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Biomedical subjects

G Gong

Publications and source records attributed to G Gong.

At least 19 recordsLinked to original sources
PubMed2006

Channel catfish BAC-end sequences for marker development and assessment of syntenic conservation with other fish species.

In the present study, 25 195 BAC ends for channel catfish (Ictalurus punctatus) were sequenced, generating 20 366 clean BAC-end sequences (BES), with an average read length of 557 bp after trimming. A total of 11 414 601 bp were generated, representing approximately 1.2% of the catfish genome. Based on this survey, the catfish genome was found to be highly AT-rich, with 60.7% A+T and 39.3% G+C. Approximately 12% of the catfish genome consisted of dispersed repetitive elements, with the Tc1/mariner transposons making up the largest percentage by base pair (4.57%). Microsatellites were detected in 17.5% of BES. Catfish BACs were anchored to the zebrafish and Tetraodon genome sequences by BLASTN, generating 16% and 8.2% significant hits (E < e(-5)) respectively. A total of 1074 and 773 significant hits were unique to the zebrafish and Tetraodon genomes, respectively, of which 417 and 406, respectively, were identified as known genes in other species, providing a major genome resource for comparative genomic mapping.

Animals↗
PubMed2006

Cavernous haemangioma of the breast.

Vascular tumours of the breast are rare and most can be classified as either angiosarcomas or haemangiomas. Cavernous haemangiomas are the most common form of mammary haemangioma. We describe a case with unilateral whole breast involvement without associated calcifications, studied with mammography, ultrasound and MRI.

Adolescent↗
PubMed2004

Further evidence for paternal inheritance of mitochondrial DNA in the sheep (Ovis aries).

The mitochondrial DNA of 172 sheep from 48 families were typed by using PCR-RFLP, direct amplification of the repeated sequence domain and sequencing analysis. The mitochondrial DNA from three lambs in two half-sib families were found to show paternal inheritance. Our findings provide direct evidence of paternal inheritance of mitochondria DNA in sheep. A total of 12 highly polymorphic microsatellite markers, which mapped on different chromosomes, were employed to type the sheep population to confirm family relationships. Possible mechanisms of paternal inheritance are discussed.

Animals↗
PubMed2003

Differentiation of Caucasians and Chinese at bone mass candidate genes: implication for ethnic difference of bone mass.

Bone mineral density (BMD) is an important risk factor for osteoporosis and has strong genetic determination. While average BMD differs among major ethnic groups, several important candidate genes have been shown to underlie BMD variation within populations of the same ethnicity. To investigate whether important candidate genes may contribute to ethnic differences in BMD, we studied the degree of genetic differentiation among several important candidate genes between two major ethnic groups: Caucasians and Chinese. The genetic variability of these two populations (1131 randomly selected individuals) was studied at six restriction sites exhibiting polymorphisms of five important candidate genes for BMD: the BsaHI polymorphism of the calcium-sensing receptor (CASR) gene, the SacI polymorphism of the alpha2HS-glycoprotein (AHSG) gene, the PvuII and XbaI polymorphisms of the estrogen receptor alpha (ESR1) gene, the ApaI polymorphism of the vitamin D receptor (VDR) gene, and the BstBI polymorphism of the parathyroid hormone (PTH) gene. The two ethnic groups showed significant allelic and genotypic differentiation of all the polymorphisms studied. The mean FST was 0.103, which significantly differed from zero (P < 0.01). The Chinese population had lower mean heterozygosity (0.331) than the Caucasian one (0.444); the CASR-BsaHI and PTH-BstBI polymorphisms contributed most significantly to this difference. Analysis of the intra- and inter-population variability suggests that various types of natural selection may affect the observed patterns of variation at some loci. If some of the candidate genes we studied indeed underlie variation in BMD, their population differentiation revealed here between ethnic groups may contribute to understanding ethnic difference in BMD.

Asian People↗
PubMed2002

Association between bone mineral density and candidate genes in different ethnic populations and its implications.

