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C Bai

Publications and source records attributed to C Bai.

At least 19 recordsLinked to original sources

A novel gene, GliH1, with homology to the Gli zinc finger domain not required for mouse development.

The Sonic hedgehog (Shh)-Gli signaling pathway regulates development of many organs, including teeth. We cloned a novel gene encoding a transcription factor that contains a zinc finger domain with highest homology to the Gli family of proteins (61-64% amino acid sequence identity) from incisor pulp. Consistent with this sequence conservation, gel mobility shift assays demonstrated that this new Gli homologous protein, GliH1, could bind previously characterized Gli DNA binding sites. Furthermore, transfection assays in dental pulp cells showed that whereas Gli1 induces a nearly 50-fold increase in activity of a luciferase reporter containing Gli DNA binding sites, coexpression of Gli1 with Gli3 and/or GliH1 results in inhibition of the Gli1-stimulated luciferase activity. In situ hybridization analysis of mouse embryos demonstrated that GliH1 expression is initiated later than the three Gli genes and has a more restricted expression pattern. GliH1 is first detected diffusely in the limb buds at 10.0 days post coitus and later is expressed in the branchial arches, craniofacial interface, ventral part of the tail, whisker follicles and hair, intervertebral discs, teeth, eyes and kidney. LacZ was inserted into the GliH1 allele in embryonic stem cells to produce mice lacking GliH1 function. While this produced indicator mice for GliH1-expression, analysis of mutant mice revealed no discernible phenotype or required function for GliH1. A search of the Celera Genomics and associated databases identified possible gene sequences encoding a zinc finger domain with approximately 90% homology to that of GliH1, indicating there is a family of GliH genes and raising the possibility of overlapping functions during development.

Alleles↗

DNA-protein crosslinks induced by nickel compounds in isolated rat lymphocytes: role of reactive oxygen species and specific amino acids.

Isolated rat lymphocytes in salts-glucose medium (pH 7.2) were incubated with nickel chloride, nickel acetate, nickel sulfate, and a soluble form of nickel subsulfide (0-2 mM) at 37 degrees C for 2 h. The soluble form of nickel subsulfide induced a significant increase in DNA-protein crosslinks (DPXLs) (111%) beginning at 0.5 mM and a maximum increase of 700% from that of the control value was reached at a 2 mM concentration, whereas nickel sulfate produced only a 65% increase of such crosslinks at the 2 mM concentration only. No significant reduction in viability of rat lymphocytes (as measured by trypan blue exclusion) due to these nickel compounds was observed at any concentration used. Time-course studies of DPXLs and cellular viability due to 2 mM nickel subsulfide indicate that DPXL formation may not be due in part to cellular necrosis. Coincubation of nickel subsulfide (2 mM) with l-histidine (16 mM), l-cysteine (4 or 8 mM), or l-aspartic acid (24 mM) significantly reduced the DPXLs induced by 2 mM nickel subsulfide. But Mg(2+) even at 24 mM failed to antagonize nickel subsulfide-induced increase in DPXLs. High concentrations of these amino acids significantly decreased the accumulation of Ni(2+) from nickel subsulfide in lymphocytes, suggesting that such reduction of cellular uptake of Ni(2+) by these amino acids is partly responsible for the potent protective effects of these amino acids against such genotoxicity of nickel subsulfide. In vitro exposure of lymphocytes to nickel subsulfide (0-2 mM) increased the formation of reactive oxygen species (ROS) in a concentration-dependent manner. Furthermore, coincubation of 2 mM nickel subsulfide with catalase, dimethylthiourea, mannitol, or vitamin C at 37 degrees C for 2 h resulted in a significant decrease of nickel subsulfide-induced formation of DPXLs, suggesting that nickel subsulfide-induced DPXLs formation in isolated rat lymphocytes is caused by the formation of ROS. The amino acid treatment also abrogated Ni(3)S(2)-induced generation of ROS. Deferoxamine (a highly specific iron chelator) treatment prevented nickel subsulfide-induced DNA-protein crosslink formation, suggesting that Ni(2+)-induced DPXL formation in rat lymphocytes is caused by the induction of Fenton/Haber-Weiss reaction, generating hydroxyl radicals. The potent protective effects of these specific amino acids against nickel subsulfide-induced DPXL formation in isolated rat lymphocytes may be due in part to impaired cellular uptake of Ni(2+), inhibition of the binding of Ni(2+) to deproteinized DNA, and a reduction in reactive oxygen species.

