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Biomedical subjects

Y Yang

Publications and source records attributed to Y Yang.

At least 469 records · Page 26Linked to original sources

Evaluation of electron beam tomographic coronary arteriography with three-dimensional reconstruction in healthy subjects.

In this study, the authors evaluated the performance characteristics of contrast-enhanced electron-beam tomography (EBT) with three-dimensional reconstruction in defining the coronary artery lumen in healthy subjects. Thirty patients with normal coronary angiograms by selective coronary arteriography (SCA) underwent contrast-enhanced EBT examination. Measured parameters included degree of luminal enhancement, intravascular contrast-to-noise ratio (CNR), and diameter and length of visualized lumen. Ventricular cavity, aortic blood pool, and coronary artery attenuation were found to be significantly different before and after intravenous injection of contrast material (p < 0.001). CNR decreased from proximal to distal segments within each vessel (p < 0.001), with a peak of 11.2 +/- 2.3 occurring in the proximal left anterior descending coronary artery (LAD) to a low of 4.8 +/- 2.0 in the distal left circumflex (LCX). Luminal diameters visualized by EBT had no significant difference with that of SCA (p > 0.05). Therefore, EBT angiography with three-dimensional reconstruction allows for noninvasive coronary arteriography revealing long segments of the major coronary arteries in normal subjects.

Adult↗

Localization of enteroviral antigen in myocardium and other tissues from patients with heart muscle disease by an improved immunohistochemical technique.

The association of enterovirus infection and heart muscle diseases has been investigated extensively by detection of viral genomic RNA using nucleic acid hybridization and the reverse transcription-polymerase chain reaction. To further understand the role of enterovirus and its persistence in these diseases, an immunohistochemical technique was optimized to investigate the expression of viral capsid proteins in situ. A monoclonal antibody (5-D8/1) against an epitope in the N-terminus of capsid protein VP1, conserved in the enterovirus genus, was employed. To enhance sensitivity, the EnVison system was used to detect antigen-antibody complex. VP1 was detected in formalin-fixed, paraffin-embedded endomyocardial biopsy or postmortem myocardial tissues and in liver, spleen, lung, kidney, and pancreas from patients with myocarditis or dilated cardiomyopathy, but not from controls. VP1 was localized in cytoplasm of myofibers, often adjacent to necrosis and infiltrate in myocarditis, and was clustered or scattered in dilated cardiomyopathy. This technique can be used for a definitive laboratory diagnosis of enterovirus-associated diseases and for studying the mechanisms of virus persistence in chronic myocardial disease.

Antibodies, Monoclonal↗

Discoordinate expression of pancreatic lipase and two related proteins in the human fetal pancreas.

The lipase gene family contains a large number of members. Among the most closely related are pancreatic triglyceride lipase (PTL) and two pancreatic lipase-related proteins (PLRP1 and PLRP2). Previous studies in rodents demonstrated divergent temporal expression of the genes encoding these proteins. PLRP1 and PLRP2 were expressed in fetal pancreas, whereas PTL was not expressed until pups were several weeks old. To determine whether the human pancreas has a similar expression pattern for these genes, we determined the levels of each mRNA in fetal pancreas at various ages. A reverse transcriptase-PCR method was developed and used to quantify the mRNA levels for the three species normalized to the mRNA encoding cyclophillin. The mRNA encoding PLRP1 and PLRP2 was present by 16 wk in the fetal pancreas. In contrast, the mRNA encoding PTL was not present in the fetal pancreas. This pattern of expression suggests that the genes encoding theses proteins have different regulatory elements controlling temporal expression and provides another example of nonparallel expression of genes encoding pancreatic exocrine proteins.

Electrophoresis, Polyacrylamide Gel↗

Identification of macrophage migration inhibitory factor as a potent endothelial cell growth-promoting agent released by ectopic human endometrial cells.

