PubMed Health⌕ Search

Biomedical subjects

Y Wu

Publications and source records attributed to Y Wu.

At least 1,045 records · Page 58Linked to original sources
PubMed1994

Radiofrequency current catheter ablation of the left atrioventricular accessory pathways with paroxysmal supraventricular tachycardia.

Seventy patients with left atrioventricular accessory pathways and paroxysmal supraventricular tachycardia (PSVT) underwent radiofrequency catheter ablation (RFCA). The success rate was 94.3%. Among these patients, 26 had manifest preexcitation syndrome, and 44 had concealed preexcitation. Eighteen patients with concealed preexcitation underwent coronary sinus (CS) pacing, and delta wave appeared in 15. The keys to successful RFCA were correct positioning of the radiofrequency (RF) catheter tip, A/V amplitude ratio, AV interval (in sinus rhythm) and VA interval (during SVT or ventricular pacing). After 1-14 months of follow-up, two patients had supraventricular tachycardia (SVT) recurrence.

Adolescent↗
PubMed1994

[Enhancing effects of Herpesvirus hominis on sodium glutamate neurotoxicity].

The neurotoxic effects of sodium glutamate (MSG, 2.5 g.kg-1 sc) and the enhancing effects of neurotropic Herpesvirus hominis (HVH, 0.2 ml/mouse ip) on MSG toxicity were studied through histomorphological observations, together with detection of the concentration of both mitochondrial protein bound Ca2+ and intracellular free Ca2+ ([Ca2+]i) by the Tb3+ fluorescent probe and Ca2+ indicator Fura-2/AM, respectively. It was found that in 10-d-old mice the neurons in arcuate hypothalamic nucleus degenerated severely after treatment with HVH+MSG, showing swollen edematous cytoplasm, dark pyknotic nuclei as well as a decrease in the amount of the neurons. The hypothalamic and spinal cord mitochondrial Tb3+ relative fluorescent intensity increased from 20 +/- 3 and 20 +/- 1 to 28 +/- 5 and 34 +/- 6, ie, the mitochondrial protein bound Ca2+ reduced significantly. MSG elevated the [Ca2+]i levels from 0.11 +/- 0.03 to 0.69 +/- 0.19 mumol.L-1 by not only stimulating the Ca2+ influx but also releasing the Ca2+ from intracellular stores. These findings suggested that MSG neurotoxicity was probably related to the overloading of neuroplasmic Ca2+, the destruction of neuronal abilities to deplete or sequester the intracellular Ca2+, as well as the irreversible neuronal injury and death.

Animals↗
PubMed1994

[Obliteration of empty sella for therapy of empty sella syndrome by transsphenoidal and transfrontal approach].

Seven cases of empty sella syndrome were reported, among them 2 cases were primary empty sella syndrome, 5 cases were secondary empty sella syndrome. 5 cases were operated with the obliteration by transsphenoidal approach, 2 cases were operated by transfrontal approach. 6 cases were cured, the symptoms in one case was not improved due to the primary hydrocephalus. This syndrome is associated with defect of sellar diaphragm, benign intracranial hypertension, long-term administration of Bromocriptine, surgery and radiotherapy of pituitary gland. Main clinical features are headache, damage of vision and visual fields, hypopituitarism. Obliteration of empty sella by transsphenoidal approach is a simple and effective method.

Adult↗
PubMed1994

Basilar artery migraine. Reversible ischemia demonstrated by Tc-99m HMPAO brain SPECT.

The authors present a case of basilar artery migraine in a 33-year-old woman who was initially misdiagnosed as having a cerebrovascular or mental disorder and subjected to MRI and cerebral angiography, which, however, did not show any pathologic findings. During admission to the university hospital, she lost consciousness. An emergency Tc-99m HMPAO brain SPECT showed a significant decrease of regional cerebral blood flow in the right temporal and occipital cortices, and right cerebellar hemisphere, where regional cerebral blood flow was decreased by 10-24% as compared to the left side. The second brain SPECT during a symptom-free phase showed the reversion of regional cerebral blood flow to normal in these areas. Basilar artery migraine was diagnosed by the finding of reversible ischemia in the territory of the right basilar artery on brain SPECT images and the clinical picture.