Acetates↗

Some applications of a chiral fluorometric reagent, (S)-TBMB carboxylic acid.

Molecular design and applications of a fluorometric chiral agent, (S)-TBMB carboxylic acid, are briefly reviewed. The agent, possessing an asymmetric 1,3-benzodioxole skeleton, was designed as a novel class of chiral agent that functions also as a benzoate chromophore for exciton chirality CD methods. The utility of this agent has been demonstrated in an application to determine enantiomeric amino acids, acyl-sn-glycerols, glycosyl-sn-glycerols, and other chiral alcohols and amines.

Amino Acids↗

Branched nanowire based guanine rich oligonucleotides.

Self-assembly and aggregation of guanine rich sequences can provide useful insights into DNA nanotechnology and telomeric structure and function. In this paper, we designed a guanine rich sequence d(GGCGTTTTGCGG). We found that it can form stable structure in appropriate condition and it exhibits an anomalous CD spectra. This structures can be imaged in ambient environment with a Nanoscope III AFM (Digital Instruments). We found it forms branch structure and long multistrand DNA nanowire after incubation at 37 degrees C for 6-12 hours in 25 mM TE (pH=8.0) + 5 mM Mg2+ + 50 mM K+. The ability to self-assemble into branches and long wires not only clearly demonstrate its potential as scaffold structures for nanotechnology, but also give aids to understand telomeric structure further. We have proposed a model to explain how these structures formed.

Circular Dichroism↗

[Significance of lung perfusion scanning with technetium labeled macroaggregated albumin and pulmonary function assay for diagnosis of early hepatopulmonary syndrome].

OBJECTIVE: To evaluate the values of pulmonary function assay and dynamic pulmonary perfusion imaging with technetium labeled macroaggregated albumin ((99m)TcMAA) in the early diagnosis of hepatopulmonary syndrome (HPS). METHODS: The pulmonary function assay and (99m)TcMAA scans were performed in 28 patients with HPS, 30 cirrhotic patients (CP) without HPS, and 21 healthy controls (HC). RESULTS: In the patients with HPS, PaO(2), SaO(2) and diffusion capacity for carbon monoxide of lungs (DLco) was significantly lower than that in CP (P<0.01) and HC (P<0.01), and alveolar-arterial gradient [P((A-a))O(2)] was significantly increased (P<0.001). Results from (99m)TcMAA scans showed that the radionuclides were distributed over the spleen, kidney, liver and brain, and the ratios of arterivenous shunt were significantly higher than that in CP (P<0.001) and NC (P<0.001). In cirrhotic patients, DLco significantly decreased (P<0.05), P((A-a))O(2) and shunt ratios increased (P<0.01 and 0.001). CONCLUSIONS: Pulmonary function assay and dynamic pulmonary perfusion imaging with (99m)TcMAA are sensitive methods for diagnosis of the early HPS.

Hepatopulmonary Syndrome↗

[Experimental study for lung fluid transport by epithelial cells and aquaporins].