The objectives of this study were (1). to identify the ethnic population in which bone mineral density (BMD) has been reported to be associated with polymorphisms of candidate genes in the literature; (2). to estimate the maximal distances between candidate genes and BMD-affecting loci, and (3). to explore the implications of phenotype-genotype association found in different ethnic populations. MEDLINE was searched for association between polymorphisms of candidate genes and BMD. The distances between marker and BMD-affecting loci were estimated with Lewontin's D'. Polymorphisms at 25 candidate loci have been reported to be associated with BMD. Eight of them are associated with BMD in both Caucasians and Asians, one with BMD in Caucasians with an allele frequency as high as 0.22, which is 0 in Asians, one with BMD in the three major ethnic populations (including Africans) and 15 with BMD in one ethnic population (not investigated in a second ethnic population yet). The maximal distance between BMD-affecting genes and marker loci was 230 (range 196-275) kb when an association is found in Caucasians and Asians. The association between vitamin D receptor gene polymorphisms and BMD is found in the three major ethnic populations, and the maximal marker-mutant distance is 79 (50-95) kb. It was concluded that most mutations affecting BMD are very old and are common in two or three major ethnic populations, which implies that these BMD-affecting loci are very close to, and are likely to be within, the candidate genes. Phenotype-genotype associations found in East Asians are unlikely to be due to admixture with Caucasians.

Asian People↗
PubMed2001

Requirement for tyrosine residues 315 and 319 within zeta chain-associated protein 70 for T cell development.

Engagement of the T cell antigen receptor (TCR) induces the transphosphorylation of the zeta chain-associated protein of 70,000 Mr (ZAP-70) protein tyrosine kinase (PTK) by the CD4/8 coreceptor associated Lck PTK. Phosphorylation of Tyr 493 within ZAP-70's activation loop results in the enzymatic activation of ZAP-70. Additional tyrosines (Tyrs) within ZAP-70 are phosphorylated that play both positive and negative regulatory roles in TCR function. Phosphorylation of Tyr residues (Tyrs 315 and 319) within the Interdomain B region of the ZAP-70 PTK plays important roles in the generation of second messengers after TCR engagement. Here, we demonstrate that phosphorylation of these two Tyr residues also play important roles in mediating the positive and negative selection of T cells in the thymus.

Animals↗
PubMed2001

Human hepatitis C virus NS5A protein alters intracellular calcium levels, induces oxidative stress, and activates STAT-3 and NF-kappa B.

The nonstructural protein 5A (NS5A) encoded by the human hepatitis C virus RNA genome is shown here to induce the activation of NF-kappaB and STAT-3 transcription factors from its cytoplasmic residence via oxidative stress. NS5A causes the disturbance of intracellular calcium. Ca2+ signaling triggers the elevation of reactive oxygen species in mitochondria, leading to the translocation of NF-kappaB and STAT-3 into the nucleus. Evidence is presented for the constitutive activation of STAT-3 by NS5A. In the presence of antioxidants [pyrrolidine dithiocarbamate (PDTC), N-acetyl l-cysteine (NAC)] or Ca2+ chelators (EGTA-AM, TMB-8), NS5A-induced activation of NF-kappaB and STAT-3 was eliminated. These results provide an insight into the mechanism by which NS5A can alter intracellular events relevant to liver pathogenesis associated with the viral infection.

Acetylcysteine↗
PubMed2001

High-energy phosphate metabolism and creatine kinase in failing hearts: a new porcine model.

BACKGROUND: This study aimed to create a pig model of heart failure secondary to severe aortic stenosis and to examine the relationship between the alterations in myocardial high-energy phosphate (HEP) metabolism and protein expression of creatine kinase (CK) isoforms. METHODS AND RESULTS: Sixteen pigs with left ventricular hypertrophy (LVH) secondary to ascending aortic banding and 10 normal pigs (N) were studied. Myocardial protein levels of CK isoforms (Western blot), HEP levels, and CK kinetics ((31)P MR spectroscopy) were measured under basal conditions. Nine of the 16 animals with LVH developed congestive heart failure (CHF), as evidenced by ascites (100 to 2000 mL). LV weight/body weight ratio (g/kg) was 2.18+/-0.15 in N hearts, 3.04+/-0.14 in hearts with LVH (P<0.01), and 4.23+/-0.36 in hearts with CHF (P<0.01 versus LVH). Right ventricle weight/body weight ratio and LV end-diastolic pressure were significantly higher in hearts with CHF (each P<0.01 versus N or LVH). Myocardial phosphocreatine/ATP ratios and the CK forward flux rates were decreased in LVH hearts, most severely in hearts with CHF. CK-M/beta-actin ratios were 2.21+/-12 (N), 1.69+/-0.15 (LVH), and 1.39+/-0.27 (CHF, P<0.05 versus N). CK-mitochondria (CK-Mt)/beta-actin ratios were 1.40+/-0.09 (N), 1.24+/-0.09 (LVH), and 1.02+/-0.08 (CHF, P<0.05 versus N or LVH). The severity of the reduction of CK flux rate was linearly related to the severity of the decrease of CK-Mt/beta-actin (r=0.68, P<0.01). CONCLUSIONS: In this new model of heart failure/hypertrophy, the abnormal myocardial HEP metabolism is related to the decreased CK-Mt protein level, which in turn is related to the severity of the hypertrophy.

