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X Ye

Publications and source records attributed to X Ye.

At least 181 records · Page 10Linked to original sources
PubMed1996

[Changes of N-methyl-D-aspartate receptor in spinal cord after trauma].

N-methyl-D-aspartate (NMDA) receptor-mediated events have implicated in the pathophysiology of posttraumatic spinal cord injury. In the present study, [3H] CPP was used as ligand to analyse the changes in NMDA receptor-binding sites in synaptic plasma membranes (SPM) isolated from rat spinal cord after impact trauma at T10. Radio-binding assays of [3H] CPP showed a specific and saturable binding site for [3H] CPP in spinal cord tissue. Scatchard analysis revealed the binding of [3H] CPP has one site with low affinity (Kd = 3.51 < or = 0.26 nM) and binding density (Bmax = 662.82 < or = 47.59 fmol/mg protein). [3H] CPP binding to NMDA receptor at the thoracic segment was significantly (P < 0.01) decreased posttrauma. Time-course studies demonstrated significantly decrease in the binding of [3H] CPP at 4 h after spinal cord injury with recovery by 24 h. Scatchard analysis results indicate that the posttrauma decrease of [3H] CPP-binding resulted from alteration in receptor binding density The data from the present study provided further evidence for a role for NMDA receptor-mediated mechanisms in the pathological consequences of spinal cord injury. The acute reduction in [3H] CPP-binding after trauma may reflect down-regulation of NMDA receptor as a consequence of posttraumatic glutamate release and may serve to limit excitotoxin-induced injury.

Animals↗
PubMed1996

[Clinical application of enzyme linked immunosorbent assay in testing antibodies against cochlear tissues and nerve tissues].

Fifty-two patients with idiopathic sensorineural hearing loss and 20 controls were examined by enzyme linked immunosorbent assay (ELISA) with cow cochlear antigen (CCAg) and cow cochlear nerve antigen (CCNAg). The antibody level against CCAg was 0.3811 +/- 0.743 in the control group and 0.9241 +/- 0.2408 in the experimental group (OD, x +/- 2s, P < 0.01). Compared with the x +/- 2s antibody level of the control group, the antibody level of 24 of 52 (46%) patients of the experimental group was positive. The antibody level against CCNAg was 0.2254 +/- 0.382 in the control group and 0.2331 +/- 0.656 in the experimental group (P > 0.05). Compared with the x +/- 2s antibody level of the control group, the antibody level of 6 of 52 patients (11.5%) of the experimental group was elevated. It is suggested that ELISA method can be used as quantitatively in the diagnosis of autoimmune inner ear diseases. Moreover, the serum antibodies against CCNAg detected in this experiment suggest that some of autoimmune inner diseases might be retrocochlear.

Adolescent↗
PubMed1995

A 62-kDa mitotic apparatus protein required for mitotic progression is sequestered to the interphase nucleus by associating with the chromosomes during anaphase.

A protein component of 62-kDa (p62) in the mitotic apparatus of the sea urchin embryo has been shown to be important for the proper progression of mitosis [Dinsmore and Sloboda, 1989: Cell 57:127-134]. To study the subcellular distribution of p62 during the cell cycle of sea urchin embryos, indirect immunofluorescence microscopy was used coupled to a modified detergent extraction procedure. The improved fluorescent images obtained by this procedure provide new information concerning the subcellular localization of p62 during the cell cycle that could not be obtained with previous conventional staining procedures [Johnston and Sloboda, 1992: J. Cell Biol. 119:843-854]. Using affinity purified antibodies to p62, we observed a cell cycle-dependent localization of p62 to the chromosomes/chromatin. Prior to nuclear envelope breakdown of the first or second cell cycle, p62 localizes to chromatin in the nucleus. During mitosis, p62 associates with the region of the spindle occupied by the microtubules of the mitotic apparatus. As anaphase proceeds, but before the nuclear envelope reforms, p62 becomes progressively associated with the chromosomes. Thus, p62 is incorporated into the forming interphase nucleus due to its association with chromosomes during late anaphase, rather than by active translocation into the newly formed daughter nuclei through the nuclear pores. The protein is not unique to marine embryos, as demonstrated by immunofluorescence of Y-1 cells, a mouse adrenal tumor cell line. In these cells, the localization of p62 is similar to the localization of the protein in echinoderm embryos, suggesting its possible function in mitotic progression in mammalian somatic cells as well.

Anaphase↗
PubMed1995

In vivo calcium phosphate formation induced by sol-gel-prepared silica.

