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Biomedical subjects

Z Tang

Publications and source records attributed to Z Tang.

At least 19 recordsLinked to original sources
PubMed2003

Lack of association of the plasminogen activator inhibitor-1 4G/5G promoter polymorphism with cardiovascular disease in the elderly.

Elevated circulating plasminogen activator inhibitor-1 (PAI-1) may increase risk of cardiovascular disease (CVD). The 4G allele of the 4G/5G PAI-1 promoter polymorphism is associated with higher levels of PAI-1. We examined the association of PAI-1 4G/5G genotype and CVD events in the elderly participants of the Cardiovascular Health Study (CHS). We measured 4G/5G genotype in a nested case-control study within the CHS. Cases included incident angina, myocardial infarction (MI), and stroke. 4G/5G genotype was not found to be associated with markers of fibrinolysis or CVD risk in the selected elderly cohort. There were no differences in genotype frequencies by case-control status (5G/5G frequency 16-22%; chi2P= 0.07). The 5G allele was not associated with incident CVD events when individuals with at least one 5G allele were compared to 4G/4G homozygotes. The presence of at least one 4G allele was likewise not associated with incident CVD when those with 4G/4G and 4G/5G genotypes were compared to 5G/5G homozygotes. Our results suggest that the PAI-1 4G/5G promoter polymorphism is not associated CVD risk factors or incident CVD events in the elderly.

Aged↗
PubMed2003

Response of Schwann cells in the inferior alveolar nerve to distraction osteogenesis: an ultrastructural and immunohistochemical study.

The biological mechanisms of nerve adaptation to distraction osteogenesis have not yet been elucidated. This study observed response of Schwann cells in the inferior alveolar nerve (IAN) following mandibular lengthening by electron microscopy and immunohistochemistry of S-100 protein, a specific marker of Schwann cells. Unilateral mandibular distraction (10mm elongation) was performed in nine young adult goats. Three animals were sacrificed at 7, 14 and 28 days after completion of distraction, respectively. The distracted IAN specimens and control nerves (from the contralateral sides) were harvested and processed for histological, ultrastructural and immunohistochemical examinations. Wallerian degeneration was observed in the distracted IAN, and Signs of axonal regeneration, as well as many activated Schwann cells were seen in the lengthened nerves. The expression of S-100 protein increased significantly at early stage of distraction osteogenesis, but almost returned to the normal level at 28 days after distraction. This study suggests that Wallerian degeneration caused by mechanical stretching may stimulate Schwann cells to enter a proliferated and activated state. Schwann cells and S-100 protein appear to play crucial roles in axonal regeneration that contributes to nerve adaptation to gradual distraction. Therefore, the IAN injury caused by mandibular gradual distraction was not serious; it seems to recover totally through a complicated repair mechanism.

Adaptation, Biological↗
PubMed2002

Heart and breast muscle mitochondrial dysfunction in pulmonary hypertension syndrome in broilers (Gallus domesticus).

This study was conducted to determine function and defects in electron transport in muscle mitochondria of meat chickens (broilers) with pulmonary hypertension syndrome (PHS). The respiratory control ratio (RCR, indicative of respiratory chain coupling) was higher in the control than in PHS breast and heart muscle mitochondria, but there were no differences in the ADP/O (an index of oxidative phosphorylation). Sequential additions of ADP improved the RCR in the control breast muscle mitochondria and the ADP/O in PHS breast and heart muscle mitochondria. Basal hydrogen peroxide production, (an indicator of electron leak), was higher in PHS breast and heart muscle mitochondria than in controls and differences in electron leak in PHS mitochondria were magnified by inhibiting electron transport at Complex I and III (cyt b(562)). Complex I activity was lower in PHS heart mitochondria but there was no difference in Complex II activity. Thus, compared to controls, PHS mitochondria exhibited site-specific defects in electron transport within Complex I and III that could contribute to lower respiratory chain coupling. Additionally, it appears that healthy broilers may exhibit higher basal levels of electron leak compared to other avian species. Together, these findings provide insight into inefficient cellular use of oxygen that may contribute to the development of PHS in broilers.

Animals↗
PubMed2001

Neuroprotection mediated by glutamate carboxypeptidase II (NAALADase) inhibition requires TGF-beta.

