Biomedical subjects

W Tian

Publications and source records attributed to W Tian.

At least 19 recordsLinked to original sources

PubMed2001

MICA genetic polymorphism and linkage disequilibrium with HLA-B in 29 African-American families.

The human major histocompatibility complex (MHC) class I chain-related gene A ( MICA) is located 46 kb upstream of HLA-B and encodes a stress-inducible protein which displays a restricted pattern of tissue expression. MICA molecules interact with NKG2D, augmenting the activation of natural killer cells, CD8(+) alpha beta T cells, and gamma delta T cells. MICA allelic variation is thought to be associated with disease susceptibility and immune response to transplants. We investigated MICA allelic variations and linkage disequilibrium with HLA-A, B, and DRB1 loci on 110 parental haplotypes from 29 African-American families. PCR/sequence-specific oligonucleotide probing (SSOP) was used to define MICA polymorphisms in exons 2, 3, and 4. Ambiguous allelic combinations were resolved by sequencing exons 2, 3, and 4. Exon 5 polymorphisms were analyzed by size sequencing. For HLA-A, B and DRB1 typing, low-resolution PCR/SSOP and allelic PCR/sequence-specific priming techniques were used. Twelve MICA alleles were observed, the most frequent of which were MICA*008, MICA*004, and MICA*002, with gene frequencies of 28.2, 26.4, and 25.5%, respectively. Thirty-eight HLA-B- MICA haplotypic combinations were uncovered, 22 of which have not been reported in the HLA homozygous typing cell lines from the 10th International Histocompatibility Workshop. Significant positive linkage disequilibria were found in 8 HLA-B- MICA haplotypes. Furthermore, haplotypes bearing HLA-B*1503, *1801, *4901, *5201, *5301, and *5703 were found to segregate with at least two different MICA alleles. Our results provide new data about MICA genetic polymorphisms in African-Americans, which will form the basis for future studies of MICA alleles in allogeneic stem cell transplantation outcome.

Alleles↗

PubMed2001

Preparation and characterisation of fluorescent chitosans using 9-anthraldehyde as fluorophore.

Chitosans with chemical composition ranging from a fraction of N-acetylated units (F(A)) of 0.01 to 0.61 were used to prepare fluorescence labelled chitosans by reductive amination with 9-anthraldehyde. Fluorescent chitosans with a low theoretical degree of substitution (DS, 0.001-1%) were prepared, and the actual DS of the products were determined by UV and (1)H NMR spectroscopy. The fluorescence excitation and emission spectra of the chitosan with F(A) of 0.09 and DS 1% showed an excitation maximum at 254 nm and an emission maximum at 413 nm. The intrinsic viscosities ([eta]) of the fluorescent chitosans were compared to those of the original chitosans, showing that the derivatisation procedure lead only to a negligible decrease in [eta]. The conformation of these fluorescent chitosans with very low DS-values is not altered and they can conveniently be directly quantified by UV or fluorescence spectroscopy.

Acetylation↗

PubMed2001

Green tea epigallocatechin gallate: a natural inhibitor of fatty-acid synthase.

We discover that epigallocatechin gallate (EGCG) from green tea is an inhibitor of fatty-acid synthase (FAS) from chicken liver. Its inhibition of FAS is composed of reversible fast-binding inhibition, through which 52 microM EGCG can inhibit 50% of the activity of FAS, and irreversible slow-binding inactivation following saturation kinetics with the dissociation constant of 0.352 mM and limiting rate constant of 0.0168 min(-1). The marked inhibition of ketoacyl reduction shows that the inhibition is related to beta-ketoacyl reductase of FAS. The observable protection of NADPH and competitive inhibition of NADPH for ketoacyl reduction indicate that EGCG may compete with NADPH for the same binding site. The synthetic inhibitor C75 does not show obvious fast-binding inhibition, but does exhibit irreversible slow-binding biphasic inactivation, which is demonstrated to be a second-order reaction. That the inactivation by C75 is protected by malonyl-CoA indicates C75 is similar to cerulenin in being a covalent inactivator of the beta-ketoacyl synthase.

4-Butyrolactone↗

PubMed2001

Complexation of trivalent lanthanide cations by D-ribose in the solid state. The crystal structure and FT-IR study of PrCl3-alpha-D-ribopyranose-5H2O.

