Biomedical subjects

Y Jiang

Publications and source records attributed to Y Jiang.

At least 379 records · Page 21Linked to original sources

PubMed1998

A simple high performance liquid chromatography assay for simultaneous determination of omeprazole and metronidazole in human plasma and gastric fluid.

Antibiotics which are actively secreted into gastric fluid may be more efficacious in the eradication of Helicobacter pylori in peptic ulcer disease. Other agents used in the treatment of this disease such as omeprazole or other anti-secretory agents may alter the secretion and/or distribution characteristics of antibiotics. In order to test the applicability of these concepts to metronidazole, a sensitive and specific high performance liquid chromatography (HPLC) assay was developed to quantitate omeprazole in plasma, and metronidazole in plasma and gastric fluid. The HPLC system consisted of a multi-phase column combining anion exchange and reversed phase separation (OmniPac Pax-500, Dionex), and a variable wavelength UV detector set at 254 nm. The mobile phase was a mixture of 0.1 M sodium phosphate buffer:methanol:acetonitrile (60:20:20) with final pH adjusted to approximately 7.0. Metronidazole and omeprazole were extracted by adsorption onto a C2-bonded silica gel solid phase extraction column, and eluted with methanol. The extract was dried, reconstituted in a solution of acetyl salicylic acid (ASA), and then injected into the HPLC system. Under these conditions, metronidazole, omeprazole and ASA were well separated and recoveries in plasma were greater than 80%. Omeprazole could not be measured in gastric fluid because of rapid decomposition. Using 0.3 ml of sample, the assay sensitivity was less than 0.1 microgram ml-1 and linear up to 10 micrograms ml-1. Both intra- and inter-assay CV were greater than 15%. It was applied successfully in determining metronidazole concentrations in clinical samples of plasma and gastric fluid.

Anti-Infective Agents↗

PubMed1998

Physicochemical, molecular-orbital and electronic properties of acephate and methamidophos.

Methamidophos (Me) and its N-acetylated derivative, acephate (Ac), are water soluble insecticides that have similar insecticidal potency, but different mammalian toxicity. Me is a potent inhibitor, while Ac is a poor inhibitor of mammalian AChE (mAChE). At physiological pH, both insecticides exhibit similar accumulation in RBC, while Ac exhibits greater binding to plasma proteins than Me. These differential effects of Ac and Me are attributed to the differences in their physicochemical, molecular-orbital and electronic properties. Ac and Me are freely soluble in aqueous solution, moderately soluble in ethyl-acetate (EtAct) and insoluble in n-hexane. The solubility of these insecticides in aqueous solution and the partitioning of these insecticides from aqueous solution into EtAct are independent of the pH of the aqueous solution. At pH 8, Me did not react with o-phthalaldehyde (a NH2 selective dye), but gamma-amino-butyric acid (pKa 10) did. Thus, despite the presence of an amino group, Ac and Me do not exhibit pH dependent solubility in aqueous and in organic solvents. Ac has two O atoms with non-bonding electrons (P = O delta- and C = O delta-) where P = O and C = O point in opposite directions. Me has only one O atom with non-bonding electrons (P = O delta-). However, because of charge translocation, the C = O group of Ac exists as C = O- and the P-NH3+ group of Me exists as P = NH2+ at a pH lower than their pKa. The P-N bond of Me, but not of Ac, is hydrolyzed at pH 2. Thus, the presence of an electron rich domain stabilizes Ac's P-N bond. The CH3S-P bond of both insecticides is similarly hydrolyzed at pH 11. This indicates that the two compounds are considerably similar except that Ac has an additional electron rich domain. At physiological pH, therefore, the functional differences between these insecticides may be due to the differences in their electronic structure. We propose that, similar to a previous model for cationic inhibitors of AChE (13), the P = O delta- group of Me forms hydrogen bonds within the oxyanion-hole causing the leaving group (-SCH3) to orient towards the "gorge" opening. This orientation allows the P atom of Me to interact with Ser200, resulting in the phosphorylation of the enzyme. For acephate, either P = O or C = O, but not both, interact within the oxyanion-hole. This destabilizes the binding of Ac to the active center, resulting in reduced AChE phosphorylation.