Inhibition of glutamate carboxypeptidase (GCP) II (EC 3.4.17.21), also termed N-acetylated alpha-linked acidic dipeptidase (NAALADase), has been shown to protect against ischemic injury presumably via decreasing glutamate and increasing N-acetyl-aspartyl-glutamate (NAAG). NAAG is a potent and selective mGlu3 receptor agonist. Activation of glial mGlu3 receptors has been shown to protect against NMDA toxicity by releasing transforming growth factors, TGF-betas. We hypothesized that GCP II inhibition could be neuroprotective also via TGF-betas, due to increased NAAG. To verify this, Enzyme-Linked Immunosorbent Assays (ELISAs) were performed on media from both control and ischemic cultures treated with the GCP II inhibitor, 2-(phosphonomethyl)-pentanedioic acid (2-PMPA). We found that 2-PMPA attenuated ischemia-induced declines in TGF-beta. To further assess the role of TGF-betas in 2-PMPA-mediated neuroprotection, a neutralizing antibody to TGF-beta (TGF-beta Ab) was used. In both in vitro and in vivo models of cerebral ischemia, TGF-beta Ab reversed the neuroprotection by 2-PMPA. Antibodies to other growth factors had no effect. Data suggests that neuroprotection by GCP II inhibition may be partially mediated by promoting TGF-beta release.

Animals↗
PubMed2001

Fermi surface of nanocrystalline embedded particles in materials: bcc Cu in Fe.

We report that a positron can act as a probe to directly reveal electronic structures of nanocrystalline embedded particles in materials. The Fermi surface (FS) of "bcc" Cu nanoparticles in an Fe matrix is observed as the first example. A two-dimensional angular correlation of the positron annihilation radiation (2D-ACAR) method is used to measure the momentum distribution which reflects the FS topology. The obtained 2D-ACAR spectra show strong and characteristic anisotropy associated with the necks of the FS around the [110] Brillouin zone boundaries of the bcc Cu, which are well reproduced by full-potential linearized argumented plane-wave calculations.

Journal Article↗
PubMed2001

Identification of a novel activation domain in the Notch-responsive transcription factor CSL.

CSL is the primary target of the Notch signaling pathway in mammalian cells. It is a DNA binding protein that generally represses transcription in the absence of Notch signaling and activates transcription upon formation of a ternary complex with NICD, the protease-generated intracellular domain of NOTCH: Previous mapping experiments identified the central third of CSL as both necessary and sufficient for DNA binding and activation by NOTCH: Here we show that CSL promotes transcription in 293T cells in the absence of added NICD and that this activity requires both the central domain plus the C-terminal third of the protein. Evidence is presented that argues against a contribution of endogenous NICD and instead supports the possibility that distinct coactivators may directly stimulate the activity of CSL in a cell type-specific manner. This conclusion supports a recent finding that Drosophila CSL (Suppressor of Hairless) can also mediate transcriptional activation in the absence of NOTCH:

3T3 Cells↗
PubMed2001

[Expression rates of three angiogenic factors in hepatocellular carcinoma and their relation with microvessel density and portal vein tumor thrombosis].

OBJECTIVE: To investigate the expression rates of the three angiogenic factors-basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), and platelet-derived endothelial cell growth factor (PD-ECGF) in hepatocellular carcinoma (HCC) and to investigate the relation of their expression rates to the microvessel density (MVD) of the tumor and to the formation of portal vein tumor thrombus (PVTT). METHODS: Immunohistochemical staining was conducted on 61specimens of hepatic cell carcinoma removed in operation. RESULTS: The expression rates of dFGF, VEGF, and PD-ECGF in HCC tissue were 45.9%, 75.4% and 70.5% respectively. The incidence rates of PVTT while all of the 3 angiogenic factor were negatively expressed, one of them was positively expressed, two of them were positively expressed, and all of them were positively expressed were 16.7%, 25.0%, 54.2% and 63.2% respectively (P < 0.05, test for trend). The MVD counts in HCC tissue in the above-mentioned four conditions were 99 +/- 56, 113 +/- 27, 140 +/- 347 and 194 +/- 52 respectively (P < 0.001, ANOVA test). CONCLUSION: As the number of positively expressed angiogenic factors in HCC tissue increases, the angiogenic capability of the tumor enhances greatly, and the incidence rate of PVTT increases too.

