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Biomedical subjects

W Xie

Publications and source records attributed to W Xie.

At least 127 records · Page 7Linked to original sources
PubMed1998

[Clinical study and denominate of traumatic herniation of corpus adiposum buccae].

OBJECTIVE: To deepen the recognition, and provide the evidence for rational name of traumatic herniation of corpus adiposum buccae. METHODS: 10 clinical cases of traumatic herniation of corpus adiposum buccae were studied. Simulat experiment on 6 fresh corpses (12 sides) were performed dissected immediately after bump (hitting) type and stab (thrusting) type of herniation of corpus adiposum buccae. RESULTS: In one side bump type and 5 sides stab type successful experiments, the buccal protuberance of masticatory fat pads (namely corpus adiposum beccae) were herniated into the mouth, with the shape, size, and position simulated with the herniated tissue of the clinical case. CONCLUSION: The herniated tissue of clinical case is the corpus adiposum buccae but not the buccal fat pad, and the rational name should be traumatic herniation of corpus adiposum buccae.

Cheek↗
PubMed1998

[Endovascular treatment of carotid-cavernous sinus fistulae].

OBJECTIVE: To treat carotid-cavernous sinus fistulae mmunications between 43 patients with endovascular procedure. METHOD: Of the 43 patients 37 were male and 6 female. Traumatic and spontaneous CCF were noted in 39 and 4 patients respectively. 36 patients with CCF were given ICA alone, both internal and external carotid arteries in 7. Fistulae occlusion in 31 patients and ICA obliteration in 12 patients were achieved with transarterial detachable balloon technique. External carotid feeding arteries were embolized with silk suture in 7 patients. RESULT: Angiographic and clinical cure wer obtained in 39 patients and improved in 4. One patient was complicated by hemiplegia postoperatively. CONCLUSION: Endovascular balloon embolization is the first method of choice in dealing with carotid-cavernous fistulae.

Adolescent↗
PubMed1998

[Clinical analysis of traumatic herniation of buccal adipose body].

Traumatic herniation of buccal adipose body is not rare, but available clinical data are not sufficient and nomenclature has not been standardized. 11 clinical cases of traumatic herniation of buccal adipose body and 1 typical cases were reported, and nomenclature and classification of the disease were discussed combining with relevant references. Finally, it suggests the diagnosis and therapy of traumatic herniation of buccal adipose body.

Adipose Tissue↗
PubMed1998

[Determination of selenium by platform graphite furnace atomic absorption spectrometry].

The matrix modifier and its amount, the ashing or atomization temperature of selenium and interference experiment are investigated. The experimental result shows that the application of Pd-Ca as mixed matrix modifier not only reduces interference but also enhances ashing temperature and increases sensitivity. The method can be used directly for the determination of selenium in cereal by platform graphite furnace atomic absorption. The characteristic mass is 39 ng,the detection limit is 0.11 microg/g, the relative standard deviation is 4.9-7.7% and the recovery is 92-100%.

Graphite↗
PubMed1998

Targeted expression of activated erbB-2 to the epidermis of transgenic mice elicits striking developmental abnormalities in the epidermis and hair follicles.

The erbB-2 proto-oncogene belongs to a receptor tyrosine kinase family that includes the epidermal growth factor receptor, erbB-2, erbB-3, and erbB-4. erbB-2 is expressed in basal cells of the squamous epithelia and the outer root sheath of the hair follicles, but its function in epidermal development has not been well studied. To investigate its role in the skin, we created transgenic mice harboring an activated erbB-2 oncogene under the control of the human keratin 14 promoter. The keratin 14 promoter directed its expression to cells in which erbB-2 is normally expressed, whereas the activated receptor gene ensured increased signaling. All transgenic founder mice exhibited extensive and striking skin phenotype, including epidermal hyperplasia, preneoplasia, papilloma, hyperkeratosis, and dyskeratosis. The majority of the hair follicles were replaced by bizarre hyperproliferative intradermal squamous invaginations, whereas the rest of the follicles exhibited severe hyperplasia and disorganization. All but one of the transgenic mice died before or shortly after birth, probably as a consequence of defects in the skin and esophagus. These observations demonstrate that the skin is sensitive to erbB-2 signaling, suggesting an important role for this receptor tyrosine kinase in epidermal growth, differentiation, and hair follicle morphogenesis.