Adenosine Triphosphate↗
PubMed2001

Growth inhibition and chemosensitivity of poorly differentiated human thyroid cancer cell line (NPA) transfected with p53 gene.

BACKGROUND: We investigated whether retroviral p53 transfection could enhance growth inhibition and chemosensitivity in a p53 mutant papillary thyroid cancer cell line (NPA). METHODS: NPA cells were transfected with either LXSN/p53 or mock infection in the presence of Adriamycin. Gene expression was confirmed by western blotting. Nude mice were injected subcutaneously with NPA cells after transfection with either LXSN/p53 or mock infection on opposite sides, and the tumor growth was compared. RESULTS: There was a dose-dependent inhibition of tumor growth with LXSN/p53 transfection. Tumor growth was inhibited more by p53 gene transfection relative to mock transfection in the presence of Adriamycin. CONCLUSION: These treatment modalities could be beneficial in the treatment of p53 mutant positive thyroid cancers.

Animals↗
PubMed2001

Bone biomechanical properties in prostaglandin EP1 and EP2 knockout mice.

Prostaglandins play an important role in regulating the bone adaptation response to mechanical stimuli. Prostaglandin E2 (PGE2) is an effective modulator of bone metabolism. Administration of PGE2 to rodents results in increased cancellous and cortical bone mass translating into enhanced mechanical strength. The PGE2 influence on bone is mediated through four well-characterized receptors (EP1, EP2, EP3, and EP4). Although the PGE2 pathways and mechanisms of action on cells involved in bone adaptation are still under investigation, it is now known that each receptor plays a unique role in regulating PGE2-related bone cell function. The EP1 subtype is coupled with Ca2+ mobilization. The EP2 subtype stimulates cyclic adenosine monophosphate (cAMP) formation. cAMP in turn is responsible for the early cellular signal that stimulates bone formation. This study compared physical and biomechanical properties of bone in EP1 and EP2 knockout mice to their corresponding wild-type controls. Ash weight was measured in the ulnae, and femurs and vertebral bodies were tested in three-point bending and compression, respectively. The results suggest: (a) EP1 receptors have a minimal influence on skeletal strength or size in mice; and (b) EP2 receptors have a major influence on the biomechanical properties of bone in mice. The absence of EP2 receptors resulted in weak bone biomechanical strength properties in the EP2 knockout model as compared with the corresponding wild-type control mice.

Animals↗
PubMed2001

Disruption of T cell signaling networks and development by Grb2 haploid insufficiency.

The developmental processes of positive and negative selection in the thymus shape the T cell antigen receptor (TCR) repertoire and require the integration of multiple signaling networks. These networks involve the efficient assembly of macromolecular complexes and are mediated by multimodular adaptor proteins that permit the functional integration of distinct signaling molecules. We show here that decreased expression of the adaptor protein Grb2 in Grb2+/- mice weakens TCR-induced c-Jun N-terminal kinase (JNK) and p38, but not extracellular signal-regulated kinase (ERK), activation. In turn, this selective effect decreases the ability of thymocytes to undergo negative, but not positive, selection. We also show that there are differences in the signaling thresholds of the three mitogen-activated protein kinase (MAPK) families. These differences may provide a mechanism by which quantitative differences in signal strength can alter the balance of downstream signaling pathways to induce the qualitatively distinct biological outcomes of proliferation, differentiation or apoptosis.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Myocardial creatine kinase kinetics and isoform expression in hearts with severe LV hypertrophy.