The growth of endometrial cells in ectopic locations (endometriosis) is dependent on the establishment of an adequate blood supply. Neovascularization (angiogenesis) is therefore a vital step toward the progression of this disease. We first revealed the presence of a potent mitogenic activity for human endothelial cells in the culture medium of immortalized human endometriotic cells. The activity, measured by the level of [(3)H]-thymidine incorporation into the DNA of human coronary artery endothelial cells, was then purified by anion exchange high-performance liquid chromatography. Electrophoretic analysis of one of the bioactive fractions that markedly enhanced endothelial cell proliferation showed three distinct bands with apparent molecular masses of 15.8, 12.6, and 6.5 kDa. N-terminal microsequencing of an internal peptide from the 12. 6-kDa protein showed 100% homology with human macrophage migration inhibitory factor (MIF). The protein was positively identified as MIF by Western blot analysis using a specific anti-MIF antibody. Anti-MIF antibody inhibited the bioactivity found in the evaluated fraction and the conditioned medium of primary endometriotic cell cultures, and commercial recombinant human MIF displayed a high mitogenic activity for endothelial cells. Our findings reveal that MIF is released by endometriotic cells and acts as a potent mitogenic factor for human endothelial cells in vitro. This may have a considerable interest, in view of the crucial role of angiogenesis in ectopic endometrial cell growth and activity and in numerous tissues undergoing dynamic physiological changes, such as human endometrium.

Amino Acid Sequence↗

High-diffraction-efficiency pseudorandom encoding.

Pseudorandom encoding (PRE) is a statistics-based procedure in which a pure-phase spatial light modulator (SLM) can yield, on the average, the prescribed diffraction pattern specified by the user. We seek to combine PRE with the optimization of an aperture-based target function. The target function is a fully complex input transmittance, unrealizable by a phase-only SLM, that generates a prescribed light intensity. The optimization is done to increase the diffraction efficiency of the overall process. We compare three optimization methods-Monte Carlo simulation, a genetic algorithm, and a gradient search-for maximizing the diffraction efficiency of a spot-array generator. Calculated solutions are then encoded by PRE, and the resulting diffraction patterns are computer simulated. Details on the complexity of each procedure are furnished, as well as comparisons on the quality, such as uniformity of the output spot array.

Computer Simulation↗

The major histocompatibility complex-encoded HFE in iron homeostasis and immune function.

HFE is a non-classical major histocompatibility complex class I molecule that complexes with a beta2-microglobulin. A functional link between HFE and iron metabolism has been established by the discovery of a physical association between HFE and the transferrin receptor. By inhibiting transferrin receptor internalization, HFE functions as a negative modulator of transferrin receptor function. In addition, HFE appears to be an iron sensor that directly or indirectly communicates the body's iron status to T cells, which then use cytokines as feedback modulators to achieve iron homeostasis. A working model for the feedback regulatory mechanism between iron metabolism and immune function is proposed.

Biological Transport, Active↗

Postnatal development of NADPH-diaphorase activity in the rat: the role of nitric oxide in the ontogeny of arginine vasopression and oxytocin.

To clarify the role of nitric oxide (NO) in the ontogeny of arginine vasopressin (AVP) and oxytocin (OXT) neurons in the hypothalamo-neurohypophysial system (HNS), we observed the coexpression pattern of NADPH-diaphorase (NADPH-d) activity and AVP- or OXT-immunoreactivity (IR) in the rat hypothalamus and posterior pituitary during the postnatal period. The enzymatic activity of NADPH-d was observed in the supraoptic nucleus (SON), paraventricular nucleus (PVN), median eminence (ME) and posterior pituitary throughout the postnatal development. AVP-containing neurons were clearly observed from postnatal day 1 in both the SON and PVN, while OXT-containing neurons were recognized from postnatal day 14. The coexistence of NADPH-d and AVP or OXT was detected in the SON from postnatal day 14. At postnatal day 21, the coexpression pattern was approximately the same as that of the SON and PVN in adult rats. Our findings indicated that the expression of NADPH-d and OXT was observed from almost the same postnatal period in both the SON and PVN. In addition, the pattern of increased numbers of NADPH-d positive fibers was similar to that of OXT-immunoreactive fibers in both the inner layer of the ME and the posterior pituitary. A good correlation was thus obtained between OXT expression and NADPH-d activity in the HNS during postnatal development. The present study suggests that NO is more closely involved in the expression and regulation of secretion of OXT than AVP.

