Pulmonary hypertension with a huge thrombosis in main stem of pulmonary artery.
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Biomedical subjects
Publications and source records attributed to H Zeng.
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Staged combustion was carried out on laboratory-scale pulverized coal combustion with different absorbents. The experiment indicated staged combustion increased emission of submicron particles, which went against the control of trace elements, especially for those of high volatile elements, such as Cu, Ni. The thermodynamics calculation also indicate the transformation of trace metal was different with different atmosphere, suboxidized and reduced species were more easily formed under reduced condition. In both conditions, absorbents show a certain absorptive ability to trace metal, and different absorbent had different ability. For unstaged combustion, kaolinite was the best for Co, Cr and Ni; dolomite for Be, and CaO for Cu. But for under staged condition, HZ- dolomite was the best for Be, Cr and Ni; Kaolinite for Co and Cu.
OBJECTIVE: To investigate the distribution and spread of MRSA in a burn ward, so as to explore the measures of the prevention, surveillance and control of hospital infection in a burn ward. METHODS: Five hundred and four specimens were isolated from the wounds and nasal vestibules of burn patients, the hands and nasal vestibules of medical staffs and lay attendants and the surfaces of various equipments. From these specimens, 58 strains of MRSA and 43 methicillin -- sensitive staphylococcus aureus (MSSA) were isolated. The genome DNA of isolated MRSA strains was analyzed by repetitive DNA -- sequence -- based PCR analysis. RESULTS: MRSA strains were isolated from the burn wounds in 22 of 41 (53.7%) patients, and 5 from the nasal vestibules. Moreover, among 19 medical staffs, MRSA strains were isolated from the hands of 9 persons, but not from the nasal vestibules. From the hands in 9 of 43 lay attendants and the nasal vestibules in 2 MRSA strains were found. Thirteen MRSA strains were isolated from 193 specimens from the surrounding items. It was indicated by repetitive DNA -- sequence -- based PCR analysis of the genome DNA of isolated MRSA strains that there existed homologous strains around the patients' wounds, in the burn wounds, on the skin of medical staffs and lay attendants and also surrounding equipments. CONCLUSION: (1) There was wide spread presence of MRSA homologous strains in the burn ward. (2) It was indicated by repetitive DNA -- sequence -- based PCR analysis of the genome DNA of isolated MRSA strains that there was cross infection among burn patients. The source of the infection of MRSA in burn ward was burn patients, and the route of the infection was hands of medical staffs and lay attendants. (3) MRSA is wide -- spread. The contamination of the hands and the environment was potential risk factor of MRSA outbreak in the burn unit.
Icariin in "Tangzhi Shuangjiang Cha" was quantitatively determined by HPLC with ODS column, a mixture of MeOH-H2O(60:40, V/V) as mobile phase and UV detection at 270 nm. There was a good linear relationship within the range of 0.1 g/L-0.5 g/L(r = 0.9993). The average recovery was 101.4%, RSD was below 2.7%(n = 3). The method is rapid, simple, accurate and reproducible. And the method is proposed to be used for quality control of "Tangzhi Shuangjiang Cha".
A reversed-phase high performance liquid chromatographic method was developed for the quantitative determination of salicylic acid, resorcinol and chloramphenicol in Junlieping tincture. The operation was carried out on an ODS column with the mobile phase of a mixture of acetonitrile-methanol-water(25:10:65, volume proportion). The eluate was detected at 278 nm wavelength. This method is simple, fast and can be used for the quality control of Junlieping tincture.
A strain Bacillus subtilis producing neutral phytase was screened from soil. The protein of phytase was purified by HPLC. Optimal pH value and temperature of the phytase for its activity were 7.5 and 55 degrees C, respectively. The Km values of the phytase for dodecasodium phytate under 37 degrees C was 0.19 mmol/L. The molecule weight of the phytase protein was determined as about 45 kD by SDS-PAGE. The N-terminal amino acids sequence of the phytase protein was determined as Lys-His-Lys-Leu-Ser-Asp-Pro-Tyr-His-Phe-Thr by amino acids sequence analysis.
The binary and ternary Eu(III) complexes have been prepared with four 1,3-diphenyl-4-acyl-5-pyazolones as ligands (where the four acyls are benzoyl, phenylacetyl, butyryl and choroacetyl, and the compounds are represented by DPBZP, DPPAP, DPBTP, DPCAP respectively). The composition of the complexes was determined by chemical and elementary analysis, and the structure of the complexes was characterized by FTIR spectra. The fluorescence spectra of the complexes were measured. It is indicated that the complexes emit with the characteristic fluorescence of Eu(III), the fluorescence intensity of the complexes are closely related to the substituents at the acyl at 4-position in pyrazolone ring of the ligands, depending on the ligands, the descending order of the fluorescence intensity is DPBZP > DPPAP > DPBTP > DPCAP, and that the second ligand, 1, 10-phenanthroline, remarkably intensifies the fluorescence of the complexes.
