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Biomedical subjects

G Hu

Publications and source records attributed to G Hu.

At least 181 records · Page 10Linked to original sources
PubMed1994

Evolutionary trail of the mitochondrial genome as based on human 16S rDNA pseudogenes.

In the course of studies on mutations in human mitochondrial (mt) DNA, we have uncovered and sequenced four new nuclear pseudogenes corresponding to bp 2457-2657 of the mt 16S rDNA. The four genes and their homologies with human mtDNA are E2 (62.4%), K10 (74.4%), E1 (84.6%) and LE6 (93.2%). When these five pseudogene sequences and another previously reported pseudogene sequence are compared with each other, they display what appears to be an ordered series of steps from a hypothetical common ancestor. The sequence of the hypothetical ancestor closely resembles that found in a wide variety of present-day mammalian mt genomes. The pseudogene sequences suggest an evolutionary trail of mt mutation dominated by base pair transitions punctuated by integration into the nuclear genome. Once integrated into the nuclear genome, the pseudogenes appear to follow the distinctive nuclear mutational pathway in which GC to AT transitions predominate and CpG sequences are preferentially eliminated.

Animals↗
PubMed1994

Expression and alternative splicing of the deleted in colorectal cancer (DCC) gene in normal and malignant tissues.

The DCC (deleted in colorectal cancer) gene was identified because it is affected by somatic mutations in colorectal tumors, including allelic losses in greater than 70% of cancers and localized mutations in a subset of cases. The DCC gene also may be inactivated in other tumor types, including cancers of the pancreas, stomach, breast, prostate, and brain, as well as some leukemias. We have characterized DCC complementary DNAs obtained from human fetal brain tissues and IMR32 human neuroblastoma cells. Based on the fetal brain complementary DNA sequence, the predicted transmembrane DCC protein product has 1447 amino acids. The extracellular domain of about 1100 amino acids has four immunoglobulin-like domains and six fibronectin type III-like domains; the 325-amino acid cytoplasmic domain does not show similarity to previously characterized proteins. Comparison of DCC complementary DNAs from IMR32 cells to those from fetal brain identified two potential alternative splice sites. Studies of adult mouse tissues revealed that DCC transcripts were present at very low levels in all tissues studied, and alternative splicing of DCC transcripts was seen in some tissues. Immunoblotting and immunoprecipitation studies with DCC-specific antisera identified protein species with molecular weights of approximately 175,000-190,000 in some rodent tissues and human tumor cell lines. DCC protein expression was highest in brain tissues and neural crest-derived cell lines and markedly reduced or absent in the majority of cancer cell lines studied. Treatment of DCC-expressing cells with tunicamycin decreased the apparent molecular weight of the immunoreactive proteins, establishing that DCC is a glycoprotein. The studies presented here demonstrate that the DCC gene encodes several related glycoprotein species that are likely to be expressed at very low levels in many normal adult tissues. Furthermore, the absence of DCC expression in some of the cancer cell lines studied may result from genetic inactivation of DCC.

3T3 Cells↗
PubMed1994

Clinical application of three-dimensional transesophageal echocardiography.

Three-dimensional transesophageal echocardiography is a new and evolving cardiac imaging technique. We reported our experiences of its clinical applications in 59 patients. A series of special temporal longitudinal views were selected by the frame grabber. Then the computer connected each digitized endocardial surface of the longitudinal views according to their spatial position and reconstructed the three-dimensional, cardiac shaded picture with gray scale. The three-dimensional transesophageal echocardiographic images were divided into three areas. The right area was right anterior to the esophagus and included such structures as the superior vena cava, right atrium, interatrial septum, and left atrium; the size, shape, and location of an atrial septal defect could be clearly shown. In the middle area the origin and the course of the two great arteries could be visualized, thus facilitating the diagnosis of transposition of the great arteries; in patients with obstruction of the right ventricular outflow tract, the circular ridgelike narrowing in the right ventricle was clearly visualized. In the left area the contour and size of the left ventricle and left atrium and the shape and point of coaptation of the mitral valve could be demonstrated; in patients with mitral valve prolapse, part of either leaflet protruded into the left atrium and appeared as a spoonlike depression in the mitral valve. Other entities subjected to three-dimensional transesophageal echocardiographic reconstruction included cor triatriatum, left atrial myxoma, aneurysm of sinus of Valsalva, dissecting aortic aneurysm, mitral stenosis, mitral regurgitation, and mitral valve prolapse.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Studies of the deleted in colorectal cancer gene in normal and neoplastic tissues.