Animals↗

Sex and skill differences in translation of English color words by Chinese students.

The present study investigated sex and skill differences in color-word translation by Chinese-speaking students in university English classes. A questionnaire was administered to estimate the correlation between subjects' performance and their color-related hobbies. To conceptualize the issue better, two more groups of correlated parameter (academic achievements plus demographic factors) were introduced in this research as well. 40 English majors (20 women, 20 men), ranging in education from level one to level four, were randomly drawn from a metropolitan university and tested in the experiments as subjects. These university students were asked to provide Chinese equivalents for a list of 33 elaborated English color terms chosen from a thesaurus by mapping on the 11 color-tone categories defined by basic color theory. The results confirm the findings in relevant studies that used native speakers as subjects by observing that (1) women possessed a richer color vocabulary both in their source language and in their target language, (2) women also provided more elaborated Chinese equivalents to the color words used as stimuli, and finally, (3) women showed a superiority in accuracy in this color-lexicon matching or translating task. As a whole, the effects of skill and age were not significant. A significant correlation was found between the learners' proficiency in English and performance in translation of color words, but this relationship was rather weak and only true for the men. Color-related hobbies did not significantly correlate with the color-decoding performance of these language learners. Neither did the demographic factors. Taken together, it is sensible to state that differences reported here were affected primarily by the sex of the learn er. conditionally by language proficiency, and presumably by the cognitive and perceptual sex differences as well. These findings further indicate that the process of color codability is a complicated but unstudied issue in language learning and that sex should be treated as an independent variable in this area of research.

Achievement↗

Usefulness of postischemic thrombolysis with or without neuroprotection in a focal embolic model of cerebral ischemia.

OBJECT: Recent studies have shown that the use of thrombolysis in the setting of acute stroke is associated with an increased risk of cerebral hemorrhage. The time of onset of symptoms to initiation of medication and the dose levels of the thrombolytic agents are important determinants for the risk of cerebral hemorrhage. The authors evaluated the time course of thrombolysis-related hemorrhages in experimental settings and tested whether the addition of neuroprotective medication augments the efficacy of thrombolysis and reduces the incidence of hemorrhages. METHODS: Male Wistar rats were subjected to right middle cerebral artery embolization with an autologous thrombus and were then randomly assigned to one of the following groups: Group 1, saline-treated (2 hours after ischemic insult) animals as controls; Groups 2 to 4, high-dose urokinase (5,000 U/kg) at 2, 3, and 6 hours after the insult; Group 5, low-dose urokinase (2,500 U/kg) at 2 hours after the insult; Group 6, 20 mg/kg topiramate (TPM) at 2 hours after the insult; Group 7, a combination of 20 mg/kg TPM at 2 hours and low-dose urokinase (2,500 U/kg) at 6 hours after the insult; and Group 8, 20 mg/kg TPM (20 mg/kg) at 2 hours and high-dose urokinase (5,000 U/kg) at 2 hours after the insult. Neurological behavior and the infarct volume in the brain were assessed following cerebral embolism and the various treatments. All animals in the single therapy and low-dose combination groups survived surgery. Three of eight animals treated with high-dose urokinase alone at 6 hours and three of six animals in the combined high-dose urokinase and TPM group developed fatal intracerebral hemorrhages. There was a significantly better neurological outcome at 24 hours in the animals treated with either medication compared with controls. The volume of the infarct in the saline-treated group was 54.2 +/- 9%. The use of TPM at 2 hours led to a decrease in the infarct to 20.1 +/- 11.2% (p < 0.01). Treatment with urokinase at 6 hours after the occlusion showed a trend toward protection; the infarct volume was 31.9 +/- 14.1% (p < 0.05). The addition of TPM to low- or high-dose urokinase achieved better neuroprotection (8.2 +/- 6% and 11.9 +/- 10.7%, respectively; both p < 0.01). CONCLUSIONS: In this study the authors show that the volume of the infarct can be significantly decreased with 2 to 6-hour delayed intraarterial thrombolysis with urokinase and that the efficacy of thrombolysis may be enhanced by combining neuroprotective agents like TPM. It is also shown that low-dose combination therapy may decrease the likelihood of cerebral hemorrhage.