Animals↗

PubMed1998

Imprinting in Angelman and Prader-Willi syndromes.

Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are caused by deficiencies of gene expression from paternal or maternal chromosome 15q11-q13, respectively. Many advances have occurred during the past year. The gene for necdin was mapped in the PWS candidate region and found to be paternally expressed in mouse and human. The bisulfite method for analysis of methylation was established for genomic sequencing and diagnostics, and the methylation of Snrpn was studied in detail in the mouse. A region near the Snrpn promoter was shown to function as a silencer in Drosophila. Point mutations were found in the gene for E6-AP ubiquitin-protein ligase (UBE3A) identifying it as the AS gene, and tissue-specific imprinting (maternal expression) was shown in the human brain and in hippocampal neurons and Purkinje cells in the mouse.

Angelman Syndrome↗

PubMed1998

The effect of anti-CD3-immunotoxin on T lymphocyte function in vitro.

Recent advances in the design of immunotoxins (IT) have yielded significant improvements. FN18-CRM9, a construct of anti-CD3 epsilon mAb FN18 and mutated diphtheria toxin CRM9 has exhibited high specificity, low systemic toxicity and unusual efficacy compared to previous iterations of immunotoxins. Others and we have examined this anti-CD3-IT for the purpose of inducing immunological tolerance through selective ablation of T cells in rhesus macaques and have obtained encouraging results. In order to characterize its mode of action, we have examined its effects on peripheral blood and lymph node T cell killing in vitro. We have studied the cytotoxic mechanism induced by this anti-CD3-IT as well as its effects on proliferation, phenotypic changes and cytokine production (IL2, IFN gamma and TNF alpha). The results indicate that anti-CD3-IT was highly specific for T cell killing at doses as low as 1 x 10(6) micrograms/ml and showed a maximal effect at 48 h after exposure. The toxicity was restricted to T cells, as B cells and other bystander cells were spared. This immunotoxin was shown to induce T cell apoptosis, as assessed by TUNEL assay, DNA content and cytotoxicity. Fas expression was upregulated on T cells within 24 h after in vitro exposure to anti-CD3-IT, suggesting an early T cell activation phase prior to T cell death. T cell killing was manifest as an early cell cycle arrest at the G1/S phase transition, which appeared to virtually eliminate the production of cytokines. These findings corroborate the temporal, specificity and quantitative patterns for anti-CD3 immunotoxin administration previously observed in vivo.

Animals↗

PubMed1998

Bone mineral density and biomechanical properties of spine and femur of ovariectomized rats treated with naproxen.

Prostaglandins have been reported to mediate the effects of ovariectomy on bone loss. We studied the effect of naproxen, an inhibitor of production of prostaglandins, on ovariectomy-induced bone loss. One hundred forty female Wistar rats 4.5 months of age were divided into groups of baseline, sham operation (sham), sham treated with naproxen at 10 mg/kg per day (in food), and ovariectomy treated with naproxen or estrogen as intramuscular injection of estradiol at 0.2 mg/kg body weight per week. They were killed 3, 6, and 9 months postsurgery. Bone mineral density (BMD) of the lumbar spine (L1-4), femoral neck, midshaft, and distal metaphysis was determined using dual-energy X-ray absorptiometry (DXA) in vitro. The compressive test of the L1 vertebral body and torsional test of the left femur were performed. The right femoral neck and femoral midshaft were processed undecalcified for determining cross-sectional moments of inertia. Naproxen treatment partially prevented ovariectomy-induced loss or less gain in BMD, in a significant manner, in the femoral neck cortical area, and also in L1 compressive strength and stiffness. Estrogen fully prevented these ovariectomy-induced effects. Naproxen showed no effect on ovariectomy-induced improvement in femoral torsional strength and stiffness and cross-sectional moments of inertia. No statistically significant difference was found between naproxen-treated sham rats and untreated sham rats. The data suggest that naproxen partially prevents ovariectomy-induced osteopenia.