OBJECTIVE: To explore the effects of aquaporins (AQP) 1, 4 on water transport between airspace and pulmonary capillary and high pressure pulmonary edema. The other purpose was to study the active alveolar fluid transport as well as alveolar fluid clearance (AFC) in different pH of airspace. METHODS: The effects of AQP1, 4 on water transport between airspace and pulmonary capillary and high pressure pulmonary edema were studied by surface fluorescence methods and gravimetric method respectively, AFC and AFC in airspace with different pH were measured by isotope method. RESULTS: AQP1 knockout inhibited water transport through pulmonary capillary and also reduced high pressure pulmonary edema. Salbutamol increased AFC, but it was reduced when propranolol was used together. AFC was improved by terbutaline, isoproterenol, salmeterol when pH > 2.5 in airspace, but the effect was reduced after pH < 2.5 in airspace. Sodium channel inhibitor, Benzamil, could also inhibit AFC. CONCLUSIONS: AQP1 knockout significantly reduced water transport through alveolar capillary, and also reduced high pulmonary edema slightly. beta adrenergic stimulant improved AFC in mechanically ventilated rats. Intact airspace is very important for the function of AFC, however, the effect of AFC was impaired after lung injury induced by pH < 2.5 in airspace.

Animals↗

Investigation of thrombomodulin and plasminogen activator inhibitor type-I in pregnancy induced hypertension and its clinical significance.

OBJECTIVE: To measure the circulating levels of thrombomodulin (TM) and plasminogen activator inhibitor type-I (PAI-I) in women with pregnancy induced hypertension (PIH). METHODS: Blood samples were drawn from 97 pregnant women in their third trimester, grouped as 25 mild PIH, 26 moderate PIH, 22 severe PIH and 24 normotensive healthy pregnant women for determining levels of TM by ELISA, PAI-I by colorimetric assay methods, and creatinine (Cr) in serum by biochemical method. RESULTS: Circulating levels of TM, PAI-I and TM/Cr ratio increased with increasing severity of PIH. There were no significant differences between mild and normotensive pregnant women. The parameters were significantly changed in the moderate and severe PIH groups. CONCLUSION: TM and PAI-I may serve as meaningful clinical markers for the assessment of the endothelial damage in PIH, which is very important in evaluating and following the development of PIH.

Adult↗

Role of aquaporins in alveolar fluid clearance in neonatal and adult lung, and in oedema formation following acute lung injury: studies in transgenic aquaporin null mice.

Aquaporin (AQP) water channels provide a major pathway for osmotically driven water movement across epithelial and microvascular barriers in the lung. We used mice deficient in each of the three principal lung aquaporins, AQP1, AQP4 and AQP5, to test the hypothesis that aquaporins are important in neonatal lung fluid balance, adult lung fluid clearance and formation of lung oedema after acute lung injury. Wet-to-dry weight ratios (W/D) in lungs from wild-type mice decreased from 7.9 to 5.7 over the first hour after spontaneous delivery. AQP deletion did not significantly affect W/D at 45 min after birth. Alveolar fluid clearance was measured in living ventilated mice in which 0.5 ml saline containing radiolabelled albumin was instilled into the airspaces. Fluid clearance was 17.4 % in 15 min and inhibited >90 % by amiloride, but clearance was not affected by AQP deletion. W/D was measured in established models of acute lung injury - acid aspiration and thiourea administration. Two hours after intratracheal administration of HCl, W/D increased from 3.7 to 7.5 but was not affected by AQP deletion. Three hours after intraperitoneal infusion of thiourea, W/D increased to 5.5 and marked pleural effusions appeared, but there were no differences in wild-type and AQP knockout mice. Hyperoxic subacute lung injury was induced by 95 % oxygen. Neither mean survival (143 h) nor W/D at 65 h (5.1) were significantly affected by AQP deletion. Despite their role in osmotically driven lung water transport, aquaporins are not required for the physiological clearance of lung water in the neonatal or adult lung, or for the accumulation of extravascular lung water in the injured lung.

Acids↗

Genetic analysis of a La homolog in Drosophila melanogaster.