Adult↗
PubMed1994

[Urinary luteinizing hormone surge and outcome of in vitro fertilization and embryo transfer].

This study was based on 150 in vitro fertilization cycles carried out between June 1991 and July 1992. All the patients had blocked or dysfunctional fallopian tubes as the cause of infertility. Clomiphene citrate, human menopausal gonadotropin and hCG were used for controlled ovarian hyperstimulation. The results showed that an urinary luteinizing hormone (LH) surge (LH > 40 IU/L) occurred in 41 cycles (27.33%), a high LH level (LH = 40 IU/L) in 16 (10.67%), and normal (LH < 40 IU/L) LH level in 93 cycles, before hCG injection. The average number of oocytes recovered was not affected by the occurrence of a spontaneous LH surge, but the cleavage rate of the fertilized eggs was significantly lower than that in the cycles without LH surge and the rate of clinical pregnancy was also lower, although of no statistical significance. Our results demonstrated that the LH surge had an adverse effect on the egg quality and therefore would probably reduce the chances of pregnancy success.

Adult↗
PubMed1994

Regional changes in [3H]zolpidem binding to brain benzodiazepine receptors in flurazepam tolerant rat: comparison with changes in [3H]flunitrazepam binding.

Regional downregulation of brain benzodiazepine (BZ) receptors was studied in rats treated with flurazepam or diazepam protocols known to produce anticonvulsant tolerance. Zolpidem, a selective BZ1 receptor agonist, was used to detect BZ1 receptors; flunitrazepam, a nonselective BZ receptor agonist, was used to detect the total BZ receptor population. Rats were treated 4 weeks with flurazepam, then sacrificed immediately or 48 hr later. After flurazepam treatment, the maximal binding capacity of [3H]zolpidem binding decreased 22% in the cerebral cortex, 32% in the cerebellum and 25% in the hippocampus. The Kd increased in the cerebellum. The maximal binding capacity of [3H]flunitrazepam binding decreased by 13% in the cerebral cortex and 14% in the hippocampus, but did not change in the cerebellum. The Kd increased in the hippocampus. At 48 hr after flurazepam treatment, there was no significant difference in [3H]zolpidem binding between treated and control rats. In rats treated 3 weeks with diazepam released from s.c. reservoirs, there was no change in [3H]zolpidem binding. The data suggest that chronic flurazepam treatment causes downregulation primarily involving BZ1 receptors. The differing effects on [3H]-zolpidem and [3H]flunitrazepam binding, especially in the cerebellum in which more than 90% of the receptors are the BZ1 subtype, may indicate a shift in BZ receptor subtypes in flurazepam-tolerant rats, suggesting a change in the subunit composition or conformation of gamma-aminobutyric acidA/BZ receptors.

Animals↗
PubMed1994

Prostacyclin production in acute, chronic, and long-term experimental portal hypertension.

BACKGROUND: Chronic portal hypertension (PHT) is characterized by a high portosystemic shunt (PSS) and increased splanchnic blood flow. It has been suggested that the splanchnic vasodilator, prostacyclin (PGI2), mediates this increased flow. We studied splanchnic PGI2 production both in normal rabbits and in three groups of rabbits after partial portal vein ligation (PVL-PHT): acute (within 30 minutes of ligation), chronic (3 weeks after ligation), and long-term (3 months after ligation) to determine whether increased splanchnic production is a mechanism for the elevated PGI2 in PHT. METHODS: Levels of 6-keto prostaglandin F1 alpha were determined by radioimmunoassay, and splanchnic hemodynamics were measured with Doppler flowmetry in four groups of rabbits: portal normotensive rabbits, and PVL-PHT rabbits 30 minutes, 3 weeks, or 3 months after partial PVL. Splanchnic PGI2 production (PGI2 PROD) was then calculated. RESULTS: Portal pressure and PSS in chronic and long-term groups were significantly elevated in all groups compared with normals (p < 0.001). Splanchnic blood flow initially fell from 84 +/- 4.8 to 37.4 +/- 7 ml/min/100 gm immediately and then rose to 144.7 +/- 9.6 ml/min/100 gm and 137 +/- 15 ml/min/100 gm at 3 weeks and 3 months after ligation, respectively. PGI2 production rose immediately after partial portal ligation from 62 +/- 10 to 164 +/- 4.1 ng/min/100 gm and remained elevated thereafter. CONCLUSIONS: The mechanism for elevated PGI2 in acute PHT is unclear, but in chronic and long-term PHT, it is probably due in part to increased splanchnic PGI2 production.