Absorptiometry, Photon↗

PubMed1998

In vitro biosynthesis of the Pseudomonas aeruginosa quorum-sensing signal molecule N-butanoyl-L-homoserine lactone.

In Pseudomonas aeruginosa, synthesis of the quorum-sensing signal molecules N-butanoyl-L-homoserine lactone (BHL) and N-hexanoyl-L-homoserine lactone (HHL) requires the Luxl homologue Rhll(Vsml). By using thin-layer chromatography in conjunction with high-performance liquid chromatography (HPLC) and mass spectrometry, we show that purified Rhll can catalyse the biosynthesis of BHL and HHL using either S-adenosylmethionine (SAM) or homoserine lactone (HSL) but not homoserine as the source of the homoserine lactone moiety. As we were unable to detect homoserine lactone in cytoplasmic extracts of Escherichia coli, we conclude that SAM is the natural substrate for Rhll-directed N-acylhomoserine lactone (AHL) biosynthesis. The N-acyl chain of BHL and HHL can be supplied by the appropriately charged coenzyme A derivative (either n-butanoyl-CoA or n-hexanoyl-CoA). The specificity of Rhll for charged CoA derivatives is demonstrated as Rhll was unable to generate AHLs detectable in our bioassays from acetyl-CoA, malonyl-CoA, n-octanoyl-CoA, n-decanoyl-CoA, DL-beta-hydroxybutanoyl-CoA or crotonoyl-CoA. Rhll was also unable to use N-acetyl-S-3-oxobutanoylcysteamine, a chemical mimic for 3-oxobutanoyl-CoA. Furthermore, the Rhll-catalysed synthesis of BHL and HHL was most efficiently driven when NADPH was included in the reaction mixture.

4-Butyrolactone↗

PubMed1998

Keratinocyte differentiation is stimulated by activators of the nuclear hormone receptor PPARalpha.

Peroxisome proliferator activated receptors (PPAR) belong to the superfamily of nuclear hormone receptors that heterodimerize with the retinoid X receptor and regulate transcription of several genes involved in lipid metabolism and adipocyte differentiation. Because of the role of 1,25-dihydroxyvitamin D3 and retinoic acid working through similar receptors (the vitamin D receptor and retinoic acid receptor, respectively) on keratinocyte differentiation, we have examined the effects of activators of PPARalpha on keratinocyte differentiation. The rate of cornified envelope formation was increased 3-fold in keratinocytes maintained in low calcium (0.03 mM) and incubated in the presence of clofibric acid, a potent PPARalpha activator. Involucrin, a cornified envelope precursor, and the cross-linking enzyme transglutaminase, were increased at both the message level (2-7-fold) and the protein level (4-12-fold) by clofibric acid. Furthermore, physiologic doses of the fatty acids oleic acid, linoleic acid, and eicosatetraynoic acid, which are also activators of PPARalpha, also induced involucrin and transglutaminase protein and mRNA. In contrast, the PPARgammaligand prostaglandin J2 had no effect on protein or mRNA levels of involucrin or transglutaminase. Levels of involucrin and transglutaminase mRNA and protein were induced by clofibric acid in keratinocytes incubated in 1.2 mM calcium, a concentration which by itself induces keratinocyte differentiation. Finally, PPARalpha activators inhibit DNA synthesis. This study demonstrates that PPARalpha activators, including putative endogenous ligands such as fatty acids, induce differentiation and inhibit proliferation in keratinocytes, and suggests a regulatory role for the PPARalpha in epidermal homeostasis.

Cell Differentiation↗

PubMed1998

Ligands and activators of nuclear hormone receptors regulate epidermal differentiation during fetal rat skin development.

