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W Z Yu

Publications and source records attributed to W Z Yu.

15 recordsLinked to original sources
PubMed2005

Nonspherical colloidal crystals fabricated by the thermal pressing of colloidal crystal chips.

Nonspherical colloids and their ordered arrays may be more attractive in applications such as photonic crystals than their spherical counterparts because of their lower symmetries, although such structures are difficult to achieve. In this letter, we describe the fabrication and characterization of colloidal crystals constructed from nonspherical polyhedrons. We fabricated such nonspherical colloidal crystals by pressing spherical polymer colloidal crystal chips at a temperature slightly lower than the glass-transition temperature (T(g)) of these polymer colloids. During this process, the polymer microspheres were distinctively transformed into polyhedrons according to their crystal structures, whereas the long-range order of the 3D lattice was essentially preserved. Because a working temperature lower than T(g) effectively prevented the colloidal crystals from fusing into films, the spherical colloidal crystals were transformed greatly under pressure, which lead to obvious change in the optical properties of colloidal crystals. Besides their special symmetry and optical properties, these nonspherical colloidal crystals can be used as templates for 2D or 3D structures of special symmetry, such as 2D nano-networks. We anticipate that this fabrication technique for nonspherical colloidal crystals can also be extended to nonspherical porous materials.

Journal Article↗
PubMed2000

Role of D(1) and D(2) dopamine receptors in the acquisition and expression of flavor-preference conditioning in sham-feeding rats.

The present study examined the effects of D(1) and D(2) antagonists on flavor-preference conditioning by the sweet taste of sucrose. All sessions were conducted under sham-feeding conditions to minimize post-ingestive influences. The rats were trained in alternating, one-bottle sessions to sham-feed a 16% sucrose solution containing one novel flavor (CS+) and a less-preferred 0.2% saccharin solution containing a different flavor (CS-). Three groups of food-restricted rats were treated with either vehicle (control group), the D(1) antagonist, SCH23390 (200 nmol/kg), or the D(2) antagonist, raclopride (200 nmol/kg) during one-bottle training. A fourth group (yoked group) was vehicle-treated and its training intakes were matched to that of the D(1) and D(2) drug groups. Preferences were assessed in two-bottle tests with the CS+ and CS- flavors presented in mixed 8% sucrose+0.1% saccharin solutions following systemic doses of 0, 200, or 800 nmol/kg of either the D(1) or D(2) antagonists. All groups significantly preferred the CS+ flavor in vehicle tests, although the preferences were weaker in the D(1), D(2), and yoked groups compared to the control group. All groups selectively reduced their CS+ intakes when treated with either D(1) or D(2) antagonists during two-bottle testing, and the CS+ preference was blocked at the higher doses. These data show that D(1) and D(2) receptor antagonists block the expression of a sucrose-conditioned preference, but produces substantially lesser effects upon the acquisition of this form of flavor conditioning.

Animals↗
PubMed2000

Pharmacology of flavor preference conditioning in sham-feeding rats: effects of dopamine receptor antagonists.

Opioid and dopamine systems are both implicated in the response to sweet solutions. Our laboratory previously reported that the opioid antagonist, naltrexone, reduced the intake of sweet solutions, yet had little or no effect on sucrose-conditioned flavor preferences in sham-feeding rats. The present study examined the role of dopamine D(1) and D(2) receptors in the expression of flavor preferences conditioned by the sweet taste of sucrose. All sessions were conducted under sham-feeding conditions to minimize postingestive influences. Training was accomplished by adding a novel flavor (CS+) to a 16% sucrose solution, a different flavor (CS-) to a less-preferred 0.2% saccharin solution in alternating, one-bottle sessions. Preferences were assessed in two-bottle tests with the CS+ and CS- flavors presented in mixed sucrose (8%)-saccharin (0.1%) solutions following systemic doses of 0, 50, 200, 400, or 800 nmol/kg of the D(2) antagonist, raclopride (Experiment 1) or the D(1) antagonist, SCH23390 (Experiment 2) under either food-restricted or unrestricted conditions. Rats significantly preferred the CS+ solutions in vehicle tests, and displayed equipotent and dose-dependent reductions in total intake and CS+ preference following either D(1) or D(2) receptor antagonism. Similar results were obtained with SCH23390 and raclopride in Experiment 3 conducted with water-restricted rats. These data indicate that dopaminergic D(1) and D(2) receptors play pivotal and functionally equivalent roles in the expression of flavor preferences conditioned by the sweet taste of sucrose.