People afflicted with certain rheumatological auto-immune diseases produce autoantibodies directed against a select group of proteins such as the La auto-antigen. Biochemical studies have revealed La to be a promiscuous RNA-binding protein that appears to play a role in a variety of intracellular activities such as processing and/or transport of RNA polymerase III precursor transcripts and translational regulation from internal ribosome entry sites (IRES). We have previously identified an RNA-binding protein that is a Drosophila melanogaster homolog of La (D-La) and shown that early transcript accumulation throughout the embryo is later refined to be most prevalent in the visceral mesoderm, gut, gonads and salivary glands. Here we report the first in vivo genetic characterization of a La homolog in a multicellular eukaryote. Lethality was observed in homozygous larvae harboring a small chromosomal deletion that removed the D-La gene, which was rescued by an inducible D-La cDNA transgene. This implies that D-La confers essential functions for larval development. In addition, loss of D-La function gives rise to defects in embryonic midgut morphogenesis; one of the midgut defects correlates with loss of Ultrabithorax ( Ubx ) expression along the second midgut constriction. Finally, genetic interactions between chromosomal deficiencies that remove D-La and certain Ubx alleles were demonstrated in adults. Our results support the hypothesis that D-La provides essential functions for proper Drosophila development and imply that the conserved La family of proteins may perform critical developmental functions in higher eukaryotes.

Adenosine Triphosphatases↗

Overexpression of M68/DcR3 in human gastrointestinal tract tumors independent of gene amplification and its location in a four-gene cluster.

Fas-mediated apoptosis is an important regulator of cell survival, and abnormalities in this system have been shown to result in a number of human pathological conditions. A secreted member of the tumor necrosis factor receptor superfamily, DcR3, was recently reported to be amplified in human lung and colon cancers as a negative regulator of Fas-mediated apoptosis. We identified this gene, which we call M68. M68 genomic DNA, mRNA, and protein levels were examined in a series of human gastrointestinal tract tumors. Using M68 immunohistochemistry and a scoring system similar to that used for HER-2/neu, we found that M68 protein was overexpressed in 30 of 68 (44%) human adenocarcinomas of the esophagus, stomach, colon, and rectum. Tumors examined by Northern blot revealed M68 mRNA highly elevated in a similar fraction of primary tumors from the same gastrointestinal tract regions, as well as in the colon adenocarcinoma cell lines SW480 and SW1116. Further, we found M68 protein to be overexpressed in a substantial number of tumors in which gene amplification could not be detected by fluorescence in situ hybridization or quantitative genomic PCR, suggesting that overexpression of M68 may precede amplification in tumors. Finally, we find that M68 lies within a four-gene cluster that includes a novel helicase-like gene (NHL) related to RAD3/ERCC2, a plasma membrane Ras-related GTPase and a member of the stathmin family, amplification or overexpression of which may also contribute to cell growth and tumor progression.

ADP-Ribosylation Factors↗

Effects of protein-deficient nutrition during rat pregnancy and development on developmental hindlimb crossing due to methylmercury intoxication.

Pregnant rats were fed either a control (20% protein) or low (3.5%) protein diet during gestation and lactation. The pups were separated from their mothers on postnatal day 21, and were given the same diet as their corresponding mothers. The groups of pups from each diet group were treated on either postnatal day 21 or postnatal day 60 with 7.5 mg methylmercury chloride (MeHgCl) per kg b.w. once daily by gavage for 10 consecutive days, and the development of ataxia (hind-limb crossing) was monitored. The offspring from mothers on the protein-deficient diet were found to be more sensitive to MeHg-induced ataxia than those on the protein-sufficient diet. The former accumulated more mercury in different brain regions than the latter. The rates of protein synthesis in different brain regions of the offspring fed the protein-deficient diet were significantly reduced compared with the rates in those fed the protein-sufficient diet. However, MeHg treatment did not significantly modify the rates of such protein synthesis further in protein-deficient rats. Thus, a significantly much higher inhibition of the intrinsic rates of protein synthesis in different brain regions due to severe protein deficiency, as observed in this study, may be partly responsible for the increased susceptibility of developing rats fed a protein-deficient diet to MeHg-induced ataxia, or hindlimb crossing, although other factor(s) might also be involved.

Animals↗

Fold-back tetraplex DNA species in DNase I-resistant DNA isolated from HeLa cells.