The crystal structure of praseodymium chloride.alpha-D-ribopyranose pentahydrate, PrCl3-C5H10O5-5 H2O, M(r)=487.47, a=9.1989(8), b=8.8214(7), c=9.8233(9) A, beta=94.060(3) degrees, V=795.2(1) A(3), Z=2, mu=0.71073 A and R=0.0418 for 1923 observed reflections and 172 parameters has been determined. The sugar provides three hydroxyl groups, ax-eq-ax for coordination. The Pr(3+) ion is nine-coordinated with five Pr-O bonds from water molecules, three from hydroxyl groups and one from chloride. The OH, CO stretching vibrations and COH bending vibrations are shifted in the complex IR spectrum and the hydroxyl groups, water molecules, chloride ions form an extensive hydrogen-bond network.

Crystallization↗

PubMed2001

Complexation of trivalent lanthanide cations by galactitol in the solid state. The crystal structure and an FT-IR study of 2NdCl3.galactitol.14H2O.

The crystal structure of 2NdCl3.galactitol.14H2O has been determined. The crystal system is triclinic, space group: -1, with unit-cell dimensions: a = 9.736(2), b = 10.396, c = 8.027 A; alpha = 108.05(3), beta = 92.68(3), gamma = 88.44(3) degrees, V= 771.6(3) A3, Z = 2. Each Nd atom is coordinated to nine oxygen atoms, three from the alditol and six from water molecules, with Nd-O distances from 2.461 to 2.552 A. The seventh water molecule is hydrogen-bonded by the hydroxyl hydrogen on O-1 (O-1-H-ll...O-10, 2.639 A). The FT-IR spectra of 2NdCl3.galactitol.14H2O and 2PrCl3.galactitol.14H2O are analogous, and show that Pr and Nd have the same coordination mode. The IR results are consistent with the crystal structures.

Carbohydrates↗

PubMed2001

Sugar interaction with metal ions. The crystal structure and Raman spectra study of SmCl3-galactitol complex.

The crystal structure of 2SmCl3.galactitol.14H2O has been determined. The crystal system is triclinic, space group: P-1. The unit cell dimensions: a = 9.683(2) A, b = 10.341(2) A, c = 7.990(2) A; alpha = 108.01(3) degrees, beta = 92.71(3) degrees, gamma = 88.42(3) degrees. Each Sm atom is coordinated to nine oxygen atoms, three from the alditol and six from water molecules, with Sm-O distance from 2.417 to 2.520 A. The seventh water molecule is hydrogen-bonded by the hydroxy hydrogen on O-3 (O(3)-H(13)...O(10), 2.635 A). After forming complexes the peaks have shifted and the relative intensities have changed in the IR and Raman spectra, which are corresponding to the changes in bond distances and bond angles of the structures. The IR and Raman spectra of Pr-, Nd- and Sm-galactitol complexes are similar, which show that the three metal ions have the same coordination mode.

Crystallography, X-Ray↗

PubMed2001

Signaling and gene regulation by urea in cells of the mammalian kidney medulla.

Signaling by urea, although incompletely understood, is relevant both to cells of the mammalian kidney inner medulla and to all cells of the organism in the setting of advanced renal failure with its attendant accumulation of urea in the systemic circulation. The molecular events initiated by urea stress are distinct from those occurring in response to hypertonic stress; urea activates a characteristic subset of signaling events, which are in large part specific to cultured renal tubular epithelial cells. Interestingly, urea is protective of hypertonic NaCl-inducible apoptosis in this model. Details of this phenomenon are reviewed. The effect of urea has been likened to that of either hypertonicity or of a peptide mitogen. In preliminary expression array analyses, the profile of genes activated by urea stress in renal medullary cells, however, was found to be unique.

Animals↗

PubMed2001

Urea and hypertonicity increase expression of heme oxygenase-1 in murine renal medullary cells.

Epithelial cells derived from the mammalian kidney medulla are responsive to urea at the levels of signal transduction and gene regulation. Hybridization of RNA harvested from control- and urea-treated murine inner medullary collecting duct (mIMCD3) cells with a cDNA expression array encoding stress-responsive genes suggested that heme oxygenase (HO)-1 mRNA was upregulated by urea. RNase protection assay confirmed this upregulation; hypertonicity also increased HO-1 mRNA expression but neither hypertonic NaCl nor urea were effective in the nonrenal 3T3 cell line. The effect on HO-1 expression appeared to be transcriptionally mediated on the basis of mRNA half-life studies and reporter gene analyses using the promoters of both human and chicken HO-1. Although urea signaling resembles that of heavy metal signaling in other contexts, the effect of urea on HO-1 transcription was independent of the cadmium response element in this promoter. Urea-inducible HO-1 expression was sensitive to antioxidants but not to scavengers of nitric oxide. Urea also upregulated HO-1 protein expression and pharmacological inhibition of HO-1 action with zinc protoporphyrin-sensitized mIMCD3 cells to the adverse effects of hypertonicity but not to urea. Coupled with the prior observation of others that HO-1 expression increases along the renal corticomedullary gradient, these data suggest that HO-1 expression may comprise an element of the adaptive response to hypertonicity and/or urea in renal epithelial cells.