Animals↗
PubMed1999

Pharmacology of flavor preference conditioning in sham-feeding rats: effects of naltrexone.

Relatively little is known about the neurochemical and pharmacological mechanisms involved in flavor preference learning. The present study examined the ability of the opioid antagonist, naltrexone to alter the acquisition and expression of flavor preferences conditioned by the sweet taste of sucrose. This was accomplished by adding a novel flavor (the CS+) to a sucrose solution, and a different flavor (the CS-) to a less-preferred saccharin solution. Rats were trained to drink these solutions with an open gastric fistula (sham-feeding), which minimized postingestive actions. Food-restricted (Experiments 1 and 2A) and ad lib-fed (Experiment 2B) rats were given either limited (Experiment 1) or unlimited (Experiment 2) access to the CS+ and CS- solutions during one-bottle training. Preferences were assessed in two-bottle tests (with the CS+ and CS- flavors presented in mixed sucrose-saccharin solutions) following vehicle or naltrexone (0.1-10 mg/kg, SC) treatment. The rats displayed significant CS+ preferences following vehicle, particularly after unlimited access training. In four of five experiments, naltrexone significantly reduced total intakes during the two-bottle, sham-feeding tests. Except for one instance, however, the drug failed to block the preference for the CS+ flavor over the CS- flavor. The effects of naltrexone (0.1 mg/kg) on the acquisition of flavor preferences were studied in sham-feeding rats under limited (Experiment 3A) and unlimited (Experiment 3B) training access conditions. Rats treated with naltrexone during training displayed similar CS+ preferences as did saline-treated rats, even though they consumed less CS+ during training. The naltrexone-trained rats also displayed smaller reductions in total or CS+ intakes than did saline-trained rats when all rats were treated with a 2.5 mg/kg dose of naltrexone during testing. As in previous studies, these results show that naltrexone significantly reduces the intake of sweet solutions, yet it has little or no effect on the acquisition or expression of flavor preferences conditioned by sucrose in sham-feeding rats.

Animals↗
PubMed1998

Antisense mapping of opioid receptor clones: effects upon 2-deoxy-D-glucose-induced hyperphagia.

Antisense oligodeoxynucleotides (AS ODNs) directed against exons 1 and 2 of the MOR-1 clone significantly and markedly reduced (81-93%) hyperphagia induced by the anti-metabolic glucose analogue, 2-deoxy-d-glucose (2DG) across a 4 h time course. AS ODNs directed against exons 3 or 4 of the MOR-1 clone had a more limited (1-2 h) duration of action upon 2DG-induced hyperphagia. 2DG-induced hyperphagia was significantly reduced by AS ODNs directed against exon 2 (44-51%), but not exons 1 or 3 of the KOR-1 clone across a 4 h time course. Whereas an AS ODN probe directed against the KOR3/ORL-1 clone produced small (36%), but significant reductions in 2DG-induced hyperphagia, an AS ODN probe directed against the DOR-1 clone was ineffective. These data provide further converging evidence for the roles of primarily mu, but also kappa1 and kappa3 opioid receptors in mediating the hyperphagic effects of glucoprivation.

Animals↗
PubMed1997

Opioid-receptor subtype agonist-induced enhancements of sucrose intake are dependent upon sucrose concentration.

