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Biomedical subjects

Q Xiao

Publications and source records attributed to Q Xiao.

At least 55 records · Page 3Linked to original sources
PubMed1998

Human placenta and fetal membranes contain peptide YY1-36 and peptide YY3-36.

Extracts of human term amniotic, placental, and chorion/decidua tissue contained, respectively, 4.36 +/- 2.79 (pmol/g wet wt; mean +/- S.E.M.: n = 5). 2.78 +/- 0.5 (n = 5) and 0.68 +/- 0.68 (n = 5) peptide YY (PYY)-like immunoreactivity. Using a specific PYY antiserum, gel filtration chromatography and reverse-phase high performance liquid chromatography (HLPC), amniotic, placental and fetal intestinal tissue extracts were demonstrated to contain PYY-like immunoreactivity consisting of equal amounts of PYY1-36 and PYY3-36. The presence of pancreatic polypeptide was not detected in any of the extracts. Positive immunohistochemical staining for PYY was seen in extravillous trophoblasts in the decidual septa and fetal membranes, the syncytiotrophoblast and cytotrophoblasts, amniotic epithelial cells and in maternal decidual stromal cells. Positive staining for PYY was found at the earliest date examined (9.5 weeks) and remained present throughout pregnancy to term. PYY1-36 and PYY3-36 may play important roles in human pregnancy, acting via endocrine or paracrine mechanisms.

Amnion↗
PubMed1998

[Development of the LCY-3E intelligent intracranial pressure monitor].

The LCY-3E intelligent intracranial pressure (ICP) monitor uses a microcomputer system for measurement and control. The ICP is transmitted by an air capsule, and detected by an universal high precision transducer. The problem of zero point drift during continuous ICP measurement was successfully solved and the electric safety of the instrument was greatly improved.

Aerospace Medicine↗
PubMed1998

[A clinical study on reducing immunologic rejection in combining corneal lamellar autografting with allografting].

OBJECTIVE: To reduce the rate of immunologic rejection, corneal lamellar autografting with allografting were combined, making immune cells less attack on allograft. METHODS: The pterygium having encroached upon the pupillary area was removed surgically, and the combination of autograft with allograft was transplanted on the peripheral and central cornea in 23 cases (24 eyes). The control group of 13 cases (13 eyes) was established in which the pterygium and dermoids were removed, and lamellar allografts were transplanted. The rate of rejection and their effects were compared. RESULTS: The rate of transparent autograft and allograft was 100%, no rejection and recurrence of pterygium occurred in any case in the combined group, while in the control group, the rejection rate was 30.8% and recurrence rate, 20.0%. CONCLUSION: The combination of lamellar autografting with allografting can reduce the rate of rejection and recurrence of pterygium.

Adult↗
PubMed1998

A divergent role of COOH-terminal domains in Nurr1 and Nur77 transactivation.

Orphan nuclear receptors such as Nurr1 and Nur77 have conserved amino acid sequences in the zinc finger DNA binding domains and similar COOH-terminal regions, but have no known ligands. These receptors can bind DNA sequences (response elements) as monomers and can also heterodimerize with the retinoid X receptor to activate transcription. We report here the identification and initial characterization of a novel COOH-terminal truncated isoform of Nurr1, Nurr1a. Internal splicing of Nurr1 generates a frameshift such that a stop codon is prematurely encoded resulting in a naturally occurring COOH-terminal truncation. Embryonic and postnatal mouse brain showed both Nurr1 and Nurr1a mRNAs expressed during development. To characterize essential COOH-terminal elements that may be deleted from Nurr1a and determine function in putative ligand binding, we created COOH-terminal deletion mutants. Nurr1, Nur77, and 3'-truncated mutants bind in gel mobility shift assays to the monomeric Nur77 response element (B1A-RE). However, in transient transfection assays, a truncation of as little as 15 Nurr1 COOH-terminal amino acids diminished transcriptional activation of B1A-thymidine kinase-chloramphenicol acetyltransferase reporter. This result was not seen for a similar Nur77 deletion mutant, Nur77-586. Unlike full-length Nurr1 and Nur77, transactivation by Nur77-586 was not augmented in response to the presence of retinoid-like receptor and 9-cis-retinoic acid. Thus, the interaction of putative ligand binding and transactivation for Nurr1 and Nur77 may function differently.

3T3 Cells↗
PubMed1998

Studies on the enzymology of aldehyde dehydrogenase-2 in genetically modified HeLa cells.