Chromosome 18q is among the chromosomal regions thought to harbor a tumor suppressor gene(s) that is frequently inactivated during the development of several cancer types, particularly those of the gastrointestinal tract. Moreover, preliminary data suggest that colorectal cancers with 18q LOH have a more aggressive clinical behavior than those cancers without 18q LOH. A candidate tumor suppressor gene from 18q, termed DCC for deleted in colorectal cancer, has been identified. The DCC gene is contained within the common region of LOH on 18q, its expression is markedly decreased or absent in colorectal cancers and cell lines, and a subset of colorectal cancers have been shown to have somatic mutations within the DCC gene. Thus, DCC represents the most promising candidate tumor suppressor gene from 18q. At present, however, many questions remain regarding the mechanisms underlying the inactivation of DCC in the majority of colorectal cancers. In addition, although studies of 18q LOH and DCC gene expression in other cancer types suggest that DCC inactivation may contribute to the pathogenesis of other tumor types, few studies have provided definitive data to demonstrate that DCC inactivation is a critical genetic event in these tumors. Moreover, little is known about the function of DCC in the regulation of normal cell growth and tumor suppression. The predicted structural similarity of DCC to the N-CAM family of cell-surface proteins suggests that it may function through cell-cell and/or cell-extracellular matrix interactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

[The physiological function of plasma apoA-I--the anti-viral effects of apoA-I and its fragments].

Apolipoprotein A-I (apoA-I), the major protein of plasma high density lipoproteins, was found to inhibit herpes simplex virus type I (HSV-I) induced cell fusion at physiological concentrations (mumol/L). Plasma apoA-I from three different species was used to study the anti-viral effects by microneutralization test. Marked inhibition of virus-induced cell fusion was observed when the virus or the cells were pretreated with apoA-I, suggesting that apoA-I may have a direct effect on the virus and the cells. This function may be related to the structure of apoA-I.

Animals↗
PubMed1993

Osteogenic protein-1 regulates L1 and neural cell adhesion molecule gene expression in neural cells.

Osteogenic protein-1 (OP-1) is a member of the TGF-beta superfamily that is expressed in the nervous system. We recently showed that human recombinant osteogenic protein-1 (hOP-1) strongly promotes the aggregation of dividing neuroblastoma x glioma hybrid NG108-15 cells, in part by inducing the major isoforms of the neural cell adhesion molecule (N-CAM) (Perides, G., Safran, R. M., Rueger, D. C., and Charness, M. E. (1992) Proc. Natl. Acad. Sci. U. S. A. 89, 10326-10330). Here we show that hOP-1 induces L1 expression approximately 6-fold in NG108-15 cells without changing the levels of N-cadherin, neurofilament 200, Thy-1, tau, and G alpha s. OP-1 induction of L1 and N-CAM was unassociated with changes in cell proliferation and was not reproduced by cellular differentiation. The increased adhesiveness of hOP-1-treated NG108-15 cells could be inhibited in part by Fab fragments of an anti-L1 polyclonal antiserum. L1 and N-CAM expression first increased 12-18 h after hOP-1 treatment, reached a maximum after 2-3 days, persisted for up to 5 days, and returned to control levels 3 days after hOP-1 withdrawal. The increases in L1 and N-CAM protein levels were preceded or accompanied by large increases in the abundance of L1 and all detectable N-CAM mRNAs. Actinomycin D prevented the induction by hOP-1 of L1 and N-CAM mRNAs, suggesting that hOP-1 regulates immunoglobulin CAM gene transcription. OP-1 is the first described growth factor that regulates both N-CAM and L1 gene expression.

Bone Morphogenetic Protein 7↗
PubMed1993

Ethanol differentially increases alpha 2-adrenergic and muscarinic acetylcholine receptor gene expression in NG108-15 cells.

Modulation of alpha 2-adrenergic and opioid neurotransmission may contribute to ethanol intoxication, tolerance, and physical dependence. We showed previously that ethanol increased the expression of functional delta-opioid receptors in NG108-15 cells (Charness, M. E., Querimit, L. A., and Diamond, I. (1986) J. Biol. Chem. 261, 3164-3169). Here we report that long-term (2 days) treatment of NG108-15 cells with ethanol increased the binding of the alpha 2-adrenergic receptor (alpha 2AR) antagonist [3H]rauwolscine and the muscarinic acetylcholine receptor (mAChR) antagonist [3H]quinuclidinyl benzilate by 2.8- and 1.4-fold, respectively. Increased receptor expression was associated with a proportionate increase in the potency of oxymetazoline and carbachol in inhibiting cAMP accumulation. Ethanol did not change the expression of G alpha i2 and reduced levels of G alpha s. Pertussis toxin pretreatment did not prevent the ethanol-induced increase in alpha 2AR, mAChR, and delta-opioid receptor expression. Ethanol caused a large (3.6-fold), dose-dependent increase in the abundance of alpha 2BAR mRNA (rat cDNA probe RNG, 4.1-kb transcript). Ethanol-induced increases in alpha 2BAR and alpha 2CAR (rat probe RG10, 2.5-kb transcript) mRNAs were first detected after 6 h of exposure to 100 mM ethanol, became maximal after 24 h, and persisted for up to 5 days. In contrast, ethanol caused only a small (1.3-fold) increase in the abundance of hm4 mAChR mRNA and did not change levels of G alpha i2 and G alpha s mRNAs. Our data indicate that clinically attainable concentrations of ethanol regulate alpha 2AR gene expression within the time frame of a single session of drinking.