Adult↗
PubMed2001

Craniosynostosis and related limb anomalies.

Many genetically determined craniosynostosis syndromes feature limb anomalies, implying that pathways of cranial suture and limb morphogenesis share some identical components. Identification of heterozygous mutations in FGFR1, FGFR2, FGFR3, TWIST and MSX2 in craniosynostosis has focused particular attention on these genes. Here we explore two themes: use of clinical/molecular analysis to provide new clues to pathophysiology and the contrasting effects of loss- and gain-of-function mutations. Apert syndrome is a severe craniosynostosis/syndactyly disorder usually caused by specific substitutions (Ser252Trp or Pro253Arg) in FGFR2. The relative severity of cranial and limb malformations varies in opposite directions for the two mutations, suggesting that these phenotypes arise by different mechanisms. Clinical and biochemical evidence supports a model in which alternative splice forms of FGFR2 mediate these distinct effects. Pro-->Arg substitutions equivalent the Pro253Arg/FGFR2 mutation occur in both FGFR1 and FGFR3, and are also associated with craniosynostosis. This suggests a common pathological mechanism, whereby enhanced affinity for a limited repertoire of tissue-specific ligand(s) excessively prolongs signalling in the cranial suture. The first MSX2 mutation in craniosynostosis was described in 1993 but this remains the only example. We have recently identified three MSX2 mutations associated with a different cranial phenotype, parietal foramina. DNA binding studies show that the craniosynostosis and parietal foramina arise from gain and loss of function, respectively.

Acrocephalosyndactylia↗
PubMed2001

Formation of binary alloy cluster ions from group-14 elements and cobalt and comparison with solid-state alloys.

By using laser ablation on mixtures of transition metal cobalt and group-14 elements, binary alloy cluster anions were produced while no binary alloy cluster cations were detected, and the homocluster cations of group-14 elements appeared at very low abundance. The differences between clustering abilities of germanium, tin and lead with cobalt are described, and the chemical bonds in the binary alloy cluster anions appear to indicate a transition from covalent to metal bonds. The cluster anion [CoPb10](-) appears in very high abundance (magic number), and an endohedral structure is proposed for this cluster. The cluster anion [CoPb12](-), also representing a magic number, probably has an icosahedral structure. Compared with solid-state Co/Ge binary alloys, the compositions of most binary alloy cluster anions are germanium-rich, in which the covalent bonds are predominant.

Journal Article↗
PubMed2001

BCL-1 rearrangement in acute lymphocytic leukemia and its clinical significance.

BCL-1 rearrangement (BCL-1/IgH gene rearrangement) in acute lymphocytic leukemia and its clinical significance was investigated. In 38 patients with acute lymphocytic leukemia (ALL), the genomic DNA of mononuclear cells isolated from peripheral blood and bone marrow was amplified by using hemi-nested polymerase chain reaction (PCR) technique and the expression of cyclin D1 protein of mononuclear cells was detected by using immunohistochemical method. Ten patients with acute granulocytic leukemia, 2 with chronic granulocytic leukemia and 10 with normal bone marrow served as control group. The results showed that BCL-1 rearrangement was detectable in 3 of 38 ALL patients (7.9%) and cyclin D1 protein positive expression was detected in 4 ALL patients (10.5%). Three ALL patients with BCL-1 rearrangement were all B-cell leukemia (B-ALL) and accompanied by cyclin D1 protein expression. No BCL-1/IgH rearrangement or cyclin D1 protein expression was detected in 12 patients with granulocytic leukemia and 10 cases of normal bone marrow. Leukocyte counts in peripheral blood of B-ALL patients with BCL-1 rearrangement and (or) cyclin D1 protein expression were significantly increased and the patients had bad reaction to chemotherapy. It was concluded that: 1) BCL-1/IgH gene rearrangement were detected in acute B lymphocytic leukemia; 2) B-ALL patients with BCL-1 rearrangement and (or) cyclin D1 protein expression had poor prognosis.

Adolescent↗
PubMed2001

Mutation and overexpression of the beta-catenin gene may play an important role in primary hepatocellular carcinoma among Chinese people.