The Asian flush reaction is known to result from a lysine for glutamine substitution in the aldehyde dehydrogenase 2 (ALDH2) gene. This mutation was studied in HeLa cells transduced with retroviruses carrying the ALDH2E (wild-type) and ALDH2K (variant) cDNAs. The cells expressed high levels of the enzyme protein that had the same pI and enzymatic characteristics as the corresponding liver enzyme. When cells expressing ALDH2E were transduced with ALDH2K expressing retrovirus, the ALDH2 activity was reduced roughly in proportion to the amount of ALDH2K mRNA expressed, indicating a dominant suppression of activity. The half-life of the wild-type enzyme was 22 hr, while that of variant enzyme was 14 hr. The half-life of the enzyme in cells expressing both cDNAs was 13 hr, indicating that the shorter half-life of the variant was also dominant These data are consistent with a model in which the wild-type homodimers have normal activity and turnover, while the heterodimers have reduced to virtually no activity and increased turnover. The model predicts residual ALDH2 activity in heterozygotes of about 13% of that in individuals homozygous for ALDH2*1, in good agreement with experimentally determined values.

Alcohol Drinking↗
PubMed1997

Growth and dissemination of Lewis lung carcinoma in plasminogen-deficient mice.

Plasminogen activation has been proposed to play a critical role in cancer invasion and metastasis. The effects of complete ablation of plasminogen activation in cancer was studied by inoculation of a metastatic Lewis lung carcinoma expressing high levels of plasminogen activator into plasminogen-deficient (Plg-/-) mice and matched control mice. Primary tumors developed in all mice with no difference in the rate of appearance between Plg-/- and control mice. However, the primary tumors in Plg-/- mice were smaller and less hemorrhagic and displayed reduced skin ulceration. In addition, dissemination of the tumor to regional lymph nodes was delayed in Plg-/- mice. Surprisingly, no quantitative differences were observed in lung metastasis between Plg-/- and control mice. In addition, Plg deficiency was compatible with metastasis of the primary tumor to a variety of other organs. Nevertheless, Plg-/- mice displayed a moderately increased survival after primary tumor resection. These findings suggest that plasmin-mediated proteolysis contributes to the morbidity and mortality of Lewis lung carcinoma in mice, but sufficient proteolytic activity is generated in Plg-/- mice for efficient tumor development and metastasis.

Animals↗
PubMed1997

Plasminogen deficiency accelerates vessel wall disease in mice predisposed to atherosclerosis.

A critical link between hemostatic factors and atherosclerosis has been inferred from a variety of indirect observations, including the expression of procoagulant and fibrinolytic factors within atherosclerotic vessels, the presence of fibrin in intimal lesions, and the cellular infiltration of mural thrombi leading to their incorporation into developing plaques. To directly examine the role of the key fibrinolytic factor, plasminogen, in atherogenesis, plasminogen-deficient mice were crossed to hypercholesterolemic, apolipoprotein E-deficient mice predisposed to atherosclerosis. We report that the loss of plasminogen greatly accelerates the formation of intimal lesions in apolipoprotein E-deficient animals, whereas plasminogen deficiency alone does not cause appreciable atherosclerosis. These studies provide direct evidence that circulating hemostatic factors strongly influence vessel wall disease in the context of a disorder in lipid metabolism.

Animals↗
PubMed1997

Organization, sequence, chromosomal localization, and promoter identification of the mouse orphan nuclear receptor Nurr1 gene.

We have cloned and characterized the organization of the mouse orphan nuclear receptor Nurr1 gene. The Nurr1 gene is approximately 7 kb long, contains eight exons and seven introns, and mapped to mouse chromosome 2. Although the exon/intron structure of Nurr1 is nearly identical to that of Nur77, Nurr1 possesses an additional untranslated exon. Primer extension was used to identify two major transcription initiation sites mapped 37 nucleotides apart in the first untranslated exon. Functional studies of chimeric Nurr1-luciferase reporter genes delineated the promoter region and underscored the importance of the +1 transcription start site. Sequence analysis of the 5' flanking region surrounding +1 revealed several possible response elements such as a hexanucleotide glucocorticoid binding site, a cAMP-response element, a CArG box, and two c-Jun-binding sites. These data help to explain the different response characteristics of two closely related early response genes, Nurr1 and Nur77.

Animals↗
PubMed1997

The distribution of NPY-containing nerves and the catecholamine contents of canine enteric nerve plexuses.