The acrylic acid (AA) was grafted onto the PE film surface through UV photograft polymerization. With certain pH value, the grafted films were made to react with the alcohol-water solution of Eu3+ and alpha-thenoyltrifluoroacetone (TTA) or with the chloroform-water solution of Tb3+ and acetyl actone (AcAc), thus causing the preparation of the red or green fluorescent films. As compared with the corresponding Eu(TTA)3.(H2O)2 or Tb(AcAc)3.(H2O)2 solid complexes, both the excitation and emission spectra of the fluorescent films changed remarkably. It's predictable that chemical bond combination has occurred between the rare earth complexes and the macromolecular material. In addition, the IR spectra of the fluorescent films were also observed.
[structure] The first total syntheses of (-)-fumiquinazolines A, B, and I have been accomplished efficiently using the Pd-catalyzed cyclization of an iodoindole carbamate to construct the imidazoindolone moiety and the dehydrative cyclization of a diamide followed by rearrangement through an amidine to construct the quinazolone moiety.
The mechanism of interaction between S-nitrosoglutathione (GSNO) and hemoglobin is a crucial component of hypotheses concerning the role played by S-nitrosohemoglobin in vivo. We previously demonstrated (Patel, R. P., Hogg, N., Spencer, N. Y., Kalyanaraman, B., Matalon, S., and Darley-Usmar, V. M. (1999) J. Biol. Chem. 274, 15487-15492) that transnitrosation between oxygenated hemoglobin and GSNO is a slow, reversible process, and that the reaction between GSNO and deoxygenated hemoglobin (deoxyHb) did not conform to second order reversible kinetics. In this study we have reinvestigated this reaction and show that GSNO reacts with deoxyHb to form glutathione, nitric oxide, and ferric hemoglobin. Nitric oxide formed from this reaction is immediately autocaptured to form nitrosylated hemoglobin. GSNO reduction by deoxyHb is essentially irreversible. The kinetics of this reaction depended upon the conformation of the protein, with more rapid kinetics occurring in the high oxygen affinity state (i.e. modification of the Cysbeta-93) than in the low oxygen affinity state (i.e. treatment with inositol hexaphosphate). A more rapid reaction occurred when deoxymyoglobin was used, further supporting the observation that the kinetics of reduction are directly proportional to oxygen affinity. This observation provides a mechanism for how deoxygenation of hemoglobin/myoglobin could facilitate nitric oxide release from S-nitrosothiols and represents a potential physiological mechanism of S-nitrosothiol metabolism.
Epithelia of the vertebrate intestinal tract characteristically maintain an inflammatory hyporesponsiveness toward the lumenal prokaryotic microflora. We report the identification of enteric organisms (nonvirulent Salmonella strains) whose direct interaction with model human epithelia attenuate synthesis of inflammatory effector molecules elicited by diverse proinflammatory stimuli. This immunosuppressive effect involves inhibition of the inhibitor kappaB/nuclear factor kappaB (IkappaB/NF-kappaB) pathway by blockade of IkappaB-alpha degradation, which prevents subsequent nuclear translocation of active NF-kappaB dimer. Although phosphorylation of IkappaB-alpha occurs, subsequent polyubiquitination necessary for regulated IkappaB-alpha degradation is completely abrogated. These data suggest that prokaryotic determinants could be responsible for the unique tolerance of the gastrointestinal mucosa to proinflammatory stimuli.