Left ventricular (LV) hypertrophy (LVH) results in a fetal shift in myocardial creatine kinase (CK) expression. Because CK plays an important role in intracellular energy production, transport, and utilization, this study was performed to characterize changes in CK expression and CK flux in severe pressure-overload LVH. Ascending aortic banding in 8-wk-old dogs resulted in LVH with a 92% increase in relative LV mass. In LVH hearts, CK-M isoform mRNA was decreased by 40% (P = 0.05) and protein was decreased by 50% (P < 0.01), whereas mitochondrial CK protein was decreased by 22% (P < 0.05). CK-B isoform mRNA was undetectable in normal hearts but was prominently expressed in LVH (P < 0.01); CK-B protein was increased by more than 10-fold in LVH (P < 0.01). Despite these changes, total CK activity was normal in LVH. Myocardial CK flux was examined using (31)P magnetic resonance spectroscopy magnetization transfer. The CK forward rate constant was similar in normal and LVH hearts at baseline and did not change in either group during dobutamine treatment. In hearts with LVH, the CK forward flux rate was reduced by approximately 60% (P < 0.05) and decreased further during dobutamine. Thus, although pressure-overload LVH caused alterations of expression of both CK mRNA and protein levels, LV performance and oxygen consumption in response to dobutamine were normal. However, myocardial free ADP was increased in LVH hearts. This finding suggests that the CK alterations result in a need for higher ADP levels to maintain ATP synthesis in the hypertrophied heart.

Animals↗
PubMed2001

Mitochondrial ATPase and high-energy phosphates in failing hearts.

This study examined high-energy phosphates (HEP) and mitochondrial ATPase protein expression in hearts in which myocardial infarction resulted in either compensated left ventricular remodeling (LVR) or congestive heart failure (CHF). The response of HEP (measured via (31)P magnetic resonance spectroscopy) to a modest increase in the cardiac work state produced by dobutamine-dopamine infusion and pacing (if needed) was examined in 17 pigs after left circumflex coronary artery ligation (9 with LVR and 8 with CHF) and compared with 7 normal pigs. In hearts with LVR, the baseline phosphocreatine (PCr)-to-ATP ratio decreased, and calculated ADP increased; these changes were most severe in hearts with CHF. HEP levels did not change in normal or LVR hearts during dobutamine-dopamine infusion. However, in hearts with CHF, the PCr-to-ATP ratio decreased further, and free ADP increased. The mitochondrial protein levels of the F(0)F(1)-ATPase subunits were normal in hearts with compensated LVR. However, in failing hearts, the alpha-subunit decreased by 36%, the beta-subunit decreased by 16%, the oligomycin sensitivity-conferring protein subunit decreased by 40%, and the initiation factor 1 subunit decreased by 41%. Thus in failing hearts, reductions in mitochondrial F(0)F(1)-ATPase protein expression are associated with increased myocardial free ADP.

Adenosine Diphosphate↗
PubMed2001

Effects of augmented delivery of pyruvate on myocardial high-energy phosphate metabolism at high workstate.

This study was performed to determine whether the fall in myocardial high-energy phosphates (HEP) that occurs during high workstates can be ascribed to either inadequate glycolytic pyruvate generation and conversion to acyl-CoA or limitation of long-chain fatty acid transport into the mitochondria. This was tested by using infusions of either pyruvate or butyrate in anesthetized dogs. Pyruvate was used because it bypasses the glycolytic sequence of reactions, activates pyruvate dehydrogenase, and increases mitochondrial NADH concentration ([NADH(m)]) in isolated myocardium, whereas butyrate enters the mitochondria without need for transport by the rate-limiting, palmitoyl-carnitine transporter. Increasing blood pyruvate from 0.16 +/- 0.016 mM to >3 mM did not alter baseline HEP levels determined with (31)P nuclear magnetic resonance, but caused an increase in the rate-pressure product and a modest increase in myocardial oxygen consumption (MVO(2)). Infusion of dobutamine + dopamine (each 20 microg x kg(-1) x min(-1) iv) increased MVO(2) and caused decreases of myocardial phosphocreatine (PCr)/ATP. Pyruvate partially reversed the decrease of HEP levels produced by catecholamine stimulation, whereas butyrate had no effect. Neither pyruvate nor butyrate caused an increase of MVO(2) during catecholamine infusion. Deoxymyoglobin was not detected by (1)H magnetic resonance spectroscopyy in any group. The data demonstrate that carbon substrate availability to the mitochondria is not the only cause of the reduction of PCr/ATP that occurs at high workstates. Supplemental pyruvate (but not butyrate) attenuated the reduction of PCr/ATP during the high workstates; this may have resulted from direct effects on intermediary metabolism or from other effects such as the free radical scavenging activity of pyruvate.