A DNase I-resistant DNA species has been isolated and purified from HeLa cells by gel electrophoresis. Our studies indicate that the DNase I-resistant DNA species was about 40-60 bp fragment sizes responding to double-strand DNA marker and has higher guanine content. The image of AFM showed that this species has been assumed to be tetraplex structure according to its apparent width and height. Its CD, UV spectrum also exhibited characteristics similar to some tetraplex structure, which was different from the standard duplex DNA. 32P-labeled probes (TTAGGG)4 and 5'-TGGGGAGGGTGGGGAGGGTGGGGAAGG-3' could be hybridized to purified DNase I-resistant species. All results suggest that the DNase I-resistant DNA species have at least two components, which adopt an intrastrand fold-back DNA tetraplex. Their sequences were similar to human telomere and human c-myc locus (NHE), respectively.

Chromatography, High Pressure Liquid↗

Atomic force microscopy analysis of intermediates in cobalt hexammine-induced DNA condensation.

The packaging pathway of cobalt hexammine-induced DNA condensation on the surface of mica was examined by varying the concentration of Co(NH3)6(3+) in a dilute DNA solution and visualizing the condensates by atomic force microscopy (AFM). Images reveal that cobalt hexammine-induced DNA condensation on mica involves well-defined structures. At 30 microM Co(NH3)6(3+), prolate ellipsoid condensates composed of relatively shorter rods with linkages between them are formed. At 80 microM Co(NH3)6(3+), the condensed features include toroids with average diameter of approximately 240 nm as well as U-shaped and rod-like condensates with nodular appearances. The results imply that the condensates, whether toroids, U-shaped or rod-like structures have similar intermediate state which includes relatively shorter rod-like segments. The average size of the condensed toroids after incubated at room temperature for 5 h (approximately 240 nm) is much larger than that incubated for 0.5 h (approximately 100 nm). The results indicate that the condensation of DNA by Co(NH3)6(3+) is a kinetic-controlled process.

Adsorption↗

A slice-by-slice blurring model and kernel evaluation using the Klein-Nishina formula for 3D scatter compensation in parallel and converging beam SPECT.

Converging collimation increases the geometric efficiency for imaging small organs, such as the heart, but also increases the difficulty of correcting for the physical effects of attenuation, geometric response and scatter in SPECT. In this paper, 3D first-order Compton scatter in non-uniform scattering media is modelled by using an efficient slice by-slice incremental blurring technique in both parallel and converging beam SPECT. The scatter projections are generated by first forming an effective scatter source image (ESSI), then forward-projecting the ESSI. The Compton scatter cross section described by the Klein-Nishina formula is used to obtain spatial scatter response functions (SSRFs) of scattering slices which are parallel to the detector surface. Two SSRFs of neighbouring scattering slices are used to compute two small orthogonal 1D blurring kernels used for the incremental blurring from the slice which is further from the detector surface to the slice which is closer to the detector surface. First-order Compton scatter point response functions (SPRFs) obtained using the proposed model agree well with those of Monte Carlo (MC) simulations for both parallel and fan beam SPECT. Image reconstruction in fan beam SPECT MC simulation studies shows increased left ventricle myocardium-to-chamber contrast (LV contrast) and slightly improved image resolution when performing scatter compensation using the proposed model. Physical torso phantom fan beam SPECT experiments show increased myocardial uniformity and image resolution as well as increased LV contrast. The proposed method efficiently models the 3D first-order Compton scatter effect in parallel and converging beam SPECT.

Biophysical Phenomena↗

Crystallization and preliminary X-ray diffraction studies of monomeric isocitrate dehydrogenase from corynrbacterium glutamicum. erratum

In the paper by Audette et al. [Acta Cryst. (1999), D55, 1584-1585] the postal code of one of the authors was printed incorrectly. The correct version is given above. Also the reaction catalyzed by isocitrate dehydrogenase was given incorrectly in the paper; the correct reaction is given below. Isocitrate + NADP(+) <--> Oxalosuccinate + NADPH. Oxalosuccinate <--> alpha-Ketoglutarate + CO(2).