Animals↗
PubMed1993

DNA polymerase-catalyzed addition of nontemplated extra nucleotides to the 3' end of a DNA fragment.

Some prokaryotic and eukaryotic DNA polymerases are capable of adding an additional nontemplated nucleotide residue at the 3' end of a DNA fragment (Clark et al., 1987; Clark, 1988). The extra nucleotide at the 3' end of the PCR product has been shown to be a critical factor determining the efficiency of cloning PCR products into plasmids and can affect mutation analyses with a PCR-denaturing gradient gel electrophoresis (DGGE) approach (Pfeiffer and Hu, 1993). In the present work, the ability of various DNA polymerases to add an extra nontemplated nucleotide at the 3' end of DNA was studied. The results show that out of the eight studied enzymes, five can add, with varying efficiencies, an extra nucleotide residue at the 3' end of DNA. Which extra nucleotide is added depends on the terminal residue and the DNA polymerase. Among the enzymes, thermostable Pfu DNA polymerase is found to be the best choice for PCR due to its relatively high fidelity (Scott et al., 1991; Coller, unpublished), and ability to produce blunt-ended DNA fragments. The relationship between the DNA polymerases' ability to add an extra nucleotide and their 3'-->5' exonuclease activity is also discussed.

Bacterial Proteins↗
PubMed1993

Studies on antibiotic 230 as a molluscicide.

In the course of studying molluscicidal effects of microorganisms, a microorganism belonging to Streptomycetaceae, Streptomyces griseolus (Strain 230) was isolated from soil and a certain microbial ingredient proved to have a molluscicidal activity. The effective substance was named antibiotic 230. As a result of several investigations on the antibiotic, the following chemical features were made clear. The chemical substance was an indol-carbazole-heterocyclic compound, the molecular weight 446 and the molecular formula C28H26N4O3. The antibiotic demonstrated a molluscicidal effect against Oncomelania snails and their eggs both in the laboratory and in the field. The compound had a wide bacteriostasis spectrum and a slight toxicity to fish in addition to the above, but it was non-toxic to plants.

Animals↗
PubMed1993

Ethanol increases delta-opioid receptor gene expression in neuronal cell lines.

Long-term treatment with ethanol increases delta-opioid receptor (DOR) expression in the NG108-15 neuroblastoma x glioma hybrid cell line. To determine the underlying mechanism, we studied the effects of ethanol on [3H]diprenorphine binding to intact cells and DOR gene expression in four related clonal neural cell lines. Incubation with 200 mM ethanol for 48 hr increased [3H]diprenorphine binding by 1.4- (N18TG2), 1.8- (NG108-15), 1.9- (N4TG1), and 3.0-fold (N1E-115). Treatment with 25, 50, or 100 mM ethanol for 1 week caused a dose-dependent increase in receptor expression. Receptor up-regulation was associated with an increase in the potency of etorphine for inhibiting prostaglandin E1-stimulated cAMP accumulation. Constitutive DOR expression differed more than 3-fold among the different cell lines and correlated positively with basal cAMP levels. Long-term ethanol treatment increased basal cAMP levels in three of the four cell lines, but did not induce cellular differentiation. Northern blot analysis demonstrated an identical pattern of multiple transcripts in the four cell lines. Ethanol increased the abundance of DOR mRNA by approximately 3-fold in N18TG2 cells and by approximately 5-fold in the remaining cell lines. These findings indicate that clinically relevant concentrations of ethanol regulate DOR expression by increasing the abundance of DOR mRNA. The disparity between the increase in gene expression and ligand binding suggests that ethanol may also modify mRNA translation or receptor processing.

Animals↗
PubMed1993

A study on the clinical effect and immunological mechanism in the treatment of Hashimoto's thyroiditis by moxibustion.