Adenosine Triphosphate↗
PubMed2001

Genetic changes in paired atypical and usual ductal hyperplasia of the breast by comparative genomic hybridization.

PURPOSE: Breast cancer is thought to develop from noninvasive precursor lesions, although the earliest steps of neoplastic transformation are still undefined. Usual ductal hyperplasia (UDH) is considered to represent a benign proliferation of ductal epithelial cells, whereas atypical ductal hyperplasia (ADH) may represent the first clonal neoplastic expansion of these cells. The aim of this study was to examine genetic alterations in UDH and ADH and to determine the relationship between these lesions in the same breast biopsy. EXPERIMENTAL DESIGN: Comparative genomic hybridization analysis was used to define copy number alterations in DNA extracted from archival sections of 18 patients. Nine patients showed ADH with adjacent UDH, and nine showed pure UDH. None showed evidence of invasive cancer or ductal carcinoma in situ. RESULTS: Five of the nine ADH lesions showed chromosome copy number alterations. 16q loss (five cases) and 17p loss (two cases) were the most frequent changes. The associated UDH lesions in these five patients also showed copy number alterations, always a subset of the changes present in the paired ADH. In one other patient, the UDH showed eight chromosomal alterations, whereas the paired ADH showed no changes. Only one of nine cases with pure UDH showed comparative genomic hybridization abnormalities. CONCLUSIONS: These data support the likelihood that UDH is a precursor of ADH, at least in some cases representing neoplastic growth. The frequencies of 16q and 17p losses suggest that alterations of candidate genes located in these chromosomal regions may play a role early in breast carcinogenesis.

Adult↗
PubMed2001

[Study on the detaining effect of hypocrelin a in the cancer cell using microspectrum].

Microspectra of mouse lymph cancer cells which one is cultured with HA and the other is cultured without HA have obtained in the range of 20,000-12,000 cm-1. The result shows tha two microspectra are quite different. This point out the cancer cell has changed because of HA. In the microspectrum of cancer cell cultured with HA, we have got the fluorescent peak of HA. This prompts HA has detained in the cancer cell. A new method which studies cells after being affected by drugs using microspectrum has also being developed.

Animals↗
PubMed2000

Coronary nitric oxide production in response to exercise and endothelium-dependent agonists.

BACKGROUND: Endothelium-derived nitric oxide (NO) contributes to epicardial coronary artery vasodilation during exercise. However, blockade of NO production does not impair the increase in coronary blood flow (CBF) during exercise, suggesting that NO is not obligatory for exercise-induced coronary resistance vessel dilation. In contrast, the increases in CBF produced by endothelium-dependent agonists are decreased after NO blockade. Consequently, this study was performed to determine whether the increase in coronary NO production in response to agonists is greater than that which occurs during exercise. METHODS AND RESULTS: We measured the oxidation products of NO (nitrate+nitrite=NO(x)) in aortic and coronary sinus plasma using chemiluminescence to assess NO(x) production across the coronary circulation in chronically instrumented dogs during a 3-stage treadmill exercise protocol and in response to intracoronary administration of the endothelium-dependent agonists acetylcholine (37.5 microg/min) and bradykinin (3.0 microg/min). No coronary NO(x) production could be detected at rest or during the first 2 stages of exercise; only at the highest level of exercise was a small increase in coronary NO(x) production measured. In contrast, coronary production of NO(x) was significantly increased in response to endothelium-dependent agonists. CONCLUSIONS: Coronary NO production in response to endothelium-dependent agonists is greater than in response to the increase in shear stress associated with exercise. These findings support previous studies suggesting that NO is not required for the coronary vasodilation that occurs in the normal heart during exercise.

Acetylcholine↗