3T3 Cells↗

PubMed2001

Urea inhibits hypertonicity-inducible TonEBP expression and action.

Tonicity-responsive genes are regulated by the TonE enhancer element and the tonicity-responsive enhancer binding protein (TonEBP) transcription factor with which it interacts. Urea, a permeant solute coexistent with hypertonic NaCl in the mammalian renal medulla, activates a characteristic set of signaling events that may serve to counteract the effects of NaCl in some contexts. Urea inhibited the ability of hypertonic stressors to increase expression of TonEBP mRNA and also inhibited tonicity-inducible TonE-dependent reporter gene activity. The permeant solute glycerol failed to reproduce these effects, as did cell activators including peptide mitogens and phorbol ester. The inhibitory effect of urea was evident as late as 2 h after the application of hypertonicity. Pharmacological inhibitors of known urea-inducible signaling pathways failed to abolish the inhibitory effect of urea. TonEBP action is incompletely understood, but evidence supports a role for proteasome function and p38 action in regulation; urea failed to inhibit proteasome function or p38 signaling in response to hypertonicity. Consistent with its effect on TonEBP expression and action, urea pretreatment inhibited the effect of hypertonicity on expression of the physiological effector gene, aldose reductase. Taken together, these data 1) define a molecular mechanism of urea-mediated inhibition of tonicity-dependent signaling, and 2) underscore a role for TonEBP abundance in regulating TonE-mediated gene transcription.

Aldehyde Reductase↗

PubMed2000

Complexation of trivalent lanthanide cations by inositols in the solid state: crystal structure and an FT-IR study of PrCl3.myo-inositol.9 H2O.

The title compound, PrCl3.C6H12O6.9 H2O crystallized in the monoclinic space group P2(1)/n with cell dimensions a = 15.8293(3), b = 8.67750(10), c = 16.2292(3) A, beta = 107.0788(8) degrees, V = 2130.92(6) A3 and Z = 4. Each Pr ion is coordinated to nine oxygen atoms, two from the inositol and seven from water molecules, with Pr-O distances from 2.4729 to 2.6899 A; the other two water molecules are hydrogen-bonded. No direct contacts exist between Pr and Cl. There is an extensive network of hydrogen bonds formed by hydroxyl groups, water molecules, and chloride ions. The IR spectra of Pr-, Nd-, and Sm-inositol complexes are similar, which shows that the three metal ions have the same coordination mode. The IR results are consistent with the crystal structure.

Crystallization↗

PubMed2000

Sugar interaction with metal ions. FT-IR study on the structure of crystalline galactaric acid and its K+, NH4+, Ca2+, Ba2+, and La3+ complexes.

The FT-IR spectra of galactaric acid and its K+, NH4+, Ca2+, Ba2+, and La3+ salts have been recorded and interpreted. Spectroscopic evidence shows that the dimeric carboxylic groups of the free acid are dissociated upon formation of the salt, and the asymmetric and symmetric stretching vibrations of the anionic COO- group in these salts are observed at about 1600 and 1400 cm-1, respectively. The two carboxylic groups of the galactarate coordinate with Ca2+ ions in a monodentate form. One of the carboxylic groups in the Ba2+ salt coordinates in a monodentate state; another group interacts with three cations in a tetradentate form. In the K+, NH4+, and La3+ salts, the COO- groups coordinate in a polydentate manner with the cations. By comparison of the spectra of the salts with that of the free acid, it is concluded that the hydroxyl groups of the galactarate skeleton take part in metal-oxygen interaction, and the hydrogen-bonding network is rearranged upon sugar metalation. The degree of participation of the sugar OH groups in metal-galactarate interaction is varied from the K+ and NH4+ salts to the Ca2+, Ba2+, and La3+ salts.

Barium↗

PubMed2000

Sugar interaction with metal ions. Crystal structure and FT-IR spectroscopic study of strontium galactarate mono-hydrate.