Acute Disease↗
PubMed1993

Rice prolamine protein body biogenesis: a BiP-mediated process.

Rice prolamines are sequestered within the endoplasmic reticulum (ER) lumen even though they lack a lumenal retention signal. Immunochemical and biochemical data show that BiP, a protein that binds lumenal polypeptides, is localized on the surface of the aggregated prolamine protein bodies (PBs). BiP also forms complexes with nascent chains of prolamines in polyribosomes and with free prolamines with distinct adenosine triphosphate sensitivities. Thus, BiP retains prolamines in the lumen by facilitating their folding and assembly into PBs.

Adenosine Triphosphate↗
PubMed1993

A major costimulatory molecule on antigen-presenting cells, CTLA4 ligand A, is distinct from B7.

CTLA4 ligands are important costimulatory molecules because soluble CTLA4Ig blocks the induction of T cell responses and induces T cell tolerance. As CTLA4 immunoglobulin (CTLA4Ig) binds B7 when the latter is expressed on fibroblasts, it was widely assumed that CTLA4Ig blocks T cell costimulation by blocking the function of B7. Here we show that the major costimulatory ligand bound by CTLA4Ig (which we term CTLA4 ligand A) on antigen-presenting cells are not encoded by the B7 gene. CTLA4 ligand A also differs from B7 in cellular distribution and in the respective levels of expression. Both B7 and CTLA4 ligand A are critically involved in T cell costimulation.

Abatacept↗
PubMed1993

Ribozyme-mediated inhibition of bcr-abl gene expression in a Philadelphia chromosome-positive cell line.

The bcr-abl fusion gene is the molecular counterpart of the Philadelphia chromosome (Ph1) and is directly involved in the pathogenesis of Ph1+ leukemia. Inhibition of bcr-abl gene expression may have profound effects on the cell biology of Ph1+ cells, as recent experiments with antisense oligonucleotides have shown. In this study we have designed and synthesized a unique ribozyme that is directed against bcr-abl mRNA. The ribozyme cleaved bcr-abl mRNA in a cell-free in vitro system. A DNA-RNA hybrid ribozyme was then incorporated into a liposome vector and transfected into EM-2 cells, a cell line derived from a patient with blast crisis of chronic myelogenous leukemia. The ribozyme decreased levels of detectable bcr-abl mRNA in these cells, inhibited expression of the bcr-abl gene product, p210bcr-abl, and inhibited cell growth. This anti-bcr-abl ribozyme may be a useful tool to study the cell biology of Ph1+ leukemia and may ultimately have therapeutic potential in treating patients with Ph1 leukemias.

Base Sequence↗
PubMed1993

Geographic association between urinary excretion of N-nitroso compounds and oesophageal cancer mortality in China.