Implantation with plugs made of a porous sol-gel-prepared silica into the femurs of goats demonstrated that a calcium phosphate was formed both on the silica plugs and within the pores inside the silica plugs 12 weeks postoperatively. This observation indicates that a highly hydrated silica surface is effectively catalytic for calcium phosphate nucleation. Calcification can be triggered in physiologic solution under stimulation of the silica gel. A high level of silicon in the uncalcified osteoid region of young bone is thus thought to provide a number of SiOH groups for initiating calcium phosphate formation. Our results provide some information about the mechanism of calcium phosphate mineralization in higher animals. We believe that heterogeneous nucleation of apatite can be induced from metastable calcium phosphate solutions including physiologic fluids on those specific surfaces of materials, where there are abundant acidic OH groups.

Animals↗
PubMed1995

Recent progress in research on Tripterygium: a male antifertility plant.

The discovery of the reversible antifertility action of an extract from Tripterygium wilfordii both in male rats and in men in 1986 stimulated worldwide interest. International and national collaborations aimed at the bioassay-directed sub-fractionation of materials extracted from the plant was then organized and to date, a series of six male antifertility diterpene epoxides have been isolated. Their chemical structures have been identified and found to be triptolide, tripdiolide, triptolidenol, tripchlorolide, 16-hydroxytriptolide and T7/19 (structure not yet published). At the ED95 dosage levels, they act mainly on metamorphosing spermatids and testicular and epdidymal spermatozoa with exfoliation and inhibition of basic nuclear protein turnover of late spermatids, delayed spermiation and sperm head-tail separation and microtubule, microfilament and membrane damages. A preliminary toxic evaluation indicated that these compounds were immunosuppressive at dose levels 5-12 times their antifertility doses. Immuno-suppression is an important weakness for an antifertility agent, but if the immuno-suppressive dose of a drug is much higher than its antifertility dose, it could yet be regarded as a safe contraceptive. Therefore, in the safety evaluation of compounds isolated from Tripterygium wilfordii, it warrants our attention to probe deeply into their precise dose/immuno-effect relationship.

Animals↗
PubMed1995

Molecular recognition in the bovine immunodeficiency virus Tat peptide-TAR RNA complex.

BACKGROUND: In lentiviruses such as human immunodeficiency virus (HIV) and bovine immunodeficiency virus (BIV), the Tat (trans-activating) protein enhances transcription of the viral RNA by complexing to the 5'-end of the transcribed mRNA, at a region known as TAR (the trans-activation response element). Identification of the determinants that account for specific molecular recognition requires a high resolution structure of the Tat peptide-TAR RNA complex. RESULTS: We report here on the structural characterization of a complex of the recognition domains of BIV Tat and TAR in aqueous solution using a combination of NMR and molecular dynamics. The 17-mer Tat peptide recognition domain folds into a beta-hairpin and penetrates in an edge-on orientation deep into a widened major groove of the 28-mer TAR RNA recognition domain in the complex. The RNA fold is defined, in part, by two uracil bulged bases; U12 has a looped-out conformation that widens the major groove and U10 forms a U.AU base triple that buttresses the RNA helix. Together, these bulged bases induce a approximately 40 degree bend between the two helical stems of the TAR RNA in the complex. A set of specific intermolecular hydrogen bonds between arginine side chains and the major-groove edge of guanine residues contributes to sequence specificity. These peptide-RNA contacts are complemented by other intermolecular hydrogen bonds and intermolecular hydrophobic packing contacts involving glycine and isoleucine side chains. CONCLUSIONS: We have identified a new structural motif for protein-RNA recognition, a beta-hairpin peptide that interacts with the RNA major groove. Specificity is associated with formation of a novel RNA structural motif, a U.AU base triple, which facilitates hydrogen bonding of an arginine residue to a guanine and to a backbone phosphate. These results should facilitate the design of inhibitors that can disrupt HIV Tat-TAR association.

Animals↗
PubMed1995

The pathological changes in peripheral organs of scrapie-infected animals.

