced but detectable expression in other organs. GFP-tagged PDRG was predominantly detected as aggregates that appeared to reside in a distinct subcellular compartment. PDRG mRNA was upregulated by ultraviolet radiation (UV) but downregulated by tumor suppressor p53. UV is known to transcriptionally upregulate the expression of certain genes by activating the transcription factor Oct-1, while p53 has been reported to suppress transcription of certain genes by directly binding to a novel head-to-tail response element. Cloning and sequence analysis of PDRG promoter revealed the presence of Oct-1-binding element and a putative head-to-tail-type p53-binding site. Indeed, UV as well as exogenous Oct-1 independently increased PDRG promoter activity, suggesting that UV could mediate PDRG upregulation via Oct-1. Exogenous wild-type p53 was found to downregulate the PDRG promoter activity indicating that wild-type p53 transcriptionally suppresses the expression of PDRG and may mediate its effect via the putative head-to-tail response element. Furthermore, stable expression of exogenous PDRG was found to decrease the clonogenic survival after UV irradiation, which highlights the significance of PDRG in facilitating UV-induced killing.

Alternative Splicing↗

PubMed2003

Crystallization and preliminary crystallographic study of rBmKalphaIT1, a recombinant alpha-insect toxin from the scorpion Buthus martensii Karsch.

Alpha-insect scorpion toxins are a distinct group of scorpion neurotoxins for which no crystal structures are yet available. A novel alpha-insect toxin named BmKalphaIT1 from the scorpion Buthus martensii Karsch (BmK) has been expressed as an inclusion body in Escherichia coli and purified by chromatography after renaturation. Recombinant BmKalphaIT1 (rBmKaIT1) was crystallized using the vapour-diffusion technique in hanging drops at 296 K. The crystals, which were grown in sodium phosphate, belonged to the orthorhombic space group P2(1)2(1)2(1), with unit-cell parameters a = 30.24 (1), b = 36.51 (3), c = 57.08 (2) A. Diffraction data were collected to 2.1 A resolution using synchrotron radiation. There appears to be one rBmKalphaIT1 molecule in the asymmetric unit.

Animals↗

PubMed2003

Antagonism of the antidepressant-like effects of clenbuterol by central administration of beta-adrenergic antagonists in rats.

RATIONALE: Stimulation of central beta(2) adrenergic receptors produces antidepressant-like effects on behavior. At present, it is not known what brain sites are involved in mediating such effects, although some recent evidence suggests the importance of the dorsal hippocampus. OBJECTIVE: Experiments were carried out to determine whether central administration of beta-adrenergic antagonists blocks antidepressant-like effects produced by peripheral administration of the beta(2)-adrenergic agonist clenbuterol. METHODS: The following were determined: 1) the ability of ICV or intrahippocampal administration of the non-selective beta adrenergic antagonists propranolol and CGP-12177, which are lipophilic and hydrophilic, respectively, to antagonize the effects of peripherally administered clenbuterol on differential-reinforcement-of-low-rate (DRL) behavior; 2) the effects of clenbuterol, administered bilaterally into the dorsal hippocampus, on DRL behavior. RESULTS: The antidepressant-like effects of clenbuterol, i.e. reduced response rate and increased reinforcement rate under the DRL schedule, were antagonized by either ICV or bilateral intrahippocampal infusions of propranolol or CGP-12177; CGP-12177 was approximately 8-fold more potent than propranolol. Direct infusion of clenbuterol into the bilateral dorsal hippocampus also produced antidepressant-like effects. CONCLUSIONS: Central beta-adrenergic receptors, in particular those in the dorsal hippocampus, are involved in the mediation of the antidepressant-like effect of clenbuterol. Probably resulting from its enhanced access to the sites of action, the hydrophilic antagonist CGP-12177 was more potent than the lipophilic antagonist propranolol, even though they exhibit similar potency in vitro.

Adrenergic beta-2 Receptor Agonists↗

PubMed2003

Polychlorinated biphenyls removal from weathered municipal solid waste incineration fly ash by collector-assisted column flotation.

Polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) are highly toxic micropollutants emitted from municipal solid waste incineration (MSWI), in particular, concentrated in the unburned carbon (UC) of MSWI fly ash. Because of concerns over their adverse health effects, a number of countries have classified MSWI fly ash as hazardous material and required further treatment before its final disposal in landfills. The technologies for removing the toxic chlorinated micropollutants in the MSWI fly ash have been studied, however, until now no mature technique has been obtained in this purpose. In this research, we used a technique of collector-assisted column flotation to remove PCBs-enriched UC from MSWI fly ash. We found that 36.9% PCBs could be removed from fresh MSWI fly ash with 61.7% UC removal efficiency, whereas only 21.7% PCBs could be removed from weathered MSWI fly ash with a low UC removal efficiency of 33.7%. By adding a mixture of two kinds of surfactants: sorbitan mono-oleate and polyoxyethylene (20) sorbitan mono-oleate to the weathered fly ash slurry as the collector assistant, 39.3% PCBs was removed at the hydrophile-lipophile balance (HLB) value of 13.5, while the UC removal efficiency increased to 49.0%. The results showed that the collector assistant could enhance PCBs and UC removal efficiencies during the column flotation process, and the mechanism has been discussed in detail. Higher PCBs and UC removal efficiencies could be expected by further optimizing the conditions of collector-assisted column flotation.

Air Pollutants↗

PubMed2003

Hypermethylation, but not LOH, is associated with the low expression of MT1G and CRABP1 in papillary thyroid carcinoma.

We previously obtained gene expression profiles of 8 matched papillary thyroid carcinoma (PTC) and normal tissues using DNA microarrays. To identify novel tumor suppressor genes involved in thyroid carcinogenesis, we here analyze genes showing lower expression in PTC tumors than in normal thyroid tissues. A search for loss of heterozygosity (LOH) in 49 regions that harbor consistently down-regulated genes revealed LOH in only 4 regions and in just a very small number of tumors. To determine whether the underexpression might be due to promoter methylation, we used combined bisulfite restriction analysis and bisulfite sequencing to study 7 underexpressed genes. Loss of expression of MT1G and CRABP1 is accompanied by hypermethylation in the 5' regions of these genes, but methylation was not seen in other genes tested. Combined treatment with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-Aza-dC) and the histone deacetylase inhibitor trichostatin A (TSA) resulted in demethylation and re-expression of the MT1G gene in the cell line K2. Treatment with 5-Aza-dC alone restored CRABP1 expression in a colorectal cancer cell line, SW48. In conclusion, LOH is a remarkably rare mechanism of loss of gene function in PTC. In contrast, hypermethylation of promoter CpG islands seems to occur at higher frequency. MT1G and CRABP1 are novel genes that are likely involved in the pathogenesis of sporadic PTC.

Adenocarcinoma, Papillary↗

PubMed2003

Effect of Bax deficiency on death receptor 5 and mitochondrial pathways during endoplasmic reticulum calcium pool depletion-induced apoptosis.

Thapsigargin (TG), by inducing perturbations in cellular Ca(2+) homeostasis, can induce apoptosis, but the molecular mechanisms remain to be fully elucidated. We have recently reported that TG-induced apoptosis appears to involve the DR5-dependent apoptotic pathway that cross talks with the mitochondrial pathway via TG-induced Bid cleavage. In this study, we have utilized Bax-proficient and -deficient HCT116 human colon cancer cells to investigate the effect of Bax deficiency on TG-induced apoptosis and TG regulation of the DR5 and mitochondrial pathways. Our results indicate that Bax-deficient cells are less sensitive to undergo apoptosis following TG treatment. Our results further demonstrate that TG-induced apoptosis is coupled with DR5 upregulation and caspases 8 and 3 activation, as well as Bid cleavage in both Bax-proficient and -deficient cells, although caspase 3 activation was reduced in Bax-deficient cells. TG also promoted the release of cytochrome c into cytosol and caspase 9 activation in Bax-proficient cells but not in Bax-deficient cells. These findings suggest that although Bax is not absolutely required for death receptor (DR)-dependent signals, it appears to be a key molecule in TG-regulated mitochondrial events. Bax-deficient cells were relatively more resistant to Apo2L/TRAIL than the Bax-proficient counterparts. However, the combination of Apo2L/TRAIL and TG was more effective in mediating apoptosis in both Bax-proficient and -deficient cells and that was coupled with activation of caspases 8 and 3. Although both agents in combination also induced cytochrome c release into cytosol and caspase 9 activation in Bax-proficient cells, these events were abrogated in Bax-deficient cells. Our results thus suggest that the combination of Apo2L/TRAIL and TG appears to bypass the Bax deficiency-induced defects in the mitochondrial (intrinsic) pathway by engaging the DR5-dependent apoptotic signals (extrinsic pathway).

Apoptosis↗

PubMed2003

Drug sensitivity and resistance genes in cancer chemotherapy: a chemogenomics approach.