Selective mu ([D-Ala2, N-Me-Phe4, Gly-ol5]-enkephalin (DAMGO)), delta1 ([D-Pen2, D-Pen5]-enkephalin (DPDPE)), delta2 ([D-Ala2, Glu4]-Deltorphin (Delt II)), kappa1 (U50488H) and kappa3 (naloxone benzoylhydrazone (NalBzOH)) opioid agonists each stimulate food intake in rats. Whereas studies with selective opioid antagonists implicate mu and kappa1 receptors in the mediation of sucrose intake, studies with selective opioid agonists implicate mu and delta receptors in the mediation of saccharin intake. The present study determined if specific delta1, delta2, kappa1, kappa3 and mu opioid-receptor subtype agonists produced similar alterations in sucrose intake as a function of sucrose concentration (0.5%, 2.5%, 10%) across a 1-h time-course. Each of these agonists significantly increased sucrose intake with variations in pattern, magnitude, and consistency as a function of sucrose concentration. Whereas the mu opioid agonist, DAMGO, and the delta1 opioid agonist, DPDPE, each enhanced sucrose intake at higher (2.5%, 10%), but not lower (0.5%), concentrations, the delta2 opioid agonist, Delt II, increased sucrose intake at lower (0.5%, 2.5%), but not higher (10%), concentrations. Kappa opioid agonists produced less consistent effects. The kappa1 opioid agonist, U50488H, increased sucrose intake at high (10%) concentrations and decreased sucrose intake at low (0.5%) concentrations, and the kappa3 opioid agonist, NalBzOH, inconsistently increased sucrose intake at the 0.5% (20 microg) and 10% (1 microg) concentrations. Thus, these data further implicate mu, delta1, and delta2 opioid mediation of palatable intake, particularly of its orosensory characteristics.

Animals↗
PubMed1997

Delta and kappa opioid receptor subtypes and ingestion: antagonist and glucoprivic effects.

Delta and kappa opioid receptors have been differentiated into further subtypes based upon both biochemical and pharmacological analgesic assays. Whereas hyperphagia elicited by the kappa1 receptor agonist, U50488H is blocked by general and kappa1 opioid antagonists, hyperphagia elicited by the kappa3 receptor agonist, naloxone benzoylhydrazone (NalBzOH) is blocked by general, but not kappa1 opioid antagonists. The first study assessed the opioid antagonist profile of hyperphagia elicited by centrally administered delta1 ([D-Pen2, D-Pen5]-enkephalin, DPDPE: 5-50 microg) and delta2 ([D-Ala2, Glu4]-Deltorphin, Delt II: 5-50 microg) agonists following central pretreatment with general (naltrexone), delta1 ([D-Ala2, Leu5, Cys6]-enkephalin, DALCE) and delta2 (naltrindole isothiocyanate, NTII) opioid antagonists. It is also important to determine whether selective opioid receptor subtype agonists are capable of altering intake in ingestive situations other than spontaneous feeding. The second study examined whether centrally administered delta1, delta2, kappa1 or kappa3 agonists altered the pattern and magnitude of hyperphagia elicited by 2-deoxy-D-glucose (2DG: 50-400 mg/kg, IP). DPDPE-induced hyperphagia was significantly reduced by naltrexone and NTII, but not DALCE. Delt II-induced hyperphagia was significantly reduced by DALCE and NTII, but not naltrexone. Pairing Delt II (5 microg) with low (100-200 mg/kg) 2DG doses significantly enhanced intake, producing a leftward (3-fold) shift in 2DG's hyperphagic dose-response curve. In contrast, DPDPE failed to alter 2DG-induced hyperphagia, and kappa1 and kappa3 opioid agonists each produced small, but significant increases in 2DG-induced hyperphagia. The antagonist data suggest the possibility of physiological and pharmacological interactions between delta receptor subtypes in mediating food intake, and it would appear that delta2 opioid receptors exert facilitatory effects upon glucoprivic hyperphagia.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1997

Interactions between angiotensin II and delta opioid receptor subtype agonists upon water intake in rats.

Delta opioid receptor agonists, like those of mu and kappa receptors, stimulate water intake. To assess the relative contributions of delta1 and delta2 receptors in the modulation of water intake stimulated by Angiotensin II (AII), the present study examined the respective actions of [D-Pen2, D-Pen5]-enkephalin (DPDPE: 5-20 ug, i.c.v.) and [D-Ala2, Glu4]-Deltorphin (Delt II: 5-20 ug, i.c.v.) upon water intake per se, and upon AII (0.02-20 ng, i.c.v.)-induced hyperdipsia in rats. Both DPDPE and Delt II dose-dependently stimulated spontaneous water intake. An ineffective (5 ug) dose of DPDPE differentially altered water intake when paired with AII, significantly increasing intake at the 0.02 ng dose, not changing intake at the 0.2 ng dose and significantly decreasing intake at the 2 ng dose. In contrast, pairing ineffective doses of Delt II (5 ug) and AII (0.2 ng) significantly increased water intake that persisted when either the Delt II dose (1 ug) or the AII dose (0.02 ng) was lowered. However, neither delta1 nor delta2 opioid agonists significantly altered the ED50 for AII-induced drinking. Thus, delta2 opioid agonism appeared more consistent and reliable than delta1 opioid agonism in stimulating water intake when paired with AII, and these data indicate interactions between delta1 and delta2 agonists and AII in mediating water intake.