The multidrug resistance-associated protein 1 (MRP1) and the canalicular multispecific organic anion transporter (cMOAT or MRP2) are ATP-binding cassette transporters that confer resistance to some anticancer drugs and efflux glutathione and glucuronate conjugates from the cell. The MRP subfamily of ABC transporters, however, contains at least four other members of which MRP3 (MOAT-D) bears the closest structural resemblance to MRP1. Although transfection studies have established that human MRP3 confers increased resistance to several anticancer agents, neither the substrate selectivity nor physiological functions of this transporter have been determined. Here we report the results of investigations of the in vitro transport properties of cloned human MRP3 using membrane vesicles prepared from MRP3-transfected HEK293 cells. It is shown that the expression of MRP3 is specifically associated with enhancement of the MgATP-dependent transport into membrane vesicles of the glucuronide estradiol 17-beta-D-glucuronide (E(2)17betaG), the glutathione conjugates 2,4-dinitrophenyl S-glutathione (DNP-SG) and leukotriene C4 (LTC4), the antimetabolite methotrexate, and the bile acid glycocholate. DNP-SG, LTC4, and E(2)17betaG are transported at moderate affinity and low capacity with Km and Vmax values of 5.7 +/- 1.7 microM and 3.8 +/- 0.1 pmol/mg/min, 5.3 +/- 2.6 microM and 20.2 +/- 5.9 pmol/mg/min, and 25.6 +/- 5.4 microM and 75.6 +/- 5.9 pmol/mg/min, respectively. Methotrexate and glycocholate are transported at low affinity and high capacity with Km and Vmax values of 776 +/- 319 microM and 288 +/- 54 pmol/mg/min and 248 +/- 113 microM and 183 +/- 34 pmol/mg/min, respectively. On the basis of these findings, the osmotic dependence of the transport measured and its inability to transport taurocholate, MRP3, like MRP1 and cMOAT, is concluded to be competent in the transport of glutathione S-conjugates, glucuronides, and methotrexate, albeit at low to moderate affinity. In contrast to MRP1, cMOAT, and all other characterized mammalian ABC transporters, however, MRP3 is active in the transport of the monoanionic human bile constituent glycocholate.
Luteinizing hormone receptor, a G protein-coupled receptor, consists of two halves, the N-terminal extracellular hormone binding domain (exodomain) and the C-terminal membrane-associated, signal-generating domain (endodomain). The exodomain has seven to nine Leu-rich repeats, which are generally thought to form a 1/3 donut-like structure and interact with human choriogonadotropin (hCG). The resulting hCG-exodomain complex adjusts the structure and its association with the endodomain, which results in signal generation in the endodomain. It is unclear whether the rigid 1/3 donut structure could provide the agility and versatility of this dynamic action. In addition, there is no clue as to where the endodomain contact point (the signal modulator) in the exodomain is. To address these issues, the exodomain was examined by Ala scan and multiple substitutions, while receptor peptides were used for photoaffinity labeling and affinity cross-linking. Our results show that the C-flanking sequence (hinge region), Thr(250)-Gln(268), of the Leu-rich repeats (LRRs) specifically interacts with hCG, preferentially hCGalpha. This interaction is inhibited by exoloop 2 of the endodomain but not by exoloops 1 and 3, suggesting an intimate relationship between Thr(250)-Gln(268), exoloop 2, and hCG. Taken together, our observations in this article suggest a new paradigm that the LRRs contact the front of hCG, while both flanking regions of the LRRs interact with the sides of hCG. This would trap hCG in the 1/3 donut structure of the LRRs and enhance the binding affinity. In addition, mutations of conserved Ser(255) in the sequence can constitutively activate the receptor. This provides a clue for the signal modulator in the exodomain. In contrast, a phenyl or phenolic group is necessary at conserved Tyr(253) for targeting the receptor to the surface.
Recent work from this laboratory both in rat primary cardiomyocytes and in ventricular tissue of transgenic mouse models of induced hypertrophy has identified two Ca(2+)/calmodulin-dependent nuclear signaling cascades. The first involves the phosphatase calcineurin (CaN). The second is the CaM kinase kinase cascade which involves CaM kinase I and CaM kinase IV. Each of these signaling cascades strongly up-regulate transcription of hypertrophy-sensitive genes in the rat ventricular cardiomyocyte. We have documented that over-expression of an active form of CaM kinase II silenced transcriptional induction of hypertrophy-sensitive genes. The purpose of this study was to generate an inducible CaM kinase II expression system and correlate its expression with the silencing of hypertrophic-sensitive reporters. A truncated form of CaM KII, CaM KII (1-290) was subcloned downstream and proximal to a promoter under transcriptional control (induction) of the tetracycline-regulated transcription factor, tet-TransActivator (tTA). Hypertrophy-sensitive reporter activity in primary cardiomyocytes was silenced when tet-inducible CaM KII was co-expressed with plasmids harboring active forms of CaN, CaM KI or CaM KIV. For instance, induced CaM KII expression silenced CaN, CaM kinase I, or CaM kinase IV driven ANF reporter activity 4.9-, 2.9-, and 6.9-fold below their maximal values, respectively. Myocyte exposure to doxycycline (DOX) blocked tTA-driven CaM KII expression and restored CaN/CaM KI or CaN/CaM KIV driven reporter activation. This study demonstrates, for the first time, that active CaM KII silences Ca(2+)-sensitive nuclear signaling cascades for transcriptional up-regulation of cardiomyocyte hypertrophy.