Scrapie is an unconventional neurodegenerative disease in sheep and goats that has been known in Europe for over 260 Years. The scrapie agents affect the brain and are transmissible from animal to animal. Key features of scrapie infections are abnormal behavior and deficits in motor function. These clinical findings can be related to the damage found in the central nervous system. In some scrapie strain-host model systems there are other manifestations of disease that appear to be related to pathological changes found in the peripheral organs, especially in the endocrine organs such as pituitary, adrenal glands, the islet of Langerhans and ovary. In those model systems in which extensive histopathological changes have been seen in peripheral organs, the titers of scrapie infectivity and the levels of the scrapie specific protein, PrPSc, are relatively low in the affected organs. These data suggest but do not prove that changes in peripheral organs are secondary to the scrapie-induced neurodegeneration that is occurring in the brain. In some scrapie strain-host combinations, obesity and aberrant glucose metabolism are seen in the preclinical and clinical phases of the incubation period. There appear to be two pathways that lead to these particular clinical manifestations. In SJL mice infected by the ME7 or 22L strains of mouse-adapted scrapie and in some scrapie-infected sheep, the mechanism is related to changes induced in the hypothalamic-pituitary-adrenal axis. The other pathway is exemplified by hamsters infected with two hamster-adapted scrapie strains, 139H and 22CH; it appears that lesions found in the hypothalamic-islets of Langerhans axis are critical. A number of reviews on the pathological changes in the central nervous system have been published and therefore, in this review article, we focus on the gross and histopathological changes in peripheral organs in several scrapie strain-host combinations. The changes induced in peripheral organs in a number of scrapie strain-host combinations expand the number of diseases in which the unconventional slow infections could serve as a model. Further work in this area could help us to understand the mechanisms and pathways of the pathological changes found in the peripheral organs of the scrapie-infected animals.

Animals↗
PubMed1994

Ablation of E2A in recombinant adenoviruses improves transgene persistence and decreases inflammatory response in mouse liver.

First-generation recombinant adenoviruses that lack E1 sequences have shown tremendous promise in animal and human models of gene therapy. Important limitations of these vectors are that recombinant gene expression is transient and inflammation occurs at the site of gene transfer. Our hypothesis for generating vectors with increased persistence is that present recombinant adenoviruses express viral proteins that stimulate cellular immune responses leading to destruction of the infected cells and repopulation of the organ with non-transgene-containing cells. This model predicts that further crippling of the virus will improve persistence and diminish pathology. We describe in this report second-generation recombinant adenoviruses harboring a beta-galactosidase-expressing transgene in which a temperature-sensitive mutation has been introduced into the E2A gene of an E1-deleted recombinant. At nonpermissive temperature, this virus fails to express late gene products, even when E1 is expressed in trans. The biology of this recombinant was studied in vivo in the context of mouse liver, a setting that is permissive for adenovirus type 5 replication. Animals that received the second-generation virus expressed the transgene for at least 70 days, whereas expression of the first-generation virus was no longer than 14 days. In addition, the inflammatory response, as measured by infiltration of CD8+ T cells, was blunted and delayed in livers infected with second-generation virus. These studies illustrate that modifications that disrupt structural protein expression in recombinant adenoviruses may be useful in enhancing their utility for gene therapy.

Adenoviridae↗
PubMed1994

Isolation and characterization of the Drosophila melanogaster gene encoding translation-initiation factor eIF-2 beta.

Drosophila melanogaster cDNA clones encoding the beta subunit of translation initiation factor 2 (eIF-2) were isolated and sequenced. The longest cDNA predicts a protein of 312 amino acids (aa), which possesses a putative RNA-binding motif and a highly charged N-terminal region composed of three basic polylysine blocks. The aa sequence comparison of D. melanogaster eIF-2 beta with its human and yeast counterparts demonstrates a high degree of similarity, especially within the C-terminal region. Northern analysis indicates quasi-constitutive expression of eIF-2 beta throughout D. melanogaster development.

Amino Acid Sequence↗
PubMed1994

Timely immunization subverts the development of peripheral nonresponsiveness and suppresses tumor development in simian virus 40 tumor antigen-transgenic mice.