Animals↗
PubMed1997

Regulation of CFTR chloride channels by syntaxin and Munc18 isoforms.

The cystic fibrosis gene encodes a cyclic AMP-gated chloride channel (CFTR) that mediates electrolyte transport across the luminal surfaces of a variety of epithelial cells. The molecular mechanisms that modulate CFTR activity in epithelial tissues are poorly understood. Here we show that CFTR is regulated by an epithelially expressed syntaxin (syntaxin 1A), a membrane protein that also modulates neurosecretion and calcium-channel gating in brain. Syntaxin 1A physically interacts with CFTR chloride channels and regulates CFTR-mediated currents both in Xenopus oocytes and in epithelial cells that normally express these proteins. The physical and functional interactions between syntaxin 1A and CFTR are blocked by a syntaxin-binding protein of the Munc18 protein family (also called n-Secl). Our results indicate that CFTR function in epithelial cells is regulated by an interplay between syntaxin and Munc18 isoforms.

Animals↗
PubMed1997

Two basic amino acids in the second inner loop of the interleukin-8 receptor are essential for Galpha16 coupling.

The involvement of basic residues of interleukin(IL)-8 receptors in coupling to the Gi and G16 proteins was investigated by using a series of IL-8 receptor mutants. Substitution of the basic amino acids in the third inner loop of the receptor does not alter the abilities of the receptor mutants to activate recombinant Galpha16 or phosphoinositide-specific phospholipase C (PLC) beta2 expressed in COS-7 cells. However, an IL-8 receptor mutant with double mutations at residues Lys158 and Arg159 of the second inner loop loses its abilities to activate Galpha16 but retains its ability to activate PLC beta2. The activation of PLC beta2 by an IL-8 receptor that is sensitive to pertussis toxin has been previously demonstrated to be mediated through Gbetagamma. Surprisingly, the IL-8 receptor mutants with substitution of Ala for either residue Lys158 or Arg159 can still activate Galpha16, which suggests that either of the two basic residues in the second inner loop of the IL-8 receptor is sufficient for Galpha16 coupling.

Amino Acid Sequence↗
PubMed1997

Roles of phospholipase C beta2 in chemoattractant-elicited responses.

The physiological roles of phospholipase C (PLC) beta2 in hematopoiesis, leukocyte function, and host defense against infection were investigated using a mouse line that lacks PLC beta2. PLC beta2 deficiency did not affect hematopoiesis, but it blocked chemoattractant-induced Ca2+ release, superoxide production, and MAC-1 up-regulation in neutrophils. In view of these effects, it was surprising that the absence of PLC beta2 enhanced chemotaxis of different leukocyte populations and sensitized the in vivo response of the PLC beta2-deficient mice to bacteria, viruses, and immune complexes. These data raise questions about the roles that PLC beta2 may play in signal transduction induced by chemoattractants in leukocytes.

Animals↗
PubMed1997

Human gamma-aminobutyric acid-type A receptor alpha5 subunit gene (GABRA5): characterization and structural organization of the 5' flanking region.

