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Biomedical subjects

J Zhao

Publications and source records attributed to J Zhao.

At least 217 records · Page 12Linked to original sources
PubMed2001

[Research on the synthesis and spectroscopy of 2-(2-phenyl propenyl) benzoxazoles].

In this paper the synthetic methods and the substituent effects on yields were discussed. It was found that the yields were not high, and the compounds with electron-drawing groups had higher yields. Some compounds with electron-giving groups such as t-Bu couldn't be synthesized by wittig-horner method. The compounds were characterized by IR, 1H NMR, MS, UV and FL. The experimental results indicated that there was not quantitative substituent effect on IR, the electron-drawing groups had great effect on the chemical shifts of propenyl hydrogen and methyl hydrogen, the strong double-electron fragments existed in MS. Some experimental phenomena of UV and FL were also studied.

Benzoxazoles↗
PubMed2001

[Study on the analysis of main and trace elements in phosphate rock by ICP-AES].

Through studying the analysis of main and trace elements in phosphate rock, a method is proposed to determine main and trace elements (total 9 elements) in phosphate rock by ICP-AES method with sample dissolved by HF-HClO4. Detected limit is 0.0024-0.36 microgram.mL-1 and RSD is 0.75%-2.57%. This method is suitable for analysis of phosphate rock.

Calcium↗
PubMed2001

[The Raman vibrational characteristics and assignments of three Schiff bases].

The Raman vibrational characteristics of three asymmetric Schiff bases were studied in this paper. By referring to the characteristic Raman spectra of substituent benzene and oxamidoxime compounds, the Raman vibrational modes of three Schiff bases were analyzed and assigned, respectively. The difference of their Raman spectra mainly arises from their different vibrational energy level resulting from the C-OH group to most extents. This result is of importance for further investigating the properties of these three new-type Schiff bases.

Benzene↗
PubMed2001

[Comparison of hard tissue changes by treatment of angle class II malocclusion with Kloehn's extraoral arch in periods of transitional dentition and permanent tooth].

OBJECTIVE: The optimal treatment period by use of extraoral arch was understood by comparison of the changes of facial hard tissue in treatment of Angle II malocclusion with Kloehn's extraoral arch and Edgwise appliance. METHODS: A group of 7-8 year old children and a group of 10-11 year-old children were selected, including 16 Angle II malocclusion cases in each group, respectively. Data of cephalograms and model analysis were compared between pretreatment and posttreatment. RESULTS: The more distance of maxillary molar and more obvious inhibition of maxilla bone growth forward in group of 7-8 year-old children (group of transitional dentition) were detected than that in group of 10-11 year-old children(group of permanent tooth). CONCLUSION: More effective treatment by use of extraoral arch was detected in the period of transitional dentition than that in permanent tooth.

English Abstract↗
PubMed2000

Analysis of FAK-associated signaling pathways in the regulation of cell cycle progression.

Focal adhesion kinase (FAK) is an important mediator of signal transduction pathways initiated by integrins in cell migration, survival and cell cycle regulation. The ability of FAK to mediate integrin signaling in the regulation of cell cycle progression depends on the phosphorylation of Tyr397, which implies a functional significance for the formation of FAK signaling complexes with Src, phosphatidylinositol-3-kinase (PI3K) and Grb7. We have previously described a FAK mutant, D395A, that selectively disrupts FAK binding to PI3K, but allows FAK association with Src. Using this mutation in a mislocalized FAK mutant background, we show here that formation of a FAK/PI3K complex is not sufficient for cell cycle progression but the formation of a FAK/Src complex plays an essential role. We also show that mutation of D395 to A disrupted FAK association with Grb7. This suggests that a FAK/Grb7 complex is not involved in the cell cycle regulation either, which is supported by direct analysis of cells expressing a dominant negative Grb7 construct. Finally, we provide evidence that the Src-dependent association of FAK with Grb2 and p130(Cas) are both required for the regulation of cell cycle progression by FAK. Together, these studies identify important FAK downstream signaling pathways in cell cycle regulation.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Abnormal contractile function in transgenic mice expressing a familial hypertrophic cardiomyopathy-linked troponin T (I79N) mutation.