The crystal structure of strontium galactarate mono-hydrate, Sr2+ x C6H8O8(2-) x H2O, Mr = 313.76, monoclinic, P2(1)/c, a = 10.268(2), b = 10.333(2), c = 10.194(2) A, beta = 117.87(3) degrees, lambda(Mo K alpha) = 0.71073 A, Z = 4, Dx = 2.180 Mg m(-3), V = 956.1(3) A3, mu = 5.676 mm(-1), F(000) = 624, T = 293(2) K, R = 0.0260 for 1690 observed reflections and 145 parameters refined, has been determined. The galactarate ion is centro-symmetrical in the crystal structure, although it contains independent half-ions. The Sr2+ ion is nine-coordinated (tricapped trigonal prism) with five Sr-O bonds from carboxylic groups, and four from hydroxyl groups. The water molecule does not take part in the coordination. Six hydrogen bonds are formed, three of them related to the water molecule. The spectroscopic evidence shows that the carboxylic acid dimers of the free acid dissociate. The asymmetric stretching vibrations of the anionic COO groups in the salt are observed at 1609 and 1548, and 1581 cm(-1), assigned to a mono-dentate and a tetra-dentate coordination, respectively. The symmetric stretching vibration is located at 1397 cm(-1). The hydroxyl groups of the galactarate skeleton take part in the metal-oxygen interaction, and the hydrogen-bonding network is rearranged upon sugar metalation.

Carbohydrates↗

PubMed2000

Production of polyesters consisting of medium chain length 3-hydroxyalkanoic acids by Pseudomonas mendocina 0806 from various carbon sources.

Pseudomonas mendocina strain 0806 was isolated from oil-contaminated soil and found to produce polyesters consisting of medium chain length 3-hydroxyalkanoates (mclPHAs). The monomers of mclPHAs contained even numbers of carbon atoms, such as 3-hydroxyhexanoate (HHx or C6), 3-hydroxyoctanoate (HO or C8), and/or 3-hydroxydecanoate (HD or C10) as major components when grown on many carbon sources unrelated to their monomeric structures, such as glucose, citric acid, and carbon sources related to their monomeric structures, such as myristic acid, octanoate, or oleic acid. On the other hand, PHA containing both even and odd numbers of hydroxyalkanoates (HA) monomers was synthesized when the strain was grown on tridecanoic acid. The molar ratio of carbon to nitrogen (C/N) had a significant effect on PHA composition: the strain produced PHAs containing 97-99% of HD monomer when grown in a glucose ammonium sulfate medium of C/N<20, and 20% HO, and 80% of the HD monomer when growth was conducted in media containing C/N>40. It was demonstrated that the HO/HD ratio in the polymers remained constant in media with a constant C/N ratio, regardless of the glucose concentration. Up to 3.6 g/L cell dry weight containing 45% of PHAs was produced when the strain was grown for 48 h in a medium containing 20 g/L glucose with a C/N ratio of 40.

Glucose↗

PubMed2000

Ras signaling in the inner medullary cell response to urea and NaCl.

The small guanine nucleotide-binding protein Ras, activated by peptide mitogens and other stimuli, regulates downstream signaling events to influence transcription. The role of Ras in solute signaling to gene regulation was investigated in the murine inner medullary collecting duct (mIMCD3) cell line. Urea treatment (100-200 mM), but not sham treatment, increased Ras activation 124% at 2 min; the effect of NaCl did not achieve statistical significance. To determine the contribution of Ras activation to urea-inducible signal transduction, mIMCD3 cells were stably transfected with an expression plasmid encoding a dominant negative-acting N17Ras mutant driven by a dexamethasone-inducible (murine mammary tumor virus) promoter. After 24 h of induction, selected cell lines exhibited sufficient N17Ras overexpression to abolish epidermal growth factor- and hypotonicity-mediated signaling to extracellular signal-regulated kinase (ERK) phosphorylation, as determined by immunoblotting. Conditional N17Ras overexpression inhibited urea- and NaCl-inducible ERK phosphorylation by 40-50%, but only at 15 min, and not 5 min, of treatment. N17Ras induction, however, almost completely inhibited urea-inducible Egr-1 transcription, as quantitated by luciferase reporter gene assay, but failed to influence tonicity-inducible (TonE-mediated) transcription. N17Ras overexpression also blocked urea-inducible expression of the transcription factor Gadd153 but did not influence osmotic or urea-inducible apoptosis. In addition, urea treatment induced recruitment of the Ras activator Sos to the plasma membrane. Taken together, these observations suggest a role for Ras signaling in the IMCD cell response to urea stress.