Because a protective barrier is essential for life, the development of the epidermis and stratum corneum must be completed prior to birth. The epidermal permeability barrier is comprised of corneocytes embedded in a lipid enriched matrix. Recent studies from our laboratory, using an explant model of fetal rat skin development that closely parallels in utero development, have shown that hormones and other activators of members of the nuclear receptor family regulate permeability barrier ontogenesis by stimulating lipid metabolism and the formation of the extracellular lipid lamellae. Using this model we sought to determine whether these hormones and nuclear activators also regulate keratinocyte differentiation during fetal development. Profilaggrin/filaggrin and loricrin expression, assessed by in situ hybridization and by immunohistochemistry, were progressively increased during epidermal ontogenesis. Whereas profilaggrin/filaggrin and loricrin were not expressed at day 17 of gestation, by day 19 both were present in the upper layers of the epidermis and both became still more abundant by day 21. These developmental changes also occurred in fetal skin explants cultured in vitro for 4 d, although the expression levels did not appear as robust as in utero. Whereas neither profilaggrin/filaggrin nor loricrin were expressed in control explants cultured for 2 d, they were seen in explants treated with either thyroid hormone, glucocorticoids, or estrogens. In contrast, dihydrotestosterone treatment delayed the expression of profilaggrin/filaggrin and loricrin. Moreover, both clofibrate, a peroxisome proliferator-activated receptor-alpha ligand, and juvenile hormone III, a farnesoid X-activated receptor activator, markedly accelerated fetal epidermal differentiation, stimulating both profilaggrin/filaggrin and loricrin expression. Our results demonstrate that several hormones and activators of nuclear hormone receptors regulate epidermal differentiation during fetal development, affecting key constituents of both keratohyalin granules and the cornified envelope. Thus, a variety of ligands/activators of nuclear receptors accelerate not only permeability barrier ontogenesis, but also the expression of structural proteins essential for stratum corneum formation.

Animals↗

PubMed1998

A high copy suppressor screen reveals genetic interactions between BET3 and a new gene. Evidence for a novel complex in ER-to-Golgi transport.

The BET3 gene in the yeast Saccharomyces cerevisiae encodes a 22-kD hydrophilic protein that is required for vesicular transport between the ER and Golgi complex. To gain insight into the role of Bet3p, we screened for genes that suppress the growth defect of the temperature-sensitive bet3 mutant at 34 degrees. This high copy suppressor screen resulted in the isolation of a new gene, called BET5. BET5 encodes an essential 18-kD hydrophilic protein that in high copy allows growth of the bet3-1 mutant, but not other ER accumulating mutants. This strong and specific suppression is consistent with the fact that Bet3p and Bet5p are members of the same complex. Using PCR mutagenesis, we generated a temperature-sensitive mutation in BET5 (bet5-1) that blocks the transport of carboxypeptidase Y to the vacuole and prevents secretion of the yeast pheromone alpha-factor at 37 degrees. The precursor forms of these proteins that accumulate in this mutant are indicative of a block in membrane traffic between the ER and Golgi apparatus. High copy suppressors of the bet5-1 mutant include several genes whose products are required for ER-to-Golgi transport (BET1, SEC22, USO1 and DSS4) and the maintenance of the Golgi (ANP1). These findings support the hypothesis that Bet5p acts in conjunction with Bet3p to mediate a late stage in ER-to-Golgi transport. The identification of mammalian homologues of Bet3p and Bet5p implies that the Bet3p/Bet5p complex is highly conserved in evolution.

Amino Acid Sequence↗

PubMed1998

Dissection of the effects of tumor necrosis factor-alpha and class II gene polymorphisms within the MHC on murine systemic lupus erythematosus (SLE).