Our previous study demonstrated that PYY was a major neuropeptide in the canine enteric nervous system, the present study defines the locations of NPY-containing enteric neurons. NPY-positive nerve cell bodies and fibers were numerous in gastric and pyloric myenteric plexuses as were positive nerve fibers in antral and pyloric muscle layers, pyloric sphincter muscle layers, and surrounding blood vessels. In contrast to findings for PYY, there were considerably fewer NPY-positive nerve cell bodies and fibers in the canine ileum and colon. Noradrenaline was the predominant catecholamine in all plexuses, the rank order of its contents being: deep muscular > submucous > myenteric plexus. The dopamine/noradrenaline ratio was constant in all plexuses; adrenaline was present in minor amounts. PYY is the more abundant neuropeptide in ileum and colon, and NPY has a greater presence in the gastric antrum, pylorus, and surrounding blood vessels. PYY and NPY may play different functional roles in the GI tract.

Animals↗
PubMed1997

Identification of downstream-initiated c-Myc proteins which are dominant-negative inhibitors of transactivation by full-length c-Myc proteins.

The c-myc gene has been implicated in multiple cellular processes including proliferation, differentiation, and apoptosis. In addition to the full-length c-Myc 1 and 2 proteins, we have found that human, murine, and avian cells express smaller c-Myc proteins arising from translational initiation at conserved downstream AUG codons. These c-Myc short (c-Myc S) proteins lack most of the N-terminal transactivation domain but retain the C-terminal protein dimerization and DNA binding domains. As with full-length c-Myc proteins, the c-Myc S proteins appear to be localized to the nucleus, are relatively unstable, and are phosphorylated. Significant levels of c-Myc S, often approaching the levels of full-length c-Myc, are transiently observed during the rapid growth phase of several different types of cells. Optimization of the upstream initiation codons resulted in greatly reduced synthesis of the c-Myc S proteins, suggesting that a "leaky scanning" mechanism leads to the translation of these proteins. In some hematopoietic tumor cell lines having altered c-myc genes, the c-Myc S proteins are constitutively expressed at levels equivalent to that of full-length c-Myc. As predicted, the c-Myc S proteins are unable to activate transcription and inhibited transactivation by full-length c-Myc proteins, suggesting a dominant-negative inhibitory function. While these transcriptional inhibitors would not be expected to function as full-length c-Myc, the occurrence of tumors which express constitutive high levels of c-Myc S and their transient synthesis during rapid cell growth suggest that these proteins do not interfere with the growth-promoting functions of full-length c-Myc.

Animals↗
PubMed1997

Secretion from cell culture of HDL and VLDL bearing apoB-33 with a large internal deletion.

Rat hepatoma McA-RH7777 cells synthesize and secrete two populations of apoB-containing lipoproteins: a larger, VLDL-sized population floating in the Sf 40-150 range and a smaller, LDL and HDL-sized population. Three permanently transfected cell lines of McA-RH7777 cells secreted (in addition to the endogenous lipoproteins) lipoproteins containing 1) a carboxyl-terminally truncated human apoB-53 (2377 amino acids in length); 2) a carboxyl-terminally truncated human apoB-31 (1420 amino acids in length); or 3) an internally deleted human apoB protein, apoB-18/95, containing a total of 1490 amino acid residues, equivalent in length to an apoB33. The apoB-18/95 protein contained amino acid residues 1-782 joined to 708 residues near the C-terminus of apoB (residues 36364343). All three of the apoB peptides, apoB53, apoB-31, and apoB-18/95, were present on smaller LDL-HDL-class lipoproteins, with buoyant densities in the HDL density range. The sizes of the HDL class lipoproteins agreed with prior observations that lipoprotein core circumference is directly proportional to apoB size. As HDL containing apoB-18/95 conformed to this rule, contiguous apoB amino acid sequence is not required for the rule to be obeyed. In addition, apoB-18/95, but not apoB-31, was also present on the VLDL-sized lipoproteins even in the absence of serum or oleate supplementation. As the latter two constructs encode equally sized apoB peptides, their particular amino acid sequences rather than just overall length must determine whether they can assemble into a VLDL particle.

Animals↗
PubMed1996

The mutation in the mitochondrial aldehyde dehydrogenase (ALDH2) gene responsible for alcohol-induced flushing increases turnover of the enzyme tetramers in a dominant fashion.

