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Biomedical subjects

W Duan

Publications and source records attributed to W Duan.

At least 55 records · Page 3Linked to original sources
PubMed1999

[A clinicopathologic study on eight cases of cystic and solid tumors of pancreas].

OBJECTIVE: To study the clinicopathologic characteristics, differentiation patterns and histogenesis of cystic and solid tumors of the pancreas (CSTP). METHODS: 8 cases of CSTP were studied using histologic (HE and PAS), immunohistochemical (S-P method) and electron microscopic techniques. RESULTS: All the patients were adolescent and young adult females, 14-33 years in age (mean 25.3 years) without recurrence after tumor resection. The mean diameter of tumors was 9.6 cm, all encapsulated. Histological examination showed presence of solid sheets, pseudopapillary, in all of the cases. Hemorrhage, foam cells, and cholesterol crystals were often found. Immunohistochemically, 8 cases were positive for alpha(1)-AT and lysozyme; 6 cases expressed vimentin, 2 cases expressed actin, and CgA-positive cells found in the tumor cell nests in one case. All of the cases showed PR, and 4 cases showed ER positive immunoreactivity in the majority of tumor cells, but negative for CK AE1, CK AE3, EMA, Synaptophysin, ACTH, gastrin, somatostatin, insulin, and glucogan in all the cases. Electron microscopy of 3 cases showed evidences of polymorphism in differentiation of the tumor cells, including the transitional appearance into ducts, acinus, and endocrine cells. Weibel-Palade body found in tumor cells in one out of 8 cases. CONCLUSIONS: (1) CSTP is a distinct clinicopathologic entity in young female patients with a benign clinical course. (2) CSTP develops from primitive pancreatic cells, with the potentiality of developing into ducts, acinus, and endocrine cells.

Actins↗
PubMed1999

[Study on relative factors in endoscopic sinus surgical procedure].

OBJECTIVE: In order to investigate the factors which affect the operative treatment effect of FESS. METHOD: 215 cases suffered functional endoscopic sinus surgery (FESS) from May 1994 to December 1997 were analysed. RESULT: The clinical curative rate was 75.8% and the improving rate was 96.3%. CONCLUSION: The effect shows that surgical procedure is closely related to following factors: mechanic of operation, drugs taken in pre-operation, kinds of anesthsia, clinical stage of chronic sinusitis, nasal poplys and skill of surgeons.

Adolescent↗
PubMed1998

A promoter recruitment mechanism for tumor necrosis factor-alpha-induced interleukin-8 transcription in type II pulmonary epithelial cells. Dependence on nuclear abundance of Rel A, NF-kappaB1, and c-Rel transcription factors.

The alveolar macrophage-derived peptide tumor necrosis factor-alpha (TNFalpha) initiates pulmonary inflammation through its ability to stimulate interleukin-8 (IL-8) synthesis in alveolar epithelial cells through an incompletely described transcriptional mechanism. In this study, we use the technique of ligation-mediated polymerase chain reaction (LMPCR) to record changes in transcription factor occupancy of the IL-8 promoter after TNFalpha stimulation of A549 human alveolar cells. Using dimethylsulfate/LMPCR, no detectable proteins bind the TATA box in unstimulated cells. By contrast, TNFalpha rapidly induces protection of G residues at -79 and -80 coincident with endogenous IL-8 gene transcription. Using DNase I/LMPCR, we observe inducible protection of nucleotides -60 to -99 (the TNF response element) and nucleotides -3 to -32 (containing the TATA box). Surprisingly, extensive TATA box protection is only seen after TNFalpha stimulation. Using a two-step microaffinity isolation/Western immunoblot DNA binding assay, we observe that the NF-kappaB subunits Rel A, NF-kappaB1, and c-Rel inducibly bind the TNF response element; these proteins undergo rapid TNFalpha-inducible increases in nuclear abundance as a consequence of IkappaBalpha proteolysis. Furthermore, the peptide aldehyde N-acetyl-Leu-Leu-norleucinal, an agent that blocks both IkappaBalpha proteolysis and NF-kappaB subunit translocation, abrogates recombinant human TNFalpha-inducible IL-8 gene transcription. These studies demonstrate that IL-8 is activated by a promoter recruitment mechanism in alveolar epithelial cells, where NF-kappaB subunit translocation is required for (and coincident with) binding of the constitutively active TATA box-binding proteins.

Binding Sites↗
PubMed1998

Seroprevalence of human herpesvirus 8 among Zambian women of childbearing age without Kaposi's sarcoma (KS) and mother-child pairs with KS.