Acute Disease↗

Illusions in quantified reasoning: how to make the impossible seem possible, and vice versa.

The mental model theory postulates that reasoners build models of the situations described in premises, and that these models normally represent only what is true. The theory has an unexpected consequence. It predicts the existence of illusions in inferences. Certain inferences should have compelling but erroneous conclusions. Two experiments corroborated the occurrence of such illusions in inferences about what is possible from disjunctions of quantified assertions, such as, "at least some of the plastic beads are not red." Experiment 1 showed that participants erroneously inferred that impossible situations were possible, and that possible situations were impossible, but that they performed well with control problems based on the same premises. Experiment 2 corroborated these findings in inferences from assertions based on dyadic relations, such as, "all the boys played with the girls."

Adult↗

How to eliminate illusions in quantified reasoning.

The mental model theory postulates that reasoners build models of situations described in premises. These models normally make explicit only what is true according to the premises. The theory has an unexpected consequence. It predicts the existence of illusions in inferences: Certain inferences should have compelling but erroneous conclusions. Previous studies have corroborated the existence of such illusions. The present study reports the first effective antidote to them. For example, most people incorrectly answer "yes" to the following problem: Only one of the following statements is true ... /At least some of the plastic beads are not red./None of the plastic beads are red./Is it possible that none of the red beads are plastic? In two experiments, we progressively eliminated this fallacy and others by using instructions designed to overcome the bias toward truth. The difference between the illusory and the control problems disappeared when the participants were instructed to work out both the case in which the first premise was true and second premise was false and the case in which the second premise was true and the first premise was false.

Attention↗

The open lid mediates pancreatic lipase function.

Pancreatic triglyceride lipase (PTL) and the homologous pancreatic lipase related protein 2 (PLRP2) provide a unique opportunity to understand the molecular mechanism of lipolysis. They differ in substrate specificity, sensitivity to bile salts, and colipase dependence despite their close amino acid and tertiary structure identity. One important structure, present in both lipases, is the lid which occupies different positions in the inactive and active forms of PTL. We investigated the role of the lid in lipase function by site-specific mutagenesis. By exchanging the lids between PTL and PLRP2, we created two chimeric lipases. Additionally, we made multiple substitution mutations in the PTL lid. PLRP2 with the PTL lid had kinetic properties similar to PLRP2. PTL with the PLRP2 lid was greatly impaired and had no activity at micellar bile salt concentrations even in the presence of colipase. Both chimeras showed interfacial activation suggesting that the closed lid position was maintained. A series of substitution mutations were made in positions Arg257 and Asp258. These mutations demonstrated the importance of these two residues to maintaining the normal activity, triglyceride acyl chain specificity, and colipase interaction of PTL. The preserved interfacial activation in the chimeras, the similar crystal structure of the two lids in the closed position, and the importance of Arg257 and Asp258 in mediating the open conformation of the lid argue that the position of the open lid influences the differences in activity against triglycerides, in sensitivity to bile salts, and in colipase dependence between PTL and PLRP2.