Deficiency in mitochondrial aldehyde dehydrogenase (ALDH2), a tetrameric enzyme, results from inheriting one or two ALDH2*2 alleles. This allele encodes a protein subunit with a lysine for glutamate substitution at position 487 and is dominant over the wild-type allele, ALDH2*1. The ALDH2*2-encoded subunit (ALDH2K) reduces the activity of ALDH2 enzyme in cell lines expressing the wild-type subunit (ALDH2E). In addition to this effect on the enzyme activity, we now report that ALDH2*2 heterozygotes had lower levels of ALDH2 immunoreactive protein in autopsy liver samples. The half-lives of ALDH2 protein in HeLa cell lines expressing ALDH2*1, ALDH2*2, or both were determined by the rate of loss of immunoreactive protein after inhibition of protein synthesis with puromycin and by pulse-chase experiments. By either measure, ALDH2E enzyme was very stable, with a half-life of at least 22 h. ALDH2K enzyme had an enzyme half-life of only 14 h. In cells expressing both subunits, most of the subunits assemble as heterotetramers, and these enzymes had a half-life of 13 h. Thus, the effect of ALDH2K on enzyme turnover is dominant. These studies indicate that the ALDH2*2 allele exerts its dominant effect both by interfering with the catalytic activity of the enzyme and by increasing its turnover. This represents the first example of a dominantly acting allele with this effect on a mitochondrial enzyme's turnover.

Aldehyde Dehydrogenase↗
PubMed1996

Fatal embryonic bleeding events in mice lacking tissue factor, the cell-associated initiator of blood coagulation.

Tissue factor (TF) is the cellular receptor for coagulation factor VI/VIIa and is the membrane-bound glycoprotein that is generally viewed as the primary physiological initiator of blood coagulation. To define in greater detail the physiological role of TF in development and hemostasis, the TF gene was disrupted in mice. Mice heterozygous for the inactivated TF allele expressed approximately half the TF activity of wild-type mice but were phenotypically normal. However, homozygous TF-/- pups were never born in crosses between heterozygous mice. Analysis of mid-gestation embryos showed that TF-/- embryos die in utero between days 8.5 and 10.5. TF-/- embryos were morphologically distinct from their TF+/+ and TF+/- littermates after day 9.5 in that they were pale, edematous, and growth retarded. Histological studies showed that early organogenesis was normal. The initial failure in TF-/- embryos appeared to be hemorrhaging, leading to the leakage of embryonic red cells from both extraembryonic and embryonic vessels. These studies indicate that TF plays an indispensable role in establishing and/or maintaining vascular integrity in the developing embryo at a time when embryonic and extraembryonic vasculatures are fusing and blood circulation begins.

Animals↗
PubMed1996

Locations and molecular forms of gastrin-releasing peptide-like immunoreactive entities in ovine pregnancy.

Large quantities of gastrin-releasing peptide-like immunoreactivity (GRP-LI) are present in ovine pregnancy fluids (allantoic fluid > fetal plasma > esophageal fluid = amniotic fluid = urine > maternal plasma) and in term endometrium (60 +/- 29 pmol.g-1) and myometrium (4.5 +/- 1.2 pmol.g-1). The larger molecular size [greater than GRP (1-27)] of this GRP-LI entity is not due to a GRP binding protein nor to a C-terminal extension of GRP. In contrast, ovine fetal colon extracts appear to contain the usual GRP (1-27) and GRP (18-27) forms. Hence, the uterus, not the fetus, is the probable source of this novel GRP-like peptide. It apparently acts as a hormone in ovine pregnancy and may play an important role in fetal-placental development.

Amino Acid Sequence↗
PubMed1996

Distribution of messenger RNAs for the orphan nuclear receptors Nurr1 and Nur77 (NGFI-B) in adult rat brain using in situ hybridization.