Analgesics↗
PubMed1993

The beta-thalassemia frameshift at codon 8 (-AA) observed in four Chinese of the Uygur nationality.

During a survey for beta-thalassemia in Kashi City, Xinjiang Province, P.R. China, four unrelated Uygur students were identified as heterozygotes for the beta-thalassemia frameshift at codon 8 (-AA). Detection was with the polymerase chain reaction combined with allele-specific oligonucleotide hybridization. This beta-thalassemia allele has not been observed in the Chinese population before and might be rather specific for the Uygur nationality.

Asian People↗
PubMed1991

Complementing amino acid substitutions within loop 6 of the alpha/beta-barrel active site influence the CO2/O2 specificity of chloroplast ribulose-1,5-bisphosphate carboxylase/oxygenase.

Photosynthesis-deficient mutant 45-3B of the green alga Chlamydomonas reinhardtii contains a chloroplast mutation that causes valine-331 to be replaced by alanine within the large subunit of ribulose-1,5-bisphosphate carboxylase/oxygenase. This amino acid substitution occurs in loop 6 of the alpha/beta-barrel active site, three residues distant from catalytic lysine-334. The mutation reduces the specific activity of the enzyme and also reduces its CO2/O2 specificity factor by 42%, but the amount of holoenzyme is unaffected. In a previous study, an intragenic-suppressor mutation, named S40-9D, was selected that causes threonine-342 to be replaced by isoleucine, thereby increasing the CO2/O2 specificity of the mutant enzyme by 36%. To determine which other residues might be able to complement the original mutation, nine additional genetically independent revertants have now been analyzed. Another intragenic suppressor, represented by mutation S61-2J, causes glycine-344 to be replaced by serine. This change increases the CO2/O2 specificity of the mutant enzyme by 25%. Of the revertants recovered and analyzed, the mutant enzyme was improved only due to true reversion or by intragenic suppression mediated by substitutions at residues 342 or 344. Changes in the physical properties of the two pairs of complementing substitutions indicate that steric effects within loop 6 are responsible for the observed changes in the CO2/O2 specificity of the enzyme.

Amino Acid Sequence↗
PubMed1989

Identification of partial mutational sites in human mitochondrial DNA in the Chinese and its significance.

A simple method for the identification of mutational sites in human mitochondrial DNA (mtDNA) was described. It was based on the human Cambridge sequence as a relative standard sequence and a single base pair substitution in mtDNA as a unique mutational form. The partial mutational sites can be determined using this method which was characterized by combining the restriction mapping with the analysis for the table of human mtDNA potential mutational sites with rapidity and simplicity. In the meanwhile, six mtDNA mutational sites found in Chinese population were identified by means of this method.

China↗
PubMed1988

Mitochondrial DNA polymorphism in Chinese.

Human mitochondrial DNA (mtDNA) restriction endonuclease fragment patterns were analyzed using placenta DNA isolated from 273 individuals representing four different nationalities, the Han, the Uygur, the Kazakh and the Hui populations. Thirty-eight fragment patterns (morphs) were observed with the enzyme ApaI, BamHI, EcoRI, HindIII, HinfI, HhaI, HapII, KpnI, Mbol, PstI, PvuII, SacI, ScaL and XhoI. Fourteen new morphs, including some only existing in individual racial and national populations were observed, which indicates that there is a significant difference in the distribution of mtDNA morphs among various national and racial populations. By comparison with the mtDNA sequences in primate species, some mtDNA ancestral morphs were found to be retained in Oriental population today. This result provided indirect evidence that Asia may be one of the human original sources. Genetic distances among four national populations computed and employed in construction of an average linkage tree suggested that the Uygur and the Kazakh populations combined to form a branch at first, then the Han and the Hui came together to form another one, and at last, these two branches converged into a stem. Again, it was found that the internal variation within the Uygur and the Kazakh populations was greater than that within the Han and the Hui populations. These results showed a relationship among the four different national populations in China based on the molecular level.

China↗