This study characterizes a transgenic animal model for the troponin T (TnT) mutation (I79N) associated with familial hypertrophic cardiomyopathy. To study the functional consequences of this mutation, we examined a wild type and two I79N-transgenic mouse lines of human cardiac TnT driven by a murine alpha-myosin heavy chain promoter. Extensive characterization of the transgenic I79N lines compared with wild type and/or nontransgenic mice demonstrated: 1) normal survival and no cardiac hypertrophy even with chronic exercise; 2) large increases in Ca(2+) sensitivity of ATPase activity and force in skinned fibers; 3) a substantial increase in the rate of force activation and an increase in the rate of force relaxation; 4) lower maximal force/cross-sectional area and ATPase activity; 5) loss of sensitivity to pH-induced shifts in the Ca(2+) dependence of force; and 6) computer simulations that reproduced experimental observations and suggested that the I79N mutation decreases the apparent off rate of Ca(2+) from troponin C and increases cross-bridge detachment rate g. Simulations for intact living fibers predict a higher basal contractility, a faster rate of force development, slower relaxation, and increased resting tension in transgenic I79N myocardium compared with transgenic wild type. These mechanisms may contribute to mortality in humans, especially in stimulated contractile states.

Animals↗
PubMed2000

Association analysis of polymorphisms in the DRD4 gene and heroin abuse in Chinese subjects.

Heroin abuse is a major social and public health problem in many parts of the world, yet relatively little is known about its etiology. Although genes play a role in determining susceptibility, they are expected to be of small effect with considerable heterogeneity. Because the dopamine system is involved in reward, its neurotransmitter receptors are candidates for etiological involvement in addiction. In the present study, we examine two polymorphisms in the dopamine D4 receptor, a VNTR in exon III and a point mutation in the promoter (-512C/T) that affects transcriptional efficiency. We examined a sample of 405 heroin-abusing subjects and 304 controls from Sichuan Province, Southwest China. One hundred twenty-one of these cases and 154 controls were previously used in a study of the DRD4 VNTR [Li et al., 1997], and the remainder are newly ascertained. The two polymorphisms were in weak but detectable linkage disequilibrium (1, 418 chromosomes, P < 0.00001, D' = 0.17). When we compared the heroin-abuse group with controls, we found no significant difference between the patients and controls for either polymorphism in the DRD4 gene or their haplotypes. We were also unable to replicate our earlier association between "long" DRD4 alleles and heroin abuse. However, division of the sample by route of administration (nasal inhalers or injectors) produced a significant difference between inhalers and controls for the DRD4 VNTR (six-fold corrected P = 0. 018 by allele) but not for injectors of heroin. The association we observed between inhalers and the DRD4 polymorphism is difficult to interpret, although it is possible that the association is explained by different levels of novelty seeking between the two subgroups.

Administration, Inhalation↗
PubMed2000

Characterization of a calcium-regulation domain of the skeletal-muscle ryanodine receptor.

A negatively charged region of the N-terminal portion of the skeletal ryanodine receptor (RyR), located between residues 1872-1923, is involved in Ca (2+)-dependent regulation of the Ca(2+)-release channel. This region is divergent between the skeletal (RyR1) and cardiac (RyR2) isoforms of the channel, and is known as D3. Ca(2+) exerts important regulatory functions on the RyR, being involved in both activation and inactivation functions of the channel, i.e. the effects occurring at micromolar and millimolar Ca(2+) concentrations respectively. To characterize the role of D3 in the Ca(2+)-dependent regulation of the Ca(2+)-release channel, we studied the functional consequences of deleting the D3 region from RyR1 (DeltaD3-RyR1) using a heterologous expression system, [(3)H]ryanodine binding assays and single-channel recordings in lipid bilayers. Deletion of the D3 region selectively affected Ca(2+)-dependent regulation of RyR1, but did not alter [(3)H]ryanodine binding or the effect of other modulators on the RyR. Compared with full-length RyR1 (wt-RyR1), the Ca(2+)-dependence curve of DeltaD3-RyR1 is broader, reflecting increased sensitivity to Ca(2+) activation and decreased sensitivity to Ca(2+) inactivation. In addition, DeltaD3-RyR1 was more resistant to inhibition by Mg(2+). Comparison of the effect of caffeine on wt-RyR1 and DeltaD3-RyR1 suggested that D3 is an important region of RyR that participates in Ca(2+)-dependent activation and inactivation of the Ca(2+)-release channel.