Overnight urine samples were collected from approximately 60 male adults in each of 69 counties of China in 1989. Two specimens were collected from each subject--one after a loading dose of proline and ascorbic acid and another after a loading dose of proline only. Levels of N-nitrosamino acids and nitrate were measured in urine samples and correlated with cumulative mortality rates for subjects aged between 0 and 64 years in the 1970s. Oesophageal cancer mortality rates were positively and significantly associated with (i) urinary levels of excreted N-nitrosoproline (NPRO) (after proline and ascorbic acid loading or proline loading only), (ii) N-nitrososarcosine levels, and (iii) nitrosation potential (the decrease in the amount of urinary NPRO after adding ascorbic acid to the proline load). There were also positive correlations between the urinary level of NPRO or other N-nitrosamino acids and that of nitrate. The urinary excretion of nitrate was associated with consumption of various nitrate-rich vegetables. The results suggest that N-nitroso compounds (NOC) or other nitrite-derived carcinogens are implicated in the aetiology of oesophageal cancer in China.

Adult↗
PubMed1993

Single base mutation that substitutes glutamic acid for glycine 1021 in the COL3A1 gene and causes Ehlers-Danlos syndrome type IV.

The proposita described here was a 24-year-old woman with an acrogeric form of the Ehlers-Danlos syndrome including a massive dissecting aortic aneurysm. She was found to have a single-base mutation that substituted glutamic acid for glycine at amino acid position 1021 in the triple-helical domain of the type III procollagen. It is the most carboxy-terminal single-base mutation characterized to date in the COL3A1 gene. Analysis of medium and cell layer proteins from proposita's cultured skin fibroblasts showed that the mutant protein was poorly secreted, migrated more slowly on a polyacrylamide gel, and was partially unstable at +25 degrees C to brief digestion with trypsin.

Adult↗
PubMed1993

A cytotoxic ribonuclease. Study of the mechanism of onconase cytotoxicity.

Onconase, or P-30, is a protein initially purified from extracts of Rana pipiens oocytes and early embryos based upon its anticancer activity both in vitro and in vivo. It is a basic single-chain protein with an apparent molecular mass of 12,000 daltons and is homologous to RNase A. In cultured 9L glioma cells, onconase inhibits protein synthesis with an IC50 of about 10(-7) M. The inhibition of protein synthesis correlates with cell death determined by clonogenic assays. 125I-Labeled onconase binds to specific sites on cultured 9L glioma cells. Scatchard analysis of the binding data shows that onconase appears to bind to cells with two different affinities, one with a Kd of 6.2 x 10(-8) and another of 2.5 x 10(-7) M. Each cell could bind about 3 x 10(5) molecules of onconase at each of the two affinity sites. The low affinity Kd is similar to the IC50 for onconase toxicity. Onconase also demonstrates a saturability of cytotoxicity at a concentration that would saturate the low affinity binding site. Incubation at 4 degrees C increased the binding of onconase to cells relative to 37 degrees C binding and also increased the sensitivity of cells to onconase toxicity, indicating that receptor binding may be an initial step in cell toxicity. Onconase cytotoxicity can be blocked by metabolic inhibitors, NaN3 and 2-deoxyglucose, and cytotoxicity is potentiated 10-fold by monensin. Ribonuclease activity appears necessary for onconase toxicity because alkylated onconase, which only retains 2% of the ribonuclease activity, was at least 100-fold less potent in inhibiting protein synthesis in cells. Onconase inhibition of protein synthesis in 9L cells coincides with the degradation of cellular 28 S and 18 S rRNA. In contrast to RNase A, onconase is resistant to two RNase inhibitors, placental ribonuclease inhibitor and Inhibit-Ace. Northern hybridization with placental ribonuclease inhibitor cDNA probe indicates that 9L glioma cells contain endogenous placental ribonuclease inhibitor mRNA. Based on these results, we propose that onconase toxicity results from onconase binding to cell surface receptors, internalization to the cell cytosol where it degrades ribosomal RNA, inhibiting protein synthesis and causing cell death.

Animals↗
PubMed1993

Tissue-specific expression of heat shock proteins of the mouse in the absence of stress.