Gene(s) in the MHC of the NZW strain (H-2z) up-regulate(s) systemic lupus erythematosus (SLE) in (NZB x NZW) F1 mice. So far, two plausible mechanisms have been implicated: (i) unique mixed haplotype class II molecules formed in the F1 mice act as a restriction element for self-reactive T cells and (ii) a unique polymorphism in the H-2-linked NZW tumor necrosis factor (TNF)-alpha allele which down-regulates TNF-alpha is contributory. Because of the difficulty in dissecting these alleles within the H-2 complex, it has not been determined which is indeed the case. We addressed this issue by establishing three different H-2-congenic (NZB x NZW) F1 mice bearing distinct haplotypes at class II and TNF-alpha regions, i.e. (NZB x NZW) F1 (H-2d/z:A(d/u)E(d/u)TNF(d/z)), (NZB x NZW.PL) F1 (H-2(d/u):A(d/u)E(d/u)TNF(d/d)) and (NZB x NZW.H-2d) F1 (H-2(d/d):A(d/d)E(d/d)TNF(d/d)). Among these, only (NZB x NZW) F1 produced a markedly lower level of TNF-alpha, due to the unique NZW TNF-alpha allele (TNF(z)). Studies of anti-DNA antibodies and lupus nephritis revealed that, compared to (NZB x NZW) F1, the disease of (NZB x NZW.H-2d) F1 was markedly reduced. In (NZB x NZW.PL) F1, the onset of renal disease was significantly delayed, while the extent of proteinuria and renal histopathology in individuals that had developed the disease was comparable to that seen in (NZB x NZW) F1. It seems likely that both class II and TNF-alpha gene polymorphisms are functioning as H-2-linked predisposing genetic elements, and that the TNF-alpha polymorphism acts to modulate an initial process of the renal disease.

Animals↗

PubMed1998

A protein encoded by the latency-related gene of bovine herpesvirus 1 is expressed in trigeminal ganglionic neurons of latently infected cattle and interacts with cyclin-dependent kinase 2 during productive infection.

Despite productive viral gene expression in the peripheral nervous system during acute infection, the bovine herpesvirus 1 (BHV-1) infection cycle is blocked in sensory ganglionic neurons and consequently latency is established. The only abundant viral transcript expressed during latency is the latency-related (LR) RNA. LR gene products inhibit S-phase entry, and binding of the LR protein (LRP) to cyclin A was hypothesized to block cell cycle progression. This study demonstrates LRP is a nuclear protein which is expressed in neurons of latently infected cattle. Affinity chromatography indicated that LRP interacts with cyclin-dependent kinase 2 (cdk2)-cyclin complexes or cdc2-cyclin complexes in transfected human cells or infected bovine cells. After partial purification using three different columns (DEAE-Sepharose, Econo S, and heparin-agarose), LRP was primarily associated with cdk2-cyclin E complexes, an enzyme which is necessary for G1-to-S-phase cell cycle progression. During acute infection of trigeminal ganglia or following dexamethasone-induced reactivation, BHV-1 induces expression of cyclin A in neurons (L. M. Schang, A. Hossain, and C. Jones, J. Virol. 70:3807-3814, 1996). Expression of S-phase regulatory proteins (cyclin A, for example) leads to neuronal apoptosis. Consequently, we hypothesize that interactions between LRP and cell cycle regulatory proteins promote survival of postmitotic neurons during acute infection and/or reactivation.

Animals↗

PubMed1998

Basis for late rise in fura 2 R signal reporting [Ca2+]i during relaxation in intact rat ventricular trabeculae.

Intact rat ventricular trabeculae were injected with the salt form of fura 2, and the fura 2 ratio signal (R) was used to report intracellular Ca2+ concentration ([Ca2+]i). The fixed end relaxation phase of a twitch is associated with a slowing of the decay of the R signal, or even a reversal, to form a distinct bump, indicating a transient rise in [Ca2+]i. The bump is most prominent at 30 degrees C, and motion artifact is not its cause. Increasing doses of 2,3-butanedione monoxime caused progressive attenuation of the twitch and bump. Increasing the bathing Ca2+ concentration potentiated the twitch and enhanced the bump. Imposed muscle shortening during relaxation caused a much quicker force decline, and this led to the appearance of a much more prominent associated bump. The amplitude of the bump depends on the amplitude of twitch force and the rate of relaxation. These findings can be explained, as in skeletal muscle, by making cross-bridge attachment and Ca2+ binding to troponin C strongly cooperative; therefore, the bump during fast relaxation is produced by a reversal of this cooperatively, leading to rapid dissociation of Ca2+ from troponin C into the myoplasm.