AIM: To study the role of beta-catenin gene mutation and expression in hepatocellular carcinogenesis. METHOD: Thirty-four hepatocellular carcinoma (HCC) specimens and adjacent para-cancerous tissues, and four normal liver tissues were analyzed. Subcellular distribution of beta-catenin was examined by immunohistochemistry staining. Mutation and semiquantitative expression of beta-catenin gene exon 3 mRNA were detected by RT-PCR-SSCP and in situ hybridization. RESULT: Immunohistochemistry showed that all normal liver tissues and para-cancerous tissues examined showed membranous-type staining for beta-catenin protein, frequently with weak expression in the cytoplasm, but no beta-catenin accumulation in nuclei was found; while in liver cancer, 21 cases (61.8%) of HCC examined showed accumulated type in cytoplasms or nuclei. On SSCP, 15 cases (44.1%) of HCC altogether displayed three kinds of characteristic mutational mobility shifts. No abnormal shifting bands were found in tissues from normal liver or para-cancerous area. The beta-catenin gene exon 3 mRNA expression index of 34 HCCs was higher than that of para-cancerous tissue and normal liver tissue. Using in situ hybridization, the signal corresponding to beta-catenin gene exon 3 mRNA was particularly strong in cytoplasm of HCC when compared with those of paracancerous tissues and normal liver tissues. CONCLUSION: beta-catenin gene mutation and overexpression may have a critical role in malignant progression of hepatic carcinogenesis among Chinese people.

Carcinoma, Hepatocellular↗
PubMed2001

Metabolism and functions of highly unsaturated fatty acids: an update.

This review briefly examines the recent progress in knowledge about the synthesis and degradation of highly unsaturated fatty acids (HUFA) and their functions. Following the cloning of mammalian Delta6-desaturase (D6D), the D6D mRNA was found in many tissues, including adult brain, maternal organs, and fetal tissue, suggesting an active synthesis of HUFA in these tissues. The cloning also confirmed the long-postulated hypothesis that the same pathway is followed in n-6 and n-3 HUFA synthesis. Dietary n-6 and n-3 HUFA both induce fatty acid oxidation enzymes in peroxisomes when compared to their respective precursor polyunsaturated fatty acids. This suggests that peroxisomes may be the primary site of HUFA degradation when HUFA are supplied in excess from the diet. Peroxisome proliferators strongly induce the enzymes for the HUFA synthesis. The mechanism of this induction is currently unknown. Recent studies revealed new HUFA functions that are not mediated by eicosanoids. These functions include endocytosis/exocytosis, ion-channel modulation, DNA polymerase inhibition, and regulation of gene expression. These new discoveries will enable us to re-examine the underlying mechanisms for the classical symptoms of essential fatty acid deficiency as well as vitamin E deficiency. Progress has also been made in understanding the mechanism by which dietary HUFA reduce body fat deposition. One mechanism is induction of genes for fatty acid oxidation, which is mediated by peroxisome proliferator-activated receptor-alpha. Another likely mechanism is that HUFA suppress genes for fatty acid synthesis by reducing both mRNA and protein maturation of sterol regulatory element binding protein-1.

Animals↗
PubMed2001

Murine homologs of deltex define a novel gene family involved in vertebrate Notch signaling and neurogenesis.

Notch signaling plays an important role in cell-fate specification in multicellular organisms by regulating cell-cell communication. The Drosophila deltex gene encodes a modulator of the Notch pathway that has been shown to interact physically with the Ankyrin repeats of Notch. We isolated four distinct cDNAs corresponding to mouse homologs of deltex - mouse Deltex1 (MDTX1), mouse Deltex2 (MDTX2), mouse Deltex2DeltaE (MDTX2DeltaE), and mouse Deltex3 (MDTX3). Deduced amino acid sequences of these four cDNAs showed a high degree of similarity to Drosophila Deltex and its human homolog, DTX1 throughout their lengths, even though they possess distinct structural features. MDTX proteins formed homotypic and heterotypic multimers. We found that these genes were expressed in the central, peripheral nervous system and in the thymus, overlapping with those of mouse Notch1. In mammalian tissue culture cells, overexpression of any of the four mouse deltex homologs suppressed the transcriptional activity of E47, a basic helix-loop-helix (bHLH) protein, in a manner similar to suppression by an activated form of human Notch1 or human DTX1. In addition, overexpression of MDTX2 and MDTX2DeltaE in C2C12 cells under differentiation-inducing conditions suppressed the expression of myogenin, one of the myogenic transcriptional factors; this was also similar to a previously reported activity of constitutively activated Notch. Furthermore, misexpression of any of the MDTX genes in Xenopus embryos resulted in an expansion of the region expressing the neural cell adhesion molecule (N-CAM) gene, a marker for the neuroepithelium. Collectively, our results suggest that these mouse deltex homologs are involved in vertebrate Notch signaling and regulation of neurogenesis.