The steady-state levels of four members of the heat shock proteins families (HSP84, HSC73, HSP71, and HSP25) were examined by immunoblot analysis of several different tissues of young and adult mice in the absence of stress. These hsps were detected in all tissues but their level was variable. The levels of HSC73 and HSP84 varied only slightly between different tissues in either young or adult mice, with the exception of skin where these hsps were found in reduced amounts. In contrasts, the stress-inducible member of the HSP70 family, HSP71, was found to be expressed in all tissues but in amounts which differed by as much as two orders of magnitude between tissues. In general, the levels of both HSP71 and HSP25 were found to be tissue dependent, with higher levels found in tissues such as stomach, intestine, colon and bladder, tissues which are exposed to toxic environmental or metabolic products, and which may concentrate these substances by water resorption and/or be exposed to them for longer periods. The levels of HSP71 and HSP25 were generally positively correlated both in young and adult mice although this correlation was not found in certain tissues such as kidney, testes, and bone. Tissues of young mice contained lower amounts of HSP25 and HSP71 than were found in the same tissues from adults. We conclude that hsps are expressed in all tissues of the mouse in the absence of stress and that some organs, particularly those exposed to potentially toxic metabolites, show a higher level of expression of HSP71 and HSP25.

Animals↗
PubMed1993

An efficient disk based data structure for rapid searching of quantitative two-dimensional gel databases.

Fast access of two-dimensional (2-D) gel quantitative databases is important for rapid searching for protein differences between sets of 2-D gels from an experiment. The GELLAB-II system organizes corresponding spots from the gels in the database into reference or "Rspot" sets. These Rspot numeric names index fixed regions in the paged composite gel database file. This is adequate for an existing database, but has several problems. (i) Building the initial database requires guessing how much disk space to pre-allocate for each corresponding spot (i.e. spots from different gels). If it ever runs out of pre-allocated space during this process, it must expand the size of each corresponding set of spots copying the old database data into the new in-place on the disk. (ii) When adding new gels or editing the database, if a new spot is created, the system may also go into this expansion mode. The time spent and wasted disk space can be appreciable--depending on the size of the database (order of 100 gel database). (iii) Because each set of corresponding spots is the same size, we waste space in most spot sets since they do not require the additional space a few spot sets require which contain additional fragmented spots. We present a new low-level disk object-based structure and algorithm, paged indexed buckets (PIB), which optimizes disk space usage while having similar retrieval speed to the original method.

Algorithms↗
PubMed1993

A fast spot segmentation algorithm for two-dimensional gel electrophoresis analysis.

An important issue in the automation of two-dimensional gel electrophoresis image analysis is the detection and quantification of protein spots. A spot segmentation algorithm must detect, define the extent of, and measure the integrated density of spots under a wide variety of actual gel image conditions. Besides these functions, the algorithm must be memory efficient to be able to process very large gel images and do this in a reasonable amount of computation time on low-cost computers, such as workstations and personal computers. We have developed a fast spot segmentation algorithm, extending the GELLAB-II segmenter, which extracts spots in a single raster scanning pass through the gel image. The performance analysis of the algorithm will be given in the paper as well as a discussion of the algorithm.

Algorithms↗
PubMed1993

Breakpoint clusters of the PML gene in acute promyelocytic leukemia: primary structure of the reciprocal products of the PML-RARA gene in a patient with t(15;17).

DNA studies of the translocation t(15;17) in acute promyelocytic leukemia (APL) have shown that the retinoic acid receptor alpha (RARA) gene on chromosome 17 is juxtaposed to the promyelocytic leukemia (PML) gene on chromosome 15. The PML breakpoints have been mapped to 3 clusters: bcr1, bcr2, and bcr3. We have examined the PML breakpoint distribution in a series of 33 Chinese patients with APL. Twenty-two patients fell within bcr1, 2 within bcr2, and 9 within bcr3. The primary structure of the reciprocal chromosome translocation joints of one patient and that of their normal counterparts have been determined and compared to those of 2 previously reported cases. These studies revealed possible topoisomerase II cleavage sites close to the breakpoints and suggested implications of DNA attachment sites to nuclear matrix. We propose that these features are relevant to the process of illegitimate recombination generating the translocation.

Base Sequence↗