Animals↗

PubMed1998

Effects of halothane on [Ca2+]i transient, SR Ca2+ content, and force in intact rat heart trabeculae.

The goal of this study was to test whether the well-known cardiodepressant effect of halothane is caused mainly by depression of the transient increase in intracellular Ca2+ concentration ([Ca2+]i) during a twitch. Intact rat ventricular trabeculae, paced at 0.5 Hz and 30 degrees C with a bathing extracellular Ca2+ concentration ([Ca2+]o) of 2 mM, were used. The [Ca2+]i was monitored with the use of fura 2 injected into the myoplasm. The sarcoplasmic reticulum (SR) Ca2+ content was estimated with the use of rapid cooling (RC)-induced contracture force and Ca2+ release. The relationship of the peak [Ca2+]i transient versus peak twitch force obtained with halothane is intermediate between those obtained with lowered [Ca2+]o and varying doses of 2,3-butanedione monoxime. The data indicate that the negative inotropic action of halothane at low (0.18 mM) dose is mainly achieved by reduction in the Ca2+ sensitivity of the contractile apparatus, whereas, at high dose (0.55 mM), halothane acts both by reducing the [Ca2+]i transient and the Ca2+ sensitivity of the contractile system. At moderate (0.37 mM) dose, the effects were midway between low and high doses. With the use of RC contracture force alone, the reduction of SR Ca2+ content caused by halothane is overestimated.

Animals↗

PubMed1998

Effects of isoflurane on [Ca2+]i, SR Ca2+ content, and twitch force in intact trabeculae.

The goal was to test whether isoflurane exerts its depressant effect on the heart by mainly affecting the intracellular Ca2+ transient [Ca2+]i. Intact rat ventricular trabeculae, paced at 0.5 Hz and 30 degreesC with extracellular [Ca2+] ([Ca2+]o) of 2 mM, were used. The [Ca2+]i was monitored using fura 2 injected into the myoplasm. The sarcoplasmic reticulum (SR) Ca2+ content was estimated using rapid cooling with or without caffeine to induce Ca2+ release and contracture. A plot of peak twitch force versus peak [Ca2+]i transient with increasing isoflurane concentration declines linearly so that a 56% reduction in the peak [Ca2+]i transient would abolish twitch force. This relationship is intermediate between those obtained with lowering [Ca2+]o, which depresses twitch force through a reduction of the [Ca2+]i transient, and adding 2,3-butanedione monoxime, which reduces the responsiveness of the contractile system to [Ca2+]i. The isoflurane effect is different from that of halothane with respect to both the above relationship and the rapid-cooling response. Isoflurane abolishes the ability of rapid cooling to liberate Ca2+ from the SR.

Animals↗

PubMed1998

Trabecular bone mineral and calculated structure of human bone specimens scanned by peripheral quantitative computed tomography: relation to biomechanical properties.

The relationship of cortical bone mineral density (BMD), and geometry to bone strength has been well documented. In this study, we used peripheral quantitative computerized tomography (pQCT) to acquire trabecular BMD and high-resolution images of trabeculae from specimens to determine their relationship with biomechanical properties. Fifty-eight human cubic trabecular bone specimens, including 26 from the vertebral bodies, were scanned in water and air. Trabecular structure was quantitated using software developed with Advanced Visual Systems interfaced on a Sun/Sparc Workstation. BMD was also obtained using a whole-body computerized tomography scanner (QCT). Nondestructive testing of the specimens was performed to assess their elastic modulus. QCT and pQCT measurements of BMD of specimens in water were strongly correlated (r2 = 0.95, p < 0.0001), with a slope (0.96) statistically not significantly different from 1. Strong correlations were found between pQCT measurements of specimens in water and in air, for BMD (r2 = 0.96, p < 0.0001), and for apparent trabecular structural parameters (r2 = 0.89-0.93, p < 0.0001). Correlations were moderate between BMD and apparent trabecular structural parameters (r2 = 0.37-0.64, p < 0.0001). Precision as coefficient of variation (CV) and standardized coefficient of variation (SCV) for these measurements was < 5%. For the vertebral specimens, the correlation was higher between elastic modulus and BMD (r2 = 0.76,p < 0.0001) than between elastic modulus and apparent trabecular structural parameters (r2 = 0.58-0.72, p < 0.0001), while the addition of apparent trabecular nodes and branches to BMD in a multivariate regression model significantly increased the correlation with the elastic modulus (r2 = 0.86, p < 0.01). Thus, pQCT can comparably and reproducibly measure trabecular bone mineral in water or air, and trabecular structure can be quantitated from pQCT images. The combination of volumetric BMD with trabecular structural parameters rather than either alone improves the prediction of biomechanical properties. Such a noninvasive approach may be useful for the preclinical study of osteoporosis.