The gamma-aminobutyric acid-type A receptor alpha5 subunit gene (GABRA5) is widely expressed in brain and localized to the imprinted human chromosome 15q11-q13. A combination of cDNA library screening and 5' RACE analysis led to identification of three distinct mRNA isoforms of GABRA5 in human adult and fetal brain tissues, each of which differs only in the noncoding 5' UTR sequence. Alignment of the genomic and cDNA sequences of GABRA5 revealed that the mRNA isoforms resulted from three alternative first exons 1A, 1B, and 1C. Northern blot analysis showed that the expression of GABRA5 was not only tissue specific but region specific in brain. CAT reporter assays revealed promoter elements in the 5' proximity of each first exon. The GABRA5 promoter regions lacked TATA and CCAAT boxes but contained several other consensus transcriptional factor recognition sequences. These findings suggest that the differential exon 1 usage of GABRA5 arises as a consequence of alternative promoter activation.

Adult↗
PubMed1997

Protein binding and signaling properties of RIN1 suggest a unique effector function.

Human RIN1 was first characterized as a RAS binding protein based on the properties of its carboxyl-terminal domain. We now show that full-length RIN1 interacts with activated RAS in mammalian cells and defines a minimum region of 434 aa required for efficient RAS binding. RIN1 interacts with the "effector domain" of RAS and employs some RAS determinants that are common to, and others that are distinct from, those required for the binding of RAF1, a known RAS effector. The same domain of RIN1 that binds RAS also interacts with 14-3-3 proteins, extending the similarity between RIN1 and other RAS effectors. When expressed in mammalian cells, the RAS binding domain of RIN1 can act as a dominant negative signal transduction blocker. The amino-terminal domain of RIN1 contains a proline-rich sequence similar to consensus Src homology 3 (SH3) binding regions. This RIN1 sequence shows preferential binding to the ABL-SH3 domain in vitro. Moreover, the amino-terminal domain of RIN1 directly associates with, and is tyrosine phosphorylated by, c-ABL. In addition, RIN1 encodes a functional SH2 domain that has the potential to activate downstream signals. These data suggest that RIN1 is able to mediate multiple signals. A differential pattern of expression and alternate splicing indicate several levels of RIN1 regulation.

3T3 Cells↗
PubMed1997

(-)-Deprenyl protection of 1-methyl-4 phenylpyridium ion (MPP+)-induced apoptosis independent of MAO-B inhibition.

Selective loss of central dopaminergic neurons in vitro and in vivo can be initiated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) through its metabolite phenylpyridium ion (MPP+). Such MPTP-mediated cytotoxicity can be blocked by (-)-Deprenyl, a monoamine oxidase (MAO)-B inhibitor, but the exact mechanisms of MPP(+)-induced cytotoxicity and (-)-Deprenyl's protection against such neurotoxicity are not fully understood. Using a hybrid clone MES 23.5, a dopaminergic cell line that does not contain MAO-B, we document that MPP+ induces apoptotic cell death. Application of (-)-Deprenyl at concentrations of 0.1-10 microM significantly reduces MPP(+)-induced apoptosis in MES 23.5 cells; (-)-Deprenyl at higher concentrations (> 100 microM) that completely inhibit MAO-B activity, however, induces apoptosis. Pretreatment with N-(2-aminoethyl)-p-chlorobenzamide (Ro 16-6491), a selective MAO-B inhibitor, does not protect MES 23.5 cells against MPP(+)-induced cell death. These results suggest that the protective action of (-)-Deprenyl against MPP+ neuro-toxicity in dopaminergic cell line may be independent of the inhibition of MAO-B.

1-Methyl-4-phenylpyridinium↗
PubMed1997

Visual acuity and contrast sensitivity for individual Sloan letters.

Sloan letter optotypes are used frequently to evaluate visual impairment, and scoring procedures have been developed that are based on the numbers of letters that are identified correctly. However, previous studies have presented conflicting evidence regarding the relative identifiability of the individual Sloan letters. To investigate this issue further, we measured psychometric functions for the identification of each of the 10 Sloan letters, with individual letters presented in random order on the gray-scale display of a Macintosh computer-based testing system. Data were obtained from three visually normal subjects under each of three conditions: (1) as a function of log contrast at a relatively large letter size; (2) as a function of log contrast at a letter size near the acuity limit; and (3) as a function of log MAR (minimum angle of resolution) at maximum letter contrast. Estimates of threshold log contrast and threshold log MAR were derived from best-fitting Weibull functions. Threshold log contrast for small letters showed the greatest interletter variability. There was relatively little interletter variability in either threshold log contrast for large letters or threshold log MAR for high-contrast letters. However, due to the relatively steep psychometric functions under these latter two conditions, the different Sloan letters had considerably different percent correct values near threshold. The overall pattern of results suggests that the contrast sensitivity functions for individual Sloan letters are displaced laterally along a log MAR axis, while their vertical positions are essentially equivalent.