Resistance to antineoplastic drugs represents a serious obstacle to successful cancer treatment. Genome-wide studies correlating drug response phenotypes with large DNA/tissue microarray and proteomic datasets have been performed to identify the genes and proteins involved in chemosensitivity or drug resistance. The goal is to identify a set of chemosensitivity and/or resistance genes for each drug that are predictive of treatment response. Therefore, validated pharmacogenomic biomarkers offer the potential for the selection of optimal treatment regimens for individual patients and for identifying novel therapeutic targets to overcome drug resistance.

Antineoplastic Agents↗

PubMed2003

The fission yeast TFIIB-related factor limits RNA polymerase III to a TATA-dependent pathway of TBP recruitment.

The RNA polymerase (pol) III-transcribed (e.g. tRNA and 5S rRNA) genes of traditionally studied organisms rely on gene-internal promoters that precisely position the initiation factor, TFIIIB, on the upstream promoter-less DNA. This is accomplished by the ability of the TFIIIB subunit, TFIIB-related factor (Brf1), to make stable protein-protein interactions with TATA-binding protein (TBP) and place it on the promoter-less upstream DNA. Unlike traditional model organisms, Schizosaccharomyces pombe tRNA and 5S rRNA genes contain upstream TATA promoters that are required to program functional pol III initiation complexes. In this study we demonstrate that S.pombe (Sp)Brf does not form stable interactions with TBP in the absence of DNA using approaches that do reveal stable association of TBP and S.cerevisiae (Sc)Brf1. Gel mobility analyses demonstrate that a TBP-TATA DNA complex can recruit SpBrf to a Pol III promoter. Consistent with this, overproduction of SpBrf in S.pombe increases the expression of a TATA-dependent, but not a TATA-less, suppressor tRNA gene. Since previous whole genome analysis also revealed TATA elements upstream of tRNA genes in Arabidopsis, this pathway may be more widespread than appreciated previously.

DNA, Fungal↗

PubMed2003

An oncolytic adenovirus selective for retinoblastoma tumor suppressor protein pathway-defective tumors: dependence on E1A, the E2F-1 promoter, and viral replication for selectivity and efficacy.

The use of oncolytic adenoviruses as a cancer therapeutic is dependent on the lytic properties of the viral life cycle, and the molecular differences between tumor cells and nontumor cells. One strategy for achieving safe and efficacious adenoviral therapies is to control expression of viral early gene(s) required for replication with tumor-selective promoter(s), particularly those active in a broad range of cancer cells. The retinoblastoma tumor suppressor protein (Rb) pathway is dysregulated in a majority of human cancers. The human E2F-1 promoter has been shown to be selectively activated/derepressed in tumor cells with a defect in the Rb pathway. Ar6pAE2fE3F and Ar6pAE2fF are oncolytic adenoviral vectors (with and without the viral E3 region, respectively) that use the tumor-selective E2F-1 promoter to limit expression of the viral E1A transcription unit, and, thus, replication, to tumor cells. We demonstrate that the antitumor activity of Ar6pAE2fF in vitro and in vivo is dependent on the E2F-1 promoter driving E1A expression in Rb pathway-defective cells, and furthermore, that its oncolytic activity is enhanced by viral replication. Selective oncolysis by Ar6pAE2fF was dependent on the presence of functional E2F binding sites in the E2F-1 promoter, thus linking antitumor viral activity to the Rb pathway. Potent antitumor efficacy was demonstrated with Ar6pAE2fF and Ar6pAE2fE3F in a xenograft model following intratumoral administration. Ar6pAE2fF and Ar6pAE2fE3F were compared with Addl1520, which is reported to be molecularly identical to an E1B-55K deleted vector currently in clinical trials. These vectors were compared in in vitro cytotoxicity and virus production assays, after systemic delivery in an in vivo E1A-related hepatotoxicity model, and in a mouse xenograft tumor model after intratumoral administration. Our results support the use of oncolytic adenoviruses using tumor-selective promoter(s) that are activated or derepressed in tumor cells by virtue of a particular defective pathway, such as the Rb pathway.

Adenoviridae↗

PubMed2003

Immunonutrients and neonates.

UNLABELLED: The gastrointestinal tract is the largest surface area of the body and the primary site for microorganisms, foreign antigens and toxins to gain entry to the host's internal milieu. The use of enteral feedings enriched with immune-enhancing ingredients is attracting considerable interest because there is increasing application of enteral feeding and appreciation of the role of the gut in the development of infection and of multiple organ failure in critically ill patients. CONCLUSION: in this review, we will discuss nutrients, such as glutamine, arginine, omega 3 fatty acids, nucleotides, probiotics, and lactoferrin, and how they might be used as immunonutrients in neonatal clinics.

Adjuvants, Immunologic↗