Adult↗

PubMed1998

Visual inertia of rotating 3-D objects.

Five experiments were designed to determine whether a rotating, transparent 3-D cloud of dots (simulated sphere) could influence the perceived direction of rotation of a subsequent sphere. Experiment 1 established conditions under which the direction of rotation of a virtual sphere was perceived unambiguously. When a near-far luminance difference and perspective depth cues were present, observers consistently saw the sphere rotate in the intended direction. In Experiment 2, a near-far luminance difference was used to create an unambiguous rotation sequence that was followed by a directionally ambiguous rotation sequence that lacked both the near-far luminance cue and the perspective cue. Observers consistently saw the second sequence as rotating in the same direction as the first, indicating the presence of 3-D visual inertia. Experiment 3 showed that 3-D visual inertia was sufficiently powerful to bias the perceived direction of a rotation sequence made unambiguous by a near-far luminance cue. Experiment 5 showed that 3-D visual inertia could be obtained using an occlusion depth cue to create an unambiguous inertia-inducing sequence. Finally, Experiments 2, 4, and 5 all revealed a fast-decay phase of inertia that lasted for approximately 800 msec, followed by an asymptotic phase that lasted for periods as long as 1,600 msec. The implications of these findings are examined with respect to motion mechanisms of 3-D visual inertia.

Contrast Sensitivity↗

PubMed1998

[A socioepidemiological survey of the oral health status and needs for dental care among elderly population in China].

The purpose of this surrey is to study the prevalence of dental disease and the needs of dental treatment, so as to develop effective programs in improving dental care in the elderly, 475 residents are selected by means of a systematic stratified sampling procedure. The aged people have poor dental health knowledge and habits. Major problems for getting their dental care include: 1. difficult to get registration; 2. long time waiting before seeing a dentist; 3. the actual needs for dental treatment are more than what expected by the elderly themselves. The study reveals that many problems are existed in terms of oral health status and dental care among the elderly, which calls for more attention.

Aged↗

PubMed1998

[Identification of Listeria monocytogenes by PCR method].

OBJECTIVE: To establish a rapid, sensitive and specific polymerase chain reaction (PCR) method for detection of Listeria monocytogenes (LM). METHODS: A pair of oligonucleotide primers were designed with hylA gene as target sequence. Fiftyfour strain of standard LM and 21 strains of irelevant bacteria were amplified and confirmed by PCR technique. Thirty-three strains of listeria isolated from food at home were identified by PCR and routine methods. RESULTS: A 743-bp DNA fragment with a conservative Hind II site could be amplified by PCR, showing excellent features of LM. Limit to detection for pure culture was 55 colony forming units (CFU). Eighteen of 54 strains were identified as LM by both methods, with a completely coincident result. PCR was strongly inhibited as used in detection for food. If food was cultured for 25 hours for proliferation in listeria enrichment broth, then the culture was chemically extracted, the purified bacteria after heat lysis could react as PCR templates and the inhibitory effects could be greatly reduced. Milk inoculated artificially with four colony forming units of LM could be specifically detected by PCR. CONCLUSION: PCR can be used in rapid, sensitive and specific identification of LM.

Animals↗