Amino Acid Sequence↗
PubMed2001

Synthesis and biodistribution of a new 99mTc nitrido complex for brain imaging.

Bis(N-isobutyl-dithiocarbamato) nitrido technetium-99m complex [99mTcN(IBDTC)2] (IBDTC: N-isobutyl dithiocarbamato) was synthesized by the reduction of 99mTcO4- into [99mTc = N]2+ with stannous chloride in the presence of succinic dihydrazide and propylenediamine tetraacetic acid, followed by the addition of sodium N-isobutyl dithiocarbamate dihydrate. The radiochemical purity of the complex was over 90% as measured by thin layer chromatography. It was stable over 6h at room temperature. Its partition coefficient indicated that it is a good lipophilic complex. Biodistribution in mice demonstrated that the complex accumulated in the brain with high uptake and good retention. The brain uptake (ID%/g) was 6.22, 5.45 and 3.88 and the brain/blood ratio was 1.51, 2.24, 1.84 at 5, 30 and 60 min post-injection, respectively. These results suggest potential usefulness of the complex as a brain perfusion imaging agent.

Animals↗
PubMed2001

Mad2-Independent inhibition of APCCdc20 by the mitotic checkpoint protein BubR1.

The mitotic checkpoint blocks the activation of the anaphase-promoting complex (APC) until all sister chromatids have achieved bipolar attachment to the spindle. A checkpoint complex containing BubR1 and Bub3 has been purified from mitotic human cells. Upon checkpoint activation, the BubR1-Bub3 complex interacts with Cdc20. In the absence of Mad2, BubR1 inhibits the activity of APC by blocking the binding of Cdc20 to APC. Surprisingly, the kinase activity of BubR1 is not required for the inhibition of APCCdc20. BubR1 also prevents the activation of APCCdc20 in Xenopus egg extracts, and restores the mitotic arrest in Cdc20-overexpressing cells treated with nocodazole. Because BubR1 also interacts with the mitotic motor CENP-E, the ability of BubR1 to inhibit APC may be regulated by kinetochore tension or occupancy.

Animals↗
PubMed2001

Comparison of blood counts in venous, fingertip and arterial blood and their measurement variation.

We compared routine blood pictures in venous, fingertip and arterial blood and their measurement variation. A pair of venous and fingertip blood samples were simultaneously collected from 24 volunteers, and another pair of venous and arterial samples from another 12 volunteers. The volunteers were healthy adults, aged 20-22 years, with males and females in equal numbers. Three aliquots of blood were taken from each person for three measurements of blood counts, including haemoglobin concentration and haematocrit, using an automatic haematology analyser. Compared to arterial blood, there was a significant increase of erythrocyte count (2.7%) and haematocrit (3.1%) in the venous blood. The total and large leucocyte counts were significantly higher (9.2% and 12.6%, respectively) in the fingertip blood than in the venous blood. There were a decreasing number of leucocytes in the fingertip blood with repeated sampling. The intermeasurement variation for total leucocyte or haemoglobin measurement was significantly larger as measured with the fingertip blood or arterial blood than with the venous blood. The intermeasurement coefficients of variation of haemoglobin (1.3%) and small leucocyte ratio or platelet (approximately 4.0%) measurements with venous and arterial blood were the smallest and largest, respectively. Volume of arterial plasma was diminished by 2-3% after microcirculation. Elevation of total leucocyte count in the fingertip blood was mainly due to the increase of granulocytes. Measurement with venous blood was of better precision than with fingertip or arterial blood.

Adult↗