Amino Acid Sequence↗

[Study of HBV X protein and RMP, an RPB5 mediate protein competitively interacting with general transcription factor TF2B].

OBJECTIVE: HBX is an essential viral protein that is important for HBV replication and might be a cofactor in the development of hepatocellular carcinoma. So many researchers are trying to find out the antagonistic factors of HBX. RMP, a newly cloned RNA polymerase II subunit RPB5 mediate protein, represses the transcription transactivation of HBV X protein. The purpose of this study was to elucidate the mechanism how RMP represses the transactivation of HBX. METHODS: In this report, DNA recombinant technique in vitro protein-protein binding assay (Pull-Down assay) and chloramphenicol acetyltransferase assay were used. RESULTS: The d10 domain of TF2B are responsible for binding to RMP, which is same as TF2B binding to the HBX protein. RMP specifically disrupts the binding between TF2B and HBX protein, vice versa HBX protein also disrupt the interaction of TF2B-RMP as demonstrated by the in vitro protein binding competition assay. Overexpression of RMP represses HBX transactivation on the reporters with HBX responsive cis-elements in transient transfected COS-1 cells. The repression can be rescued by overexpression of TF2B. CONCLUSION: The results clearly suggested that transcription co-activator HBX protein and corepressor RMP competitively associated with TF2B. Disrupting the interaction between transcription co-repressor RMP with TF2B is probably one of the mechanisms to account for the transcriptional transactivation of HBX protein.

Binding, Competitive↗

[The application of polymerase chain reaction-single strain conformation polymorphism in the pedigree analysis of familial hypercholerolemia patients].

OBJECTIVE: To discuss the value of polymerase chain reaction-single strand conformation polymorphism(PCR-SSCP) in the pedigree analysis of familial hypercholesterolemia(FH) patients. METHODS: For 4 patients with FH detected by PCR-SSCP and DNA sequence analysis (1 homozygote has point mutation in exon 7, 1 heterozygote in exon 14, and 2 heterozygotes in 3' part of exon 4 ), members of each pedigree, altogether 23 individuals, were analysed using PCR-SSCP. RESULTS: Every member of the 4 pedigrees was examined genetically. Besides the 4 probands, another 1 homozygote and 8 heterozygotes were found. CONCLUSION: The PCR-SSCP method can be used in the pedigree analysis of FH probands. The early diagnosis of siblings and relatives can help to provide genetic consultation and direction so as to pay attention to development of hypercholesterolemia.

Adolescent↗

Changes in dopamine transporter and c-Fos expression in the nucleus accumbens of alcohol-tolerant rats.

BACKGROUND: We have shown that neurochemical functions of 5-HT3 receptors in regulating dopamine (DA) release in the nucleus accumbens (ACC) after alcohol exposure compensate for the dysfunction of serotonergic activity to restore the original properties in processing alcohol tolerance, and that the development of alcohol dependence may be mediated by ACC 5-HT3 receptors. In the present study, the effects of chronic alcohol consumption on the functions of the dopamine transporter (DAT) and the expression of c-Fos proteins were investigated using in vivo brain microdialysis and immunocytochemistry. METHODS: Perfusion of cocaine and 1-(2-Bis-(4-fluorophenyl) methoxy) ethyl)-4-(3-phenylpropyl) piperizine (GBR 12909) through the microdialysis probe membrane increased the extracellular levels of DA in ACC of alcohol-treated rats that had developed alcohol tolerance by drinking 10% EtOH for 30 days. RESULTS: The magnitudes of DA reuptake or DAT inhibitors, cocaine, and GBR 12909 that induced DA availability in the ACC were significantly higher in alcohol-treated rats than in controls. When compared with control rats, the alcohol-treated rats exhibited higher levels of DA and its metabolite, DOPAC, in the ACC. Increased expression of the c-Fos-like protein was found in the ACC of alcohol-treated rats. These results show that (1) chronic alcohol consumption desensitizes or decreases the DAT of DA terminals in the ACC and that (2) EtOH causes cellular hyperexcitability of ACC dopaminergic neurons with increased Fos expression during alcohol tolerance. CONCLUSION: The findings suggested that an abnormality of the dopaminergic neurons in the ACC that are involved with DAT dysfunction is associated with the development of alcohol tolerance.