Tolerance to tumor cell-expressed molecules and selection of cells that evade immune surveillance during tumor progression create effective barriers to immunotherapy. We investigated the cytotoxic T-lymphocyte response to simian virus 40 (SV40) tumor (T/t) antigen in two lineages of transgenic mice bearing the same rat insulin promoter-SV40 T/t antigen (RIP Tag) hybrid gene. RIP1-Tag2 mice, which express Tag as embryos, are tolerant to Tag, whereas RIP1-Tag4 mice, which express the transgene in pancreatic islet beta cells several weeks after birth and develop insulinomas, can be immunized to generate active Tag-specific cytotoxic T lymphocytes as determined by in vitro assays. Indeed, RIP1-Tag4 mice immunized with Tag by SV40 infection prior to the time of endogenous transgene expression also mount an effective in vivo cellular immune response to the Tag-expressing pancreatic beta cells, and Tag-induced tumor growth is significantly delayed (up to 1 year). However, after the transgene is expressed, RIP1-Tag4 mice are unable to mount a tumor-inhibiting response upon immunization, although Tag-specific cytotoxic T cells can still be demonstrated in vitro. Our data suggest that Tag-specific T cells are rendered unresponsive in vivo in RIP1-Tag4 mice and that the establishment of this unresponsiveness to Tag can be prevented by SV40 immunization only before the onset of the transgene expression. In the older, successfully immunized mouse, decreased immune surveillance and selection of cells with down-regulation of major histocompatibility complex class I expression most likely set the stage for insulinoma development.

Animals↗
PubMed1994

Effect of infection with the 139H scrapie strain on the number, area and/or location of hypothalamic CRF- and VP-immunostained neurons.

Scrapie is a transmissible neurodegenerative disease which shares some characteristics with Alzheimer disease (AD). Recent studies show abnormal enlargement of the adrenal glands and kidneys in 139H-affected hamsters. Using immunocytochemical techniques with antibodies to corticotropin-releasing factor (CRF) and vasopressin (VP), we observed the following: (1) a significantly higher number of CRF-immunostained neurons in the preoptic nucleus of hypothalamus of 139H-affected hamsters than controls; (2) the area of VP-immunostained (ir-VP) neurons in the lateral hypothalamus, which includes the internuclear group of magnocellular neurons and the nucleus circularis, was significantly lower for 139H-affected hamsters than for controls; and (3) no significant difference between 139H-affected and control hamsters with regard to the number of ir-VP neurons in the dorsal-medial hypothalamus (DMH), including the paraventricular hypothalamus, or the supraoptic nuclei. However, the population of ir-VP neurons in the DMH shifted to the anterior part of the hypothalamus in 139H-affected hamsters. Three-dimensional models of the immunostaining were prepared and these provide clear depictions of the changes noted. The changes in the CRF and VP systems in 139H-affected hamsters suggest that the neuroendocrine system can be affected by unconventional slow infections.

Animals↗
PubMed1994

Histopathological changes in the islets of Langerhans in scrapie 139H-affected hamsters.

Previous studies showed that the 139H strain of scrapie injected into hamsters caused obesity, a marked hypertrophy of the islets of Langerhans, generalized endocrinopathy and marked hypoglycaemia-hyperinsulinaemia. In the current study, female weanling Syrian hamsters (LVG/LAK strain) were inoculated intracerebrally with scrapie strain 139H or 263K, or with normal hamster brain. Sections of the pancreas stained with haematoxylin and eosin or Gomori's one-step trichrome were examined by light microscopy. The 139H-affected hamsters showed extensive vacuolization, cellular hypertrophy, cellular atrophy, cytoplasmic vesicles and nuclear pathological changes in the islets of Langerhans. Also observed were abnormal structures, termed blood vessel cores, in the islets of 139H-affected hamsters. These structures were almost always centrally located within islets and were surrounded by B cells, some of which were abnormally elongated. None of these pathological changes were seen in the islets of Langerhans in control or 263K-affected hamsters. The level of scrapie-specific protease resistant protein (PrPSc) in pancreas was much lower than that in brain, a finding consistent with previous data showing low scrapie infectivity titres in pancreas.

Animals↗
PubMed1994

Hyperplasia and hypertrophy of B cells in the islets of Langerhans in hamsters infected with the 139H strain of scrapie.

Previous studies showed that in hamsters the 139H, but not the 263K, scrapie strain caused a marked increase in pancreatic size and led to obesity, hypoglycaemia and striking hyperinsulinaemia. In the preceding paper (Ye et al., 1994), the islets of Langerhans in 139H-affected hamsters showed cellular atrophy, fibrosis, cytoplasmic vesicles and nuclear pathological changes. In the present study, the profiles of pancreatic islets were classified into three sizes with an image analyzer. The number and total area covered by "small" islet profiles were less in 139H-affected than in normal hamsters. In contrast, the number and the area of "medium" and "large" islet profiles were significantly greater in 139H than in normal hamsters. With antibodies to insulin, glucagon, somatostatin and pancreatic polypeptide, the proportions of B, A, D and F cells were determined. With somatostatin-positive cells arbitrarily given a value of 1, the ratio of B:A:D:F cells in the islets was 27:5:1:0.04 in normal hamsters and 122:7:1:0.04 in 139H-affected hamsters. The increase in B cells would account for the islet enlargement and the hypoglycaemia-hyperinsulinaemia seen in 139H-affected hamsters.