Nurr1 and Nur77 (NGFI-B) are orphan nuclear receptors, belonging to the steroid/thyroid hormone receptor gene superfamily. They have conserved amino acid sequence in the zinc-finger DNA binding domains and similar COOH-terminal regions, but have no known ligands. However, different expression patterns during brain development and tissue distributions of these messenger RNAs imply that they might reflect a different transcriptional role in the brain. In this study, the regional and cellular expression of messenger RNAs encoding these two proteins in rat brain has been determined by in situ hybridization. Nurr1 messenger RNA is highly expressed in the piriform and entorhinal cortices, hippocampus, medial habenular and paraventricular thalamic nuclei. Moderate labeling was detected in layers II-V of most of the cerebral cortex, and in the dorsal lateral geniculate nucleus, substantia nigra (pars compacta and reticularis) and interpeduncular nucleus. No Nurr1 hybridization signal was seen in the rhombencephalon. In the cerebellum, Nurr1 messenger RNA is present in the internal granular cell layer and Purkinje cell layer. In contrast, Nur77 has a widespread distribution, with the highest level of expression in the cerebral cortex. Moderate hybridization signals were detected in the hippocampus, the lateral dorsal and posterior nuclei, reuniens thalamic nuclei, and paraventricular and supraoptic hypothalamic nuclei. In the rhombencephalon, higher signals were present in the medial and lateral vestibular, dorsal cochlear and facial, and raphe magnus nuclei. Nur77 signal was also detected in the nucleus of the spinal tract of the trigeminal nerve. In the cerebellum, Nur77 messenger RNA is highly expressed in the Purkinje cell layer and lateral deep nucleus of the cerebellum. Our results show that Nurr1 and Nur77 messenger RNAs have both overlapping and different distribution patterns within the brain, suggesting that they might regulate different sets of responsive genes.

Animals↗
PubMed1996

A novel fluorescence-activated cell sorter-based screen for yeast endocytosis mutants identifies a yeast homologue of mammalian eps15.

A complete understanding of the molecular mechanisms of endocytosis requires the discovery and characterization of the protein machinery that mediates this aspect of membrane trafficking. A novel genetic screen was used to identify yeast mutants defective in internalization of bulk lipid. The fluorescent lipophilic styryl dye FM4-64 was used in conjunction with FACS to enrich for yeast mutants that exhibit internalization defects. Detailed characterization of two of these mutants, dim1-1 and dim2-1, revealed defects in the endocytic pathway. Like other yeast endocytosis mutants, the temperature-sensitive dim mutant were unable to endocytose FM4-64 or radiolabeled alpha-factor as efficiently as wild-type cells. In addition, double mutants with either dim1-delta or dim2-1 and the endocytosis mutants end4-1 or act1-1 displayed synthetic growth defects, indicating that the DIM gene products function in a common or parallel endocytic pathway. Complementation cloning of the DIM genes revealed identity of DIM1 to SHE4 and DIM2 to PAN1. Pan1p shares homology with the mammalian clathrin adaptor-associated protein, eps15. Both proteins contain multiple EH (eps15 homology) domains, a motif proposed to mediate protein-protein interactions. Phalloidin labeling of filamentous actin revealed profound defects in the actin cytoskeleton in both dim mutants. EM analysis revealed that the dim mutants accumulate vesicles and tubulo-vesicular structures reminiscent of mammalian early endosomes. In addition, the accumulation of novel plasma membrane invaginations where endocytosis is likely to occur were visualized in the mutants by electron microscopy using cationized ferritin as a marker for the endocytic pathway. This new screening strategy demonstrates a role for She4p and Pan1p in endocytosis, and provides a new general method for the identification of additional endocytosis mutants.

Actins↗
PubMed1996

Gastrin-releasing peptide-like immunoreactivity is present in human maternal and fetal placental membranes.

Extracts of human term amnion, placenta, and chorion/decidual tissue (n = 5) contained gastrin-releasing peptide-like immunoreactivity (GRPLI) in amounts of 4.7 +/- 2.9 (pmol/g wet wt; mean +/- SEM), 3.6 +/- 1.1 and 2.9 +/- 1.5, respectively. Using C-terminally directed antisera and gel filtration chromatography and reverse-phase high-performance liquid chromatography (HPLC), each tissue contained molecular forms consistent with the presence of GRP1-27 and GRP18-27 but also contained larger amounts of two GRPLI peaks, which apparently are novel GRP-like peptides. In contrast, tissue extracts of human fetal lung contained only GRP1-27, GRP14-27, and GRP18-27. Using RT-PCR and specific GRP primers and probes, messenger RNA encoding for GRP was readily demonstrable from 6-weeks gestation throughout pregnancy to term in full-thickness membranes, placental villi, and decidua. Positive immunohistochemical staining for GRP occurred in extravillous trophoblasts in decidual septa and fetal membranes, cytotrophoblasts, syncytiotrophoblast, and certain stromal cells in placental villi and amniotic epithelium. GRPLI and GRP messenger RNA were present from the earliest dates examined (6-9 weeks) throughout pregnancy to term. Given the proven trophic nature of GRP and related peptides, these peptides may play important roles in maternal, placental, and fetal development during human pregnancy.

Amnion↗