Alcoholism↗

[TBX5 mutation in Chinese patients with Holt-Oram syndrome].

OBJECTIVE: To analyse TBX5 mutation in Chinese patients with Holt-Oram syndrome(HOS). METHODS: Seven HOS families were analysed with single strand conformation polymorphism(SSCP) and sequencing. RESULTS: Three SSCP changes were detected and identified as the TBX5 gene mutation at three new sites. One of the changes is a frameshift mutation caused by a base cytidine deletion at the cDNA sequence of 416, which altered all the codons after the point, thus it can not encode the protein of normal amino acid sequence; another is a missense mutation induced by a base substitution(C-->A) at the cDNA sequence of 145, which made the codon of that point change from CAG-->AAG, and encoded amino acid changed from glutamine(Gln) to lysine(Lys), consequently the change weakened the function of TBX5 protein; the third is also a missense mutation which resulted from a base substitution (T-->C) at the cDNA sequence of 161, this change made the codon of that point change from ATC-->ACC, it changed the encoded amino acid from isoleucine(Ile) to threonine(Thr), which reduced the function of TBX5 protein. CONCLUSION: HOS in Chinese is caused by mutation in TBX5.

Abnormalities, Multiple↗

DeltaFosB-induced cataract.

PURPOSE: The objective of this study was to investigate a possible relationship between posterior subcapsular cataract (PSC) formation and expression of the transcription factor DeltaFosB. METHODS: Western blot analysis was performed on bitransgenic NSE-tTA, TetOp-DeltaFosB, and single-transgenic NSE-tTA control mice to determine the pattern of DeltaFosB expression within the eye. Light and scanning electron microscopy and biochemical analyses were also performed. RESULTS: In mice expressing DeltaFosB, cataract developed that initially appeared to be posterior subcapsular and gradually matured to involve the entire lens. The enlarged posterior ends of developing secondary fibers curved away from the visual axis to form an elevated opaque posterior plaque. As a result, posterior suture formation did not occur. At a later time, the attenuated posterior capsule overlying the plaque ruptured and the lens nucleus subluxated into the vitreous. Retinal damage was also observed but only from postnatal day 65, a time when extensive lens degeneration had already occurred. DeltaFosB expression was observed well before the detection of morphologic change in both the lens and the retina. Within the lens, DeltaFosB expression was found in both the epithelium and fibers. The development of cataracts was a direct consequence of DeltaFosB expression and was not due to the disruption of an endogenous gene by transgene integration since cataracts could be prevented by silencing expression of DeltaFosB by feeding bitransgenic animals doxycycline (Dox). Moreover, cataracts were observed in bitransgenic mice derived from two independent TetOp-DeltaFosB founder lines but not in single NSE-tTA transgenic controls. Cataractogenesis was not a consequence of abnormal development, because mice conceived and raised on Dox to prevent expression of DeltaFosB also were subject to formation of PSC when expression of DeltaFosB was turned on in adult animals by removing Dox. Examination of biochemical parameters indicated that the earliest change observed was the disruption of calcium homeostasis with a significant increase in Ca(2+) influx, followed by a gradual but marked decrease in protein content. Significant changes in certain metabolic parameters and protein composition were also observed. CONCLUSIONS: The DeltaFosB-induced cataract in which the major morphologic early event was the disruption of normal posterior fiber formation, may be a good model for PSC. By identifying DeltaFosB-regulated target genes, it should be possible to achieve a better understanding of the molecular mechanisms through which PSC is formed.

Animals↗