Adult↗
PubMed1997

Experimental immune-mediated damage of septal cholinergic neurons.

Degeneration of cholinergic neurons in the medial septum and the diagonal band of Broca is a frequent neuropathological feature of Alzheimer's disease. To determine whether an immune process can injure these basal forebrain cholinergic neurons, we serially immunized guinea pigs with septal cholinergic hybrid cells (SN-56). Following immunization, a relatively selective damage of septal cholinergic neurons, reduction in septal choline acetyltransferase (ChAT) activity and decrease in acetylcholine release in hippocampus were detected. Serum IgG from guinea pigs immunized with SN-56 cells and stereotactically injected into the medial septal region of rats produced a loss of ChAT activity in the medial septum, frontal cortex and hippocampus, together with impairment of learning and long term spatial memory. These data suggest that relatively selective damage to septal cholinergic neurons can be caused by an immune-mediated process in experimental animals.

Alzheimer Disease↗
PubMed1997

High-level expression of cecropin CMIV in E. coli from a fusion construct containing the human tumor necrosis factor.

Cecropin CMIV gene was fused to the 3'-terminus of the mutated tumor necrosis factor (TNFb) gene and the fusion gene was directly under the control of an inducible T7 promoter in pET-11d. This fusion gene was overexpressed in Escherichia coli with an expression level of approximate 40%-50% of total cellular proteins, and was produced mainly in the form of inclusion body. Peptide with antibacterial activity was obtained by cleaving the fusion protein with CNBr.

Escherichia coli↗
PubMed1997

Targeted expression of a dominant negative epidermal growth factor receptor in the mammary gland of transgenic mice inhibits pubertal mammary duct development.

The epidermal growth factor (EGF) system has been thought to play an important role in normal mammary development and carcinogenesis. To study the role of the EGF receptor (EGFR) in mammary development, we developed a transgenic mouse model in which a C-terminal truncated mouse EGFR (EGFR-TR) was expressed in the mouse mammary epithelium under the control of the mouse mammary tumor virus long terminal repeat. The EGFR-TR lacks most of the cytoplasmic domain of the receptor, including the entire protein tyrosine kinase domain. In cultured cells, we show that it acts in a dominant negative manner in EGF-signaled EGFR autophosphorylation. Several lines of mice were characterized and shown to express the transgene at the mRNA and protein levels not only in the mammary gland but also in the salivary glands, epididymis, and prostate. In postpubertal virgin female mice, the expression of the EGFR-TR in the mammary glands was greater than the expression of the endogenous wild type EGFR. In these virgin mice, inhibition in mammary ductal development and a decrease of mammary epithelial DNA synthesis were observed beginning at 5-6 weeks. The inhibition of duct development was most apparent by 15-16 weeks, resulting in a significant defect in ductal branching and outgrowth and an apparent overall decrease in the size of the mammary glands. However, during pregnancy, expression of the endogenous wild type EGFR was markedly increased relative to the EGFR-TR and, at this stage, normal presecretory alveoli developed from the hypoplastic duct tree. Postpartum, normal lactation occurred. Despite EGFR-TR expression in other tissues, no morphological abnormalities were observed. This model demonstrates that the EGFR-TR behaves as a dominant negative regulator of the EGFR system in vivo and that the EGFR system plays an important role in mammary ductal development.

Aging↗