The seroprevalence of human herpesvirus 8 (HHV-8) among a group of Zambian women of reproductive age and among mother-child pairs in which either one of them has Kaposi's sarcoma (KS) was determined. A cross-sectional group of 378 pregnant women was randomly recruited into the study, and 183 (48.4%) had HHV-8 antibodies. Among the human immunodeficiency virus (HIV)-1-infected women, 51.1% were HHV-8-seropositive, whereas of HIV-1-negative women, 47.3% were HHV-8-seropositive. In addition, 21 women index patients with KS and 5 young children index patients with KS were studied. All children with KS had mothers who were HHV-8-seropositive, while not all children whose mothers had KS were infected with HHV-8. Our study suggests that there is a high HHV-8 seroprevalence among Zambian women, and the rate is almost the same in HIV-1-positive and -negative women. This high seroprevalence may be a contributing factor toward the increased frequency of KS in this population.

Adolescent↗
PubMed1998

Effects of clausenamide on anisodine-induced acetylcholine decrease and memory deficits in the mouse brain.

OBJECTIVES: To study the action mechanism of a new cognition enhancer clausenamide and the effect of clausenamide on regional acetylcholine (ACh) levels, and to examine anisodine-induced ACh decrease in mice of memory deficits, and to compare the effect of (-)clausenamide on ACh with that of (+)clausenamide. METHODS: Animal amnesia model was induced by i.p. anisodine and brain ACh content was measured by high performance liquid chromatography with electrochemical detection. RESULTS: Single administration of (-)clausenamide or (+)clausenamide (10, 20, 50 mg/kg, i.g.) had no effect on the ACh level in the frontal cortex, hippocampus and striatum. However, pretreatment with (-)clausenamide (10, 20, 50 mg/kg, i.g.) significantly ameliorated the reduction of ACh induced by anisodine (10 mg/kg, i.p.) in a dose-dependent manner. Physostigmine (0.2 mg/kg, s.c.), as a cholinesterase inhibitor significantly increased the ACh levels and reversed the anisodine-induced ACh decrease. In contrast, (+)clausenamide had no effect on ACh decrease in all examined brain regions. (-)Clausenamide ameliorated anisodine-induced memory deficits in step-through test in mice. CONCLUSION: There is significant difference in the action of (-)clausenamide and (+)clausenamide. The protective action of (-)clausenamide against anisodine-induced amnesia is due to its ability to reverse the ACh reduction.

Acetylcholine↗
PubMed1998

[Effects of (-), (+)clausenamide on anisodine-induced acetylcholine decrease and associated memory deficits in the mouse brain].

The effect of a new cognition enhancer clausenamide on regional acetylcholine (ACh) levels and anisodine-induced ACh decrease were examined in mice of memory deficits. In the mean time, the effect of (-)clausenamide on ACh was compared with that of (+)clausenamide. Animal amnesia model was induced by i.p. anisodine, brain acetylcholine content was measured by high performance liquid chromatography with electrochemical detection. It was found that single administration of (-)clausenamide or (+)clausenamide(10, 20, 50 mg.kg-1, ig) showed no effect on the ACh level in the frontal cortex, hippocampus and striatum in normal condition. However, pretreatment with (-)clausenamide (10, 20, 50 mg.kg-1, ig) significantly ameliorated the reduction of ACh in these regions induced by anisodine (10 mg.kg-1, i.p.) in a dose-dependent manner. In the meantime, (-) clausenamide ameliorate anisodine-induced memory deficits in step-through test in mice. In contrast, (+)clausenamide showed no effect on these sides. The results indicate that there is significant difference between the actions of (-)clausenamide and (+)clausenamide; The protective action of (-)clausenamide against anisodine-induced amnesia is due to its ability to reverse ACh reduction.

Acetylcholine↗
PubMed1995

Homozygous deletions of the MTS1 gene are rare in non-astrocytic brain tumors.

Several studies support a role for the multiple tumor suppressor gene (MTS1) in the malignant progression of different tumor types. In this study we have examined the status of the MTS1 gene in a variety of non-astrocytic tumors of the central nervous system. It was not possible, using multiplex PCR with primers for MTS1 and D9S196, a chromosome 9q marker, to demonstrate deletions of MTS1 in 59 primary non-astrocytic tumors. Two out of 5 (40%) secondary tumors showed evidence of homozygous deletion of MTS1. The results obtained here for primary non-astrocytic tumors contrast with those previously described for astrocytic tumors where a high frequency of deletions of MTS1 was associated with tumor progression.

Astrocytoma↗
PubMed1995

Binding of thyroxine to pig transthyretin, its cDNA structure, and other properties.