Animals↗
PubMed2000

Quaternized trimethylaminated polystyrene-coated zirconia as a strong anion exchange material for HPLC.

The synthesis and characterization of a new, base-stable, strong anion exchange phase by amination of polystyrene-coated zirconia (PS-ZrO2) are described. Even though the ion exchange capacity of the quaternized trimethylaminated PSZrO2 (QTMA-PS-ZrO2) is only 0.07 mequiv/g, it is able to separate various inorganic anions, benzoic acid derivatives, and nucleotides in their deprotonated states. The effects of ionic strength, eluent pH, and counterion type are discussed. In the presence of both phosphate and fluoride ions in the eluent, band broadening caused by Lewis acid/base interactions between zirconia and analytes is greatly suppressed. The mixed retention modes (ion exchange, hydrophobic interaction, and Lewis acid/base interactions) on QTMA-PS-ZrO2 offer a different selectivity toward various anionic analytes than do other zirconia- and nonzirconia-based ion exchangers.

Antiporters↗
PubMed2000

NPAT links cyclin E-Cdk2 to the regulation of replication-dependent histone gene transcription.

In eukaryotic cells, histone gene expression is one of the major events that mark entry into S phase. While this process is tightly linked to cell cycle position, how it is regulated by the cell cycle machinery is not known. Here we show that NPAT, a substrate of the cyclin E-Cdk2 complex, is associated with human replication-dependent histone gene clusters on both chromosomes 1 and 6 in S phase. We demonstrate that NPAT activates histone gene transcription and that this activation is dependent on the promoter elements (SSCSs) previously proposed to mediate cell cycle-dependent transcription. Cyclin E is also associated with the histone gene loci, and cyclin E-Cdk2 stimulates the NPAT-mediated activation of histone gene transcription. Thus, our results both show that NPAT is involved in a key S phase event and provide a link between the cell cycle machinery and activation of histone gene transcription.

CDC2-CDC28 Kinases↗
PubMed2000

The high mobility group I/Y protein is hypophosphorylated in endoreduplicating maize endosperm cells and is involved in alleviating histone H1-mediated transcriptional repression.

During maize endosperm development, cells shift from a mitotic cycle to endoreduplication, driving the massive synthesis of storage proteins (zeins) and starch. In this developmental context, we studied changes in expression levels of histone H1 and high mobility group I/Y (HMG-I/Y), two chromatin architectural proteins that are known to affect gene transcription. Almost no change was found in the level of histone H1 during endosperm development, despite a dramatic increase in DNA content (endoreduplication); hence, the histone H1/DNA ratio decreased substantially. Concurrently with a reduction in the Cdc2 kinase activity at the shift to endoreduplication, significant changes were found in the level and mobility of the HMG-I/Y protein; the faster migrating forms were, at least partly, hypophosphorylated. Purified maize HMG-I/Y protein was found to be phophorylated in vitro by the Cdc2 kinase and bound efficiently to the gamma-zein promoter AT-rich tract (gammaZ-AT). Using an in vitro transcription assay, we demonstrated the capability of the maize HMG-I/Y protein to relieve the inhibitory effect exerted by histone H1 on templates containing the gammaZ-AT sequence. These data suggest that during maize endosperm development transcription and perhaps replication are controlled, at least partly, by the activity of the Cdc2 kinase and the interplay between histone H1 and HMG-I/Y proteins.

Base Sequence↗
PubMed2000

First-principles study of Li-intercalated carbon nanotube ropes

We studied Li-intercalated carbon nanotube ropes by first-principles methods. Results show charge transfer between Li and C and small structural deformation due to intercalation. Both the interior of the nanotube and the interstitial space are susceptible for intercalation. The Li intercalation potential of a single-walled nanotube rope is comparable to that of graphite and almost independent of the Li density up to around LiC2, as observed in recent experiments. This density is significantly higher than that of Li-intercalated graphite, making the nanorope a promising candidate for the anode material in battery applications.

Journal Article↗
PubMed2000

Smad7 and Smad6 differentially modulate transforming growth factor beta -induced inhibition of embryonic lung morphogenesis.