Journal Article↗

Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation.

The secreted factor Sonic hedgehog (SHH) is both required for and sufficient to induce multiple developmental processes, including ventralization of the CNS, branching morphogenesis of the lungs and anteroposterior patterning of the limbs. Based on analogy to the Drosophila Hh pathway, the multiple GLI transcription factors in vertebrates are likely to both transduce SHH signaling and repress Shh transcription. In order to discriminate between overlapping versus unique requirements for the three Gli genes in mice, we have produced a Gli1 mutant and analyzed the phenotypes of Gli1/Gli2 and Gli1/3 double mutants. Gli3(xt) mutants have polydactyly and dorsal CNS defects associated with ectopic Shh expression, indicating GLI3 plays a role in repressing Shh. In contrast, Gli2 mutants have five digits, but lack a floorplate, indicating that it is required to transduce SHH signaling in some tissues. Remarkably, mice homozygous for a Gli1(zfd )mutation that deletes the exons encoding the DNA-binding domain are viable and appear normal. Transgenic mice expressing a GLI1 protein lacking the zinc fingers can not induce SHH targets in the dorsal brain, indicating that the Gli1(zfd )allele contains a hypomorphic or null mutation. Interestingly, Gli1(zfd/zfd);Gli2(zfd/+), but not Gli1(zfd/zfd);Gli3(zfd/+) double mutants have a severe phenotype; most Gli1(zfd/zfd);Gli2(zfd/+) mice die soon after birth and all have multiple defects including a variable loss of ventral spinal cord cells and smaller lungs that are similar to, but less extreme than, Gli2(zfd/zfd) mutants. Gli1/Gli2 double homozygous mutants have more extreme CNS and lung defects than Gli1(zfd/zfd);Gli2(zfd/+) mutants, however, in contrast to Shh mutants, ventrolateral neurons develop in the CNS and the limbs have 5 digits with an extra postaxial nubbin. These studies demonstrate that the zinc-finger DNA-binding domain of GLI1 protein is not required for SHH signaling in mouse. Furthermore, Gli1 and Gli2, but not Gli1 and Gli3, have extensive overlapping functions that are likely downstream of SHH signaling.

Abnormalities, Multiple↗

[A study on the deficiency of anticoagulant proteins in Chinese patients with deep venous thrombosis].

OBJECTIVE: To investigate the incidence of anticoagulant proteins deficiency in Chinese patients with venous thrombosis. METHODS: Eighty-seven patients with otherwise unexplained venous thrombophilia were studied. Both the antigen and antivitity of PC, PS, and antithrombin III (ATIII) were determined using commercial kits (Stago, or IL) activated PC, sensitivity ratio (APC-SR) by Coatest chromogenix, and factor V gene mutation by polymerase chain reaction with restriction fragments long polymorphism (PCR-RFLP). RESULTS: Of all the patients twenty-five were found to be abnormal. These consisted of 3 ATIII deficiencies, 5 PC deficiencies, 10 PS deficiencies, 2 resistance of activated protein C (APC-R), 1 combined ATIII and PC deficiency, 1 combined ATIII and PS deficiency, 1 combined PC and PS deficiency, 1 combined APC-R and PC deficiency and 1 combined APC-R and PS deficiency. The overall prevalence of ATIII, PC and PS deficiencies was 26.4%. The patients with anticoagulant proteins deficiency had earlier onset (35.2 +/- 9.7 vs 42.1 +/- 10.9; P < 0.01) and more recurrent thrombosis (P < 0.05), as well as more pulmonary embolism (44.0% vs 16.1%; P < 0.01) than those of without anticoagulant protein deficiency. CONCLUSION: The overall prevalence of ATIII, PC, and PS deficiency in Chinese venous thrombosis patients was higher than that of Western patients. It suggests that the etiology of thrombophilia may be different between Chinese and Western.

Adolescent↗