Thyroxine binding to proteins in pig plasma during electrophoresis was observed in the albumin, but not in the prealbumin and post-albumin regions. Transthyretin could be identified in medium from in vitro pig choroid plexus incubations by size and number of subunits and a very high rate of synthesis and secretion. Its electrophoretic mobility was intermediate between that of thyroxine-binding globulin and albumin. It bound thyroxine, retinol-binding protein, anti-(rat transthyretin) antibodies and behaved similarly to transthyretins from other vertebrate species when plasma was extracted with phenol. Inhibition experiments with the synthetic flavonoid F 21388, analysing the binding of thyroxine, suggested that transthyretin is not a major thyroxine carrier in the bloodstream of pigs. Cloning and sequencing of transthyretin cDNA from both choroid plexus and liver showed that the same transthyretin mRNA is expressed in pig choroid plexus and liver. The amino acid sequence derived from the nucleotide sequence revealed that pig transthyretin differs from the transthyretins of all other studied vertebrate species by an unusual C-terminal extension consisting of the amino acids glycine, alanine and leucine. This extension results from the mutation of a stop codon into a codon for glycine. The unusual C-terminal extensions do not seem to interfere with the access of thyroxine to its binding site in the central channel of transthyretin.

Amino Acid Sequence↗
PubMed1995

Evolution of transthyretin in marsupials.

The evolution of the expression and the structure of the gene for transthyretin, a thyroxine-binding plasma protein formerly called prealbumin, was studied in three marsupial species: the South American polyprotodont Monodelphis domestica, the Australian polyprotodont Sminthopsis macroura and the Australian diprotodont Petaurus breviceps. The transthyretin gene was found to be expressed in the choroid plexus of all three species. In liver it was expressed in P. breviceps and in M. domestica, but not in S. macroura. This, together with previous studies [Richardson, S. J., Bradley, A. J., Duan, W., Wettenhall, R. E. H., Harms, P. J., Babon, J. J., Southwell, B. R., Nicol, S., Donnellan, S. C. & Schreiber, G. (1994) Am. J. Physiol. 266, R1359-R1370], suggests the independent evolution of transthyretin synthesis in the liver of the American Polyprotodonta and the Australian Diprotodonta. The results obtained from cloning and sequencing of the cDNA for transthyretin from the three species suggested that, in the evolution of the structure of transthyretin in vertebrates, marsupial transthyretin structures are intermediate between bird/reptile and eutherian transthyretin structures. In marsupials, as in birds and reptiles, a hydrophobic tripeptide beginning with valine and ending with histidine was found in transthyretin at a position which has been identified in eutherians as the border between exon 1 and intron 1. In humans, rats and mice, the nine nucleotides, coding for this tripeptide in marsupials/reptiles/birds, are found at the 5' end of intron 1. They are no longer present in mature transthyretin mRNA. This results in a change in character of the N-termini of the subunits of transthyretin from hydrophobic to hydrophilic. This change might affect the accessibility of the thyroxine-binding site in the central channel of transthyretin, since, at least in humans, the N-termini of the subunits of transthyretin are located in the vicinity of the channel entrance [Hamilton, J. A., Steinrauf, L. K., Braden, B. C., Liepnieks, J., Benson, M. D., Holmgren, G., Sandgren, O. & Steen, L. (1993) J. Biol. Chem. 268, 2416-2424].

Amino Acid Sequence↗
PubMed1995

Homozygous deletions of the multiple tumor suppressor gene 1 in the progression of human astrocytomas.

The multiple tumor suppressor gene 1 (MTS1) located on chromosome 9p has recently been implicated as a candidate tumor suppressor gene in many different tumor types. Cytogenetic analysis and deletion mapping studies have revealed that deletion of chromosome 9p occurs in a significant number of primary human astrocytomas. Using multiplex PCR with primers for exon 2 of MTS1 and for D9S196 from chromosome 9q, we have analyzed 78 primary astrocytic tumors for the deletion of MTS1. After controlling for the contamination of tumor samples with normal cells, homozygous loss of MTS1 was found in 13 of 25 anaplastic astrocytomas (WHO grade III) and in 27 of 46 cases of glioblastomas (WHO grade IV) but in none of seven astrocytomas (WHO grade II). These data suggest that MTS1 is an important tumor suppressor gene in the malignant progression of astrocytomas.

Adult↗
PubMed1995

Wallaby transthyretin.