Animals↗

PubMed2000

Urea protects from the proapoptotic effect of NaCl in renal medullary cells.

Hypertonic NaCl upregulated two sensitive and specific biochemical indices of apoptosis, caspase-3 activation and annexin V binding, in a time- and dose-dependent fashion in renal medullary mIMCD3 cells. Pretreatment with urea (200 mM for 30 min) protected from the proapoptotic effect of hypertonic stress (200 mosmol/kgH(2)O) in this model. The protective effect of urea was dose dependent and was effective even when applied a short time (< or =1 h) following NaCl exposure; this protective effect was not observed in the nonrenal 3T3 cell line. In both mIMCD3 and 3T3 cells, urea failed to protect from the proapoptotic stressor, ultraviolet (UV)-B irradiation. The ability of urea to protect from hypertonic stress was approximately comparable to the protective effect of peptide mitogens epidermal growth factor and insulin-like growth factor (IGF), but it potentiated the IGF effect. Interestingly, the tyrosine kinase inhibitor, genistein, potentiated the proapoptotic effect of urea yet abrogated the proapoptotic effect of hypertonic stress. In aggregate, these data indicate that urea protects from the proapoptotic effect of hypertonic stress in a potentially cell type-specific and stimulus-specific fashion.

3T3 Cells↗

PubMed2000

MAPK signaling and the kidney.

Following an overview of the biochemistry of mitogen-activated protein kinase (MAPK) pathways, the relevance of these signaling events to specific models of renal cell function and pathophysiology, both in vitro and in vivo, will be emphasized. In in vitro model systems, events activating the principal MAPK families [extracellular signal-regulated and c-Jun NH(2)-terminal kinase and p38] have been best characterized in mesangial and tubular epithelial cell culture systems and include peptide mitogens, cytokines, lipid mediators, and physical stressors. Several in vivo models of proliferative or toxic renal injury are also associated with aberrant MAPK regulation. It is anticipated that elucidation of downstream effector signaling mechanisms and a clearer understanding of the immediate and remote upstream activating pathways, when applied to these highly clinically relevant model systems, will ultimately provide much greater insight into the basis for specificity now seemingly absent from these signaling events.

Adaptor Proteins, Signal Transducing↗

PubMed2000

Anatomical variation of the posterior interosseous nerve: a cadaver dissection study.

An anatomical variation of the posterior interosseous nerve was found in a cadaver. The posterior interosseous nerve entered the supinator muscle 3 cm distal to the radiohumeral joint, but exited from two sites. Fifty percent of the nerve exited under the distal edge of the supinator muscle. The other 50% of the nerve pierced through the supinator muscle, 4.2 cm distal to the articular surface of the radial head and then joined the remaining posterior interosseous nerve as it emerged from the supinator muscle distally. Variations were not found concerning the order and the manner of branches to the muscles. This variation in the posterior interosseous nerve could be an additional compression site for this nerve and therefore responsible for some of the atypical presentations of symptoms and for partial recovery after surgical decompression. Careful surgical dissection is recommended to avoid injury to this branch.

Aged↗

PubMed2000

The Oklahoma repair technique: a biomechanical study of a new suture repair technique.

We designed and evaluated the biomechanical advantages of a new (Oklahoma) suture technique for repairing flexor tendons in fresh, frozen cadaver specimens. Forty flexor digitorum profundi tendons from the middle three fingers were sharply cut and repaired with a number 3-0 braided polyester using the new technique and the Modified Kessler technique with and without an epitenon repair. The repaired tendons were then stressed to failure. The Modified Kessler with epitendon repair initiated gap formation on an average of 15.3 +/- 2.7 newtons and failed at 40.9 +/- 4.3 newtons. The Oklahoma suture technique with a running epitenon repair initiated gap formation on average of 48.6 (SD +/- 4.0) newtons and required an average load of 57.9 (SD +/- 3.0) newtons to fail. Thus, it was significantly stronger than the modified Kessler technique with epitendon repair (P < 0.01). The tendons repaired with the Oklahoma and epitenon repair suture technique did not form a 2 mm gap prior to failure. The epitendon repair increased the resistance to gap formation by 80% to 100% and the repair failure by 17.5% to 25% for both types of repairs. We concluded that the addition of the epitendon repair increases the tensile strength of the repair regardless of the core suture technique, and it should be used. In comparison with the Modified Kessler repair technique, the Oklahoma repair technique has superior tolerance to gap initiation, 2 mm gap formation, and physical failure of the repaired tendon.

Analysis of Variance↗