71 cases of Hashimoto's thyroiditis were treated by moxibustion and their immune function and thyroid function were observed. It was found that moxibustion was able to reduce the thyroid antibodies in the peripheral blood of the patients with hypothyroidism and to recover their thyroid function. It was also found that moxibustion could lower the thyroid antibody secretory levels and ADCC (antibody-dependent cell-mediated cytotoxicity) activities of the lymphocytes. In addition, the action of moxibustion in reducing the secretion of thyroid antibodies was related to its action of regulating the proportions of T lymphocyte subsets. The results indicate that the treatment of Hashimoto's thyroiditis by moxibustion is probably accomplished through its effect in regulating the relationship among the T lymphocyte subsets.

Adult↗
PubMed1992

Polymorphism at codon 72 of the p53 gene in human acute myelogenous leukemia.

A common polymorphism at codon 72 of the p53 gene in patients with acute myelogenous leukemia (AML) was analyzed by single-strand conformation polymorphism assay and sodium dodecyl sulfate polyacrylamide-gel electrophoresis of immunoprecipitated 35S-labeled P53 protein. No association between this polymorphism and a marked predisposition to AML was found. The half-lives of these two polymorphic forms of P53 were equivalent in normal phytohemagglutinin-stimulated lymphocytes, while the P53 Pro72 isoform was found to be twice as stable as the Arg72 isoform in Daudi cells.

Base Sequence↗
PubMed1992

Lack of effects of selenium on N-nitrosomethylbenzylamine-induced tumorigenesis, DNA methylation, and oncogene expression in rats and mice.

The effects of dietary selenium deficiency and excess on N-nitrosomethylbenzylamine-(NMBA) induced esophageal neoplasia in rats and forestomach tumors in mice and the effects of dietary selenium on DNA adduct formation and on the activities of DNA adduct-repairing enzyme and oncogene expression in rat esophagus were investigated. The esophageal and forestomach tumors were induced by administration of NMBA by gavage with a total dose of 39 mg/kg body wt in rats and 12 mg/kg body wt in mice. Neither selenium dietary deficiency (Se < 0.02 ppm) nor selenium excess (2.0 ppm) showed any significant effect on the incidence of tumors or number of tumors per tumor-bearing animal. For the DNA adduct formation studies, rats were given a dose of NMBA intraperitoneally after six weeks on the different selenium-containing diets. No significant difference in the amount of the DNA adduct O6-methyldeoxyguanosine was found among the different selenium-treated groups. In a parallel group of rats that did not receive NMBA, the levels of esophageal O6-methyldeoxyguanosine DNA methyltransferase were not significantly altered by dietary selenium levels. The c-myc oncogene expression in rat esophagus was induced by the administration of NMBA (3 mg/kg body wt) by gavage once a week for eight weeks. Dietary selenium did not show any effects on its expression. On the basis of the results of these studies, dietary selenium has no effects in the NMBA-induced tumor model.

Animals↗
PubMed1992

P53 gene mutations in acute myelogenous leukaemia.

A polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) assay was used to identify the exons which contained point mutations in the conserved regions (exons 4-8) of the p53 gene in 49 acute myelogenous leukaemia (AML) patients. SSCP analysis in our study was consistent with the results of subsequent direct DNA sequencing in detecting point mutational change in exons 5 and 8 of one AML patient and in exons 7 and 8 of two additional AML patients. The mutations were located at codons 245 and 273, which have been found in many other tumours, and codons 178 and 290, which have not been reported previously. All of the p53 proteins in which we detected point mutations were immunoprecipitated by the p53 monoclonal antibody PAb 240, which has been shown to recognize a mutant conformation of p53 protein. Thus, our results indicate that functional inactivation of the p53 gene by point mutational change might be one of the mechanisms underlying disease progression of AML.

Base Sequence↗
PubMed1992

The production of hybridoma cell line secreting monoclonal antibodies against Xanthomonas campestris pv. oryzae and its application in the classification of strains.

By the fusion of mouse myeloma cells (SP2/0-Ag14) and spleen cells derived from BALB/c mice immunized with the preparation of Xanthomonas campestris pv. oryzae Ks-6-6, Os-213, Yz-32 and Yz-24, we obtained 12 hybridoma cell lines secreting monoclonal antibodies. None of the McAbs cross-reacted with the other varieties of plant pathogenetic and non-pathogenetic bacteria. The McAbs could distinguish three variant serotypes of strains. Antibody titers of ascites were about 1:10(3)-1:10(6) when measured by ELISA method. The McAbs could differentiate 6 epitopes. Based on the epitopes, the 63 strains of X. campestris pv. oryzae we collected were grouped into nine groups.

Animals↗