A cDNA library was constructed from liver RNA of the Australian diprotodont marsupial Macropus eugenii, the Tammar wallaby. A cloned full-length transthyretin cDNA was sequenced. The derived amino-acid sequence showed 68% overall similarity to that of human transthyretin, with 86% similarity in the thyroxine binding site. Comparisons of nucleotide and amino acid sequences from several vertebrate species indicated that the greatest differences were in the region corresponding to the disordered N-terminus of mature human transthyretin. The evolutionary trees deduced from parsimony analyses of amino acid and nucleotide sequences of transthyretins, are consistent with that derived from fossil records.

Amino Acid Sequence↗
PubMed1994

Evolution of marsupial and other vertebrate thyroxine-binding plasma proteins.

Binding of radioactive thyroxine to proteins in the plasma of vertebrates was studied by electrophoresis followed by autoradiography. Albumin was found to be a thyroxine carrier in the blood of all studied fish, amphibians, reptiles, monotremes, marsupials, eutherians (placental mammals), and birds. Thyroxine binding to transthyretin was detected in the blood of eutherians, diprotodont marsupials, and birds, but not in blood from fish, toads, reptiles, monotremes, and Australian polyprotodont marsupials. Globulins binding thyroxine were only observed in the plasma of some mammals. Apparently, albumin is the phylogenetically oldest thyroxine carrier in vertebrate blood. Transthyretin gene expression in the liver developed in parallel, and independently, in the evolutionary lineages leading to eutherians, to diprotodont marsupials, and to birds. In contrast, high transthyretin mRNA levels, strong synthesis, and secretion of transthyretin in choroid plexus from reptiles and birds indicate that transthyretin gene expression in the choroid plexus evolved much earlier than in the liver, probably at the stage of the stem reptiles. NH2-terminal sequence analysis suggests a change of transthyretin pre-mRNA splicing during evolution.

Amino Acid Sequence↗
PubMed1993

The expression of the transthyretin gene in liver evolved during the radiation of diprotodont marsupials in Australia.

Thyroid hormone-binding proteins in blood plasma were identified in 28 different marsupial species by their capacity to bind radioactive thyroxine. All species contained albumin. Transthyretin was not found in the blood from any of 12 polyprotodont marsupial species, but was abundant in the blood from all of 16 diprotodont marsupial species investigated. Transthyretin mRNA was absent from the liver of the stripe-faced dunnart, a polyprotodont marsupial, but abundant in the liver of the diprotodont grey kangaroo. Diprotodont marsupials probably evolved in Australia from polyprotodont marsupials after their transantarctic migration from South America, about 40 million years ago. It is suggested that hepatic transthyretin expression evolved in marsupials during the radiation of herbivorous, diprotodont species in Australia. The earlier appearance of transthyretin gene expression in the choroid plexus of the stem reptiles, about 300 million years ago, contrasts with hepatic transthyretin synthesis, a relatively late evolutionary event, occurring independently in at least three lineages.

Animals↗
PubMed1993

Transthyretin expression evolved more recently in liver than in brain.

1. Transthyretin was found to be synthesized and secreted by choroid plexus from rats, echidnas, and lizards, but not toads. 2. Transthyretin was observed in blood from placental mammals, birds, and marsupials, but not reptiles and monotremes. 3. The obtained data suggest that transthyretin synthesis by the liver evolved independently in the lineage leading to the placental mammals and marsupials and in that leading to the birds. 4. It is proposed that transthyretin gene expression in mammalian liver appeared about 200 million years later than its first occurrence in the choroid plexus of the stem reptiles.

Amino Acid Sequence↗
PubMed1993

Transthyretin gene expression in choroid plexus first evolved in reptiles.

The presence of transthyretin in mammals and birds, but not amphibia, suggested that transthyretin expression first appeared in stem reptiles. Therefore, transthyretin synthesis was studied in a lizard. Transthyretin synthesis in choroid plexus pieces from Tiliqua rugosa was demonstrated by incorporation of radiactive amino acids. Oligonucleotides corresponding to conserved regions of transthyretin were used as primers in polymerase chain reaction with lizard choroid plexus cDNA. Amplified DNA was used to screen a lizard choroid plexus cDNA library. A full-length transthyretin cDNA clone was isolated and sequenced. A three-dimensional model of lizard transthyretin was obtained by homology modeling. The central channel of transthyretin, containing the thyroxine-binding site, was found to be completely conserved between reptiles and mammals. Transthyretin expression was not detected in lizard liver. These data suggest that transthyretin first evolved in the choroid plexus of the brain. Due to a change in tissue distribution of gene expression, occurring much later during evolution, transthyretin also became a plasma protein, synthesized in the liver.

Amino Acid Sequence↗