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The glucocorticoid modulatory element (GME) of the rat tyrosine aminotransferase gene is located at -3.6 kb and 1 kb upstream of the glucocorticoid response elements (GREs). The GME has the unique transcriptional properties of modulating both the dose-response curve of agonists bound to the glucocorticoid receptor (GR) and the residual agonist activity of GR-bound antisteroids. The expression of GME activity involves the binding of two novel proteins (GMEB-1 and GMEB-2) that we have recently cloned. However, the mechanistic details are limited. The DNA sequence requirements for GME activity (CGTC) also remain poorly defined, which restricts efforts to identify other GME modulated genes. To help understand the mechanism for the unusual activities of the GME and to identify permissive gene environments for GME activity, we compared the changes in GME activity and GRE action (i.e. the fold induction by GR) caused by modifying several parameters. Phasing between the GME and downstream tandem GREs was unimportant, in contrast to other cis-acting elements like the GRE, while GME activity decreased rapidly when placed at increasingly larger distances 3' to a tandem GRE. A minimal promoter was less effective in supporting GME than GRE activity. Although CREB binds to the GME, overexpression of CREB reduced GRE, but not GME, activity and a CRE was inactive when substituted for the GME. No effect of the GME was observed on the binding of GRs to a single GRE. However, the GME upstream of a single GRE was also unable to produce a left shift in the Dex dose-response curve under conditions where the GME was active with two GREs. In the absence of any GREs, the GME displayed intrinsic activity by elevating basal level expression. Collectively, these results indicate that an optimal position for a functional GME is within 250 bp upstream of a tandem GRE driving a complex promoter. Furthermore, as the changes in GME activity did not correlate with those for fold induction from the GRE, the mechanisms for expression of GME and GRE activities appear to utilize parallel, as opposed to common pathways.
The glucocorticoid modulatory element binding proteins 1 and 2 (GMEB-1 and GMEB-2) are of interest both for their multiple activities (e.g. modulation of transactivation by the glucocorticoid receptor and initiation of parvovirus replication) and their membership in the emerging family of KDWK proteins. The genomic sequence of these proteins was desired in order to begin studies on the control of GMEB expression and to pursue previous evidence for significant homologies between the GMEBs. We now report the genomic sequence of human GMEB-1 and rat GMEB-2. The structure of both genes, including portions of the introns, is highly conserved. However, GMEB-1 and GMEB-2 were found to reside on chromosomes 1 and 20, respectively, demonstrating that they are encoded by distinctly different genes. Several isoforms of the GMEBs have been reported or detected in this study, and the splicing patterns were determined. The tissue distribution of each GMEB is not the same and is highest in fetal and developing tissues, consistent with previous suggestions that both homo- and hetero-oligomers may possess biological activity. The promoter region of both genes has been identified and both display high levels of transcription activity in transiently transfected cells when fused upstream of a promoterless reporter. These results indicate that the GMEBs are proteins that evolved from a single parent gene, have been highly conserved since the divergence of rats and humans and probably play important roles in development and differentiation.
The inability to deliver a therapeutic gene to a sufficient percentage of hematopoietic stem cells is the major obstacle to using gene therapy to treat blood disorders. Providing genetically corrected stem cells with a reversible growth advantage could solve this problem. To this end we have employed small synthetic molecules that can reversibly dimerize and activate fusion proteins which contain a growth factor receptor signaling domain. We have shown that the thrombopoietin receptor (mpl) signaling domain can be used in this system to expand transduced multipotential progenitor cells from mouse bone marrow. In the present study we tested a similar retroviral vector in human CD34-selected cord blood cells. Following transduction, cells cultured in the presence of the dimerizing molecule AP1903 expanded 13.8- to 186-fold relative to cells cultured in the absence of AP1903. The cell type that emerged in suspension culture was erythroid. Contrary to our results in the murine system, cell expansion was transient. Activation of mpl caused the disappearance of BFU-E followed by a transient increase in CFU-E. In contrast, mpl activation had no discernable effect on transduced myeloid progenitor cells. AP1903-mediated expansion was restricted to transduced cells, as demonstrated by immunohistochemical staining. These findings indicate that synthetic dimerizing molecules can be used to expand primary human hematopoietic cells. (Blood. 2000;95:430-436)