Transforming growth factors beta (TGF-beta) are known negative regulators of lung development, and excessive TGF-beta production has been noted in pulmonary hypoplasia associated with lung fibrosis. Inhibitory Smad7 was recently identified to antagonize TGF-beta family signaling by interfering with the activation of TGF-beta signal-transducing Smad complexes. To investigate whether Smad7 can regulate TGF-beta-induced inhibition of lung morphogenesis, ectopic overexpression of Smad7 was introduced into embryonic mouse lungs in culture using a recombinant adenovirus containing Smad7 cDNA. Although exogenous TGF-beta efficiently reduced epithelial lung branching morphogenesis in control virus-infected lung culture, TGF-beta-induced branching inhibition was abolished after epithelial transfer of the Smad7 gene into lungs in culture. Smad7 also prevented TGF-beta-mediated down-regulation of surfactant protein C gene expression, a marker of bronchial epithelial differentiation, in cultured embryonic lungs. Moreover, we found that Smad7 transgene expression blocked Smad2 phosphorylation induced by exogenous TGF-beta ligand in lung culture, indicating that Smad7 exerts its inhibitory effect on both lung growth and epithelial cell differentiation through modulation of TGF-beta pathway-restricted Smad activity. However, the above anti-TGF-beta signal transduction effects were not observed in cultured embryonic lungs with Smad6 adenoviral gene transfer, suggesting that Smad7 and Smad6 differentially regulate TGF-beta signaling in developing lungs. Our data therefore provide direct evidence that Smad7, but not Smad6, prevents TGF-beta-mediated inhibition of both lung branching morphogenesis and cytodifferentiation, establishing the mechanistic basis for Smad7 as a novel target to ameliorate aberrant TGF-beta signaling during lung development, injury, and repair.

Animals↗
PubMed2000

Spectral Response to Protonation of 4-(4-(4-(Didodecylamino)phenylazo)phenyl)butyric Acid in Its Langmuir-Blodgett Monolayer.

4-(4-(4-(Didodecylamino)phenylazo)phenyl)butyric acid is synthesized, and its Langmuir-Blodgett (LB) monolayer is successfully fabricated. The drastic changes in electronic spectra of this compound are found in acidic solution and in LB monolayer upon exposure to HCl vapor (mainly the decrease in absorption at 416 nm and great increase at 540 nm). The UV-visible and infrared spectra reveal a mechanism of protonation to either azo group or amino group. This phenomenon has been suggested to have its prospective application in fundamental interfacial materials for pH sensors. Copyright 2000 Academic Press.

Journal Article↗
PubMed2000

Cytosolic adaptor protein Dab2 is an intracellular ligand of endocytic receptor gp600/megalin.

gp600/megalin, an endocytic receptor, belongs to the low-density lipoprotein receptor family. It is most abundant in the renal proximal tubular cells, where it is implicated in the reabsorption of a number of molecules filtered through the glomerulus. The cytoplasmic tail (CT) of gp600/megalin contains a number of sequence similarities, which indicate that gp600/megalin might be involved in signal transduction. To find intracellular proteins that would interact with the gp600/megalin CT, a human kidney cDNA library was screened by using the yeast two-hybrid system. The phosphotyrosine interaction domain (PID) of the Disabled protein 2 (Dab2), a mammalian structural analogue of Drosophila Disabled, was found to bind to the gp600/megalin CT in this system. The interaction between these two proteins was confirmed by a binding assay in vitro and by the co-immunoprecipitation of both proteins from renal cell lysates. The gp600/megalin CT contains three PsiXNPXY motifs (in which Psi represents a hydrophobic residue) that are potentially able to interact with PID. Analysis of the CT deletion and point-mutation variants of gp600/megalin by the two-hybrid system revealed that the third PsiXNPXY motif is most probably involved in this interaction. Dab2 is a mitogen-responsive phosphoprotein thought to be an adaptor molecule involved in signal transduction, and a suggested negative regulator of cell growth. Dab2 is the first intracellular ligand identified for gp600/megalin; gp600/megalin is the first known transmembrane receptor that interacts with the cytosolic protein Dab2. We speculate that their interaction might involve gp600/megalin in signal transduction pathways or might mediate the intracellular trafficking of this receptor.

Adaptor Proteins, Signal Transducing↗