Animals↗
PubMed1994

A numerical analysis of a focused ultrasound technique to measure perfusion.

A noninvasive technique to measure perfusion using a focused ultrasound heating source and a thermistor placed on the surface of a tissue is proposed. The method is numerically examined in a model of the canine kidney. The perfusion measurement is shown to depend on several transducer and tissue thermal properties. A two level fractional factorial design simulation is used to map out a parameter value combination that maximizes the sensitivity of the measurement. A technique to numerically assess the uncertainty in the measurement due to uncertainties in the tissue and transducer parameter values is also described. The effects of the medulla and a subcapsular surface layer in the kidney are examined. It is determined that the maximum error in the measured perfusion rate due to all the factors considered is 17 percent for a kidney with a nominal perfusion rate of 300 mL/100g-min and a surface layer of 0.04 cm thickness.

Animals↗
PubMed1994

[Effect of trifluoroacetoprimaquine on erythrocytic schizonts of rodent malaria].

Effect of trifluoroacetoprimaquine oxalate (M8506) and primaquine (PQ) on blood schizonts of Plasmodium berghei were determined using the method of 4-day suppressive test within extended observation period of 60 d. When mice infected with Plasmodium berghei ANKA strain were treated ig with M8506 or PQ at a same daily dose of 20 mg/kg for 4 d, the cure rates were 100% and 90%, respectively. The two drugs also showed prominent suppressive effects on chloroquine-resistant P. berghei NS line and pyronarine-resistant P. berghei RP line, but the parasitemia still remained positive or all of the mice treated recrudesced, indicating the existence of cross resistance between trifluoroacetoprimaquine and other erythrocytic schizonticides, including chloroquine and pyronaridine.

Animals↗
PubMed1994

A numerical study of rapid heating for high temperature radio frequency hyperthermia.

Hyperthermia is a promising adjuvant cancer treatment modality. However, unresolved engineering problems with the production and regulation of temperature distributions within tissues in vivo have frustrated repeated efforts to implement clinical hyperthermia protocols. A major technical problem with hyperthermia production in vivo is the cooling effect caused by circulating blood in larger vessels. Larger blood vessels, when located in heated tumors, can prevent achievement of sufficiently high temperatures, resulting in loss of therapeutic effect. One possible way of circumventing this problem is the delivery of a critical heat dose during a short-term, high-temperature treatment episode to minimize cooling from blood flow. We investigated the concept of such rapid, high-temperature heating of tissue in a two-dimensional finite element numerical model. The model demonstrates the feasibility of interstitial radiofrequency delivery of a therapeutic heat dose, equivalent to 30 min at 43 degrees C, to a 1 cm3 tumor during a 60-s period. The model assumes circulation of cooling fluid through hollow electrodes. A post processor has been designed to display a 3-D image of the temperature distribution, electric field, and thermal dose delivered to a unit volume within the heated tissue.

Blood Circulation↗
PubMed1994

Down-regulation of MHC class I antigen in insulinoma cells controlled by the R1 element of the H-2 enhancer.

Tumorigenesis in mice of the rat insulin promoter [RIP]-simian virus 40 tumor antigen [SV40 Tag] transgenic lineages, RIP1-Tag2 and RIP1-Tag4, is a process initiated by expression of SV40 Tag in pancreatic beta cells, evolution of islet cell hyperplasia and insulinoma appearance. Analysis of major histocompatibility complex [MHC] class I gene expression during this process revealed a normal level of MHC class I molecules at the surface of pancreatic islet cells of RIP1-Tag4 mice, while hyperplastic islets from the same mice contained cells expressing a normal level and cells expressing a low level of MHC class I antigen. Insulinomas themselves expressed very low levels or no MHC class I gene product. Thus, down-regulation of MHC class I gene appears to accompany tumor progression of SV40 Tag-transformed beta islet cells. MHC class I antigen expression in a series of clonally derived cell lines of beta cell origin from different SV40 Tag-induced insulinomas ranged from quite low to undetectable, although expression was inducible by interferon-gamma. Nuclear run-on and transient transfection analyses indicated that expression of the MHC class I gene in these cells in controlled at the transcriptional level, and that the decreased expression is paralleled by reduced binding of transcription factors to the R1 element of the H-2 enhancer.

Animals↗