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Biomedical subjects

Y Zhong

Publications and source records attributed to Y Zhong.

At least 73 records · Page 4Linked to original sources
PubMed2000

[Effect of amniotic membrane on filtering bleb after trabeculectomy in rabbit eyes].

OBJECTIVE: To investigate the effects of amniotic membrane on filtering blebs after trabeculectomy. METHODS: Twelve rabbits underwent bilateral trabeculectomies. One eye was randomly sutured preserved human amniotic membrane between the sclera and the scleral flap and the other eye served as the control. The filtering blebs and filtering function were observed at the 1st, 2nd and 3rd week after the operation. The scar development situation between bleb and episclera was observed under the light microscope. RESULTS: The blebs in amniotic membrane group were eminence, effuse and had a good filtering function at the 1st, 2nd and 3rd week after the operation. The blebs in control group were cicatrized and had a bad filtering function. Histological observation showed no scar development, less fibroblast cell and more inflammatory cells infiltration at the site of trabeculectomy in amniotic membrane group. On the contrary, the control group showed more fibroplasia and fibroblast hyperplasia. CONCLUSION: Amniotic membrane can reduce the scar, improve filtering function.

Amnion↗
PubMed1999

Analysis of C-cadherin regulation during tissue morphogenesis with an activating antibody.

The regulation of cadherin-mediated adhesion at the cell surface underlies several morphogenetic processes. To investigate the role of cadherin regulation in morphogenesis and to begin to analyze the molecular mechanisms of cadherin regulation, we have screened for monoclonal antibodies (mAbs) that allow us to manipulate the adhesive state of the cadherin molecule. Xenopus C-cadherin is regulated during convergent extension movements of gastrulation. Treatment of animal pole tissue explants (animal caps) with the mesoderm-inducing factor activin induces tissue elongation and decreases the strength of C-cadherin-mediated adhesion between blastomeres (Brieher, W.M., and B.M. Gumbiner. 1994. J. Cell Biol. 126:519-527). We have generated a mAb to C-cadherin, AA5, that restores strong adhesion to activin-treated blastomeres. This C-cadherin activating antibody strongly inhibits the elongation of animal caps in response to activin without affecting mesodermal gene expression. Thus, the activin-induced decrease in C-cadherin adhesive activity appears to be required for animal cap elongation. Regulation of C-cadherin and its activation by mAb AA5 involve changes in the state of C-cadherin that encompass more than changes in its homophilic binding site. Although mAb AA5 elicited a small enhancement in the functional activity of the soluble C-cadherin ectodomain (CEC1-5), it was not able to restore cell adhesion activity to mutant C-cadherin lacking its cytoplasmic tail. Furthermore, activin treatment regulates the adhesion of Xenopus blastomeres to surfaces coated with two other anti-C-cadherin mAbs, even though these antibodies probably do not mediate adhesion through a normal homophilic binding mechanism. Moreover, mAb AA5 restores strong adhesion to these antibodies. mAb AA5 only activates adhesion of blastomeres to immobilized CEC1-5 when it binds to C-cadherin on the cell surface. It does not work when added to CEC1-5 on the substrate. Together these findings suggest that the regulation of C-cadherin by activin and its activation by mAb AA5 involve changes in its cellular organization or interactions with other cell components that are not intrinsic to the isolated protein.

Activins↗
PubMed1999

American ginseng and breast cancer therapeutic agents synergistically inhibit MCF-7 breast cancer cell growth.

BACKGROUND AND OBJECTIVES: American ginseng (Panax quinquefolius L.) purportedly alleviates menopause symptoms because of putative estrogenicity. METHODS: Using a standardized American ginseng (AG) extract in MCF-7 breast cancer cells, the objectives were to evaluate the ability of AG to induce the estrogen- regulated gene pS2 by Northern blot analysis, determine the effect on cell growth using the MTT assay, and evaluate the cell cycle effects by flow cytometry. RESULTS: AG and estradiol equivalently induced RNA expression of pS2. AG, in contrast to estradiol, caused a dose-dependent decrease in cell proliferation (P < 0.005). AG had no adverse effect on the cell cycle while estradiol significantly increased the proliferative phase (percent S-phase) and decreased the resting phase (G(0)-G(1) phase) (P < 0.005). Concurrent use of AG and breast cancer therapeutic agents resulted in a significant (P < 0.005) suppression of cell growth for most drugs evaluated. CONCLUSIONS: In vitro use of AG and breast cancer therapeutics synergistically inhibited cancer cell growth.

Antineoplastic Agents, Hormonal↗
PubMed1999

The utility of short tandem repeat loci beyond human identification: implications for development of new DNA typing systems.

Since the first characterization of the population genetic properties of repeat polymorphisms, the number of short tandem repeat (STR) loci validated for forensic use has now grown to at least 13. Worldwide variations of allele frequencies at these loci have been studied, showing that variations of interpopulation diversity at these loci do not compromise the power of identification of individuals. However, data collected for validation of these loci for forensic use has utility beyond human identification; the origin and past migration history of modern humans can be reconstructed from worldwide variations at these loci. Furthermore, complex forensic cases previously unresolvable can now be investigated with the help of the validated STR loci. Here, we provide the absolute power of the validated set of 13 STR loci for addressing these issues using multilocus genotype data on 1,401 individuals belonging to seven populations (US European-American, US African-American, Jamaican, Italian, Swiss, Chinese and Apache Native-American). Genomic research is discovering new classes of polymorphic loci (such as the single nucleotide polymorphisms, SNPs) and lineage markers (such as the mitochondrial DNA and Y-chromosome markers); our aim, therefore, was to determine how many SNP loci are needed to match the power of this set of 13 STR loci. We conclude that the current set of STR loci is adequate for addressing most problems of human identification (including interpretations of DNA mixtures). However, if suitable number of SNPs are used that would match the power of the STR loci, they alone cannot resolve more complex cases unless they are supplemented by the validated STR loci.

Chromosome Mapping↗
PubMed1999

The interactions of the N-terminal fusogenic peptide of HIV-1 gp41 with neutral phospholipids.

We have studied the interactions with neutral phospholipid bilayers of FPI, the 23-residue fusogenic N-terminal peptide of the HIV-1LAI transmembrane glycoprotein gp41, by CD, EPR, NMR, and solid state NMR (SSNMR) with the objective of understanding how it lyses and fuses cells. Using small unilamellar vesicles made from egg yolk phoshatidylcholine which were not fused or permeabilised by the peptide we obtained results suggesting that it was capable of inserting as an alpha-helix into neutral phospholipid bilayers but was only completely monomeric at peptide/lipid (P/L) ratios of 1/2000 or lower. Above this value, mixed populations of monomeric and multimeric forms were found with the proportion of multimer increasing proportionally to P/L, as calculated from studies on the interaction between the peptide and spin-labelled phospholipid. The CD data indicated that, at P/L between 1/200 and 1/100, approximately 68% of the peptide appeared to be in alpha-helical form. When P/L = 1/25 the alpha-helical content had decreased to 41%. Measurement at a P/L of 1/100 of the spin lattice relaxation effect on the 13C nuclei of the phospholipid acyl chains of an N-terminal spin label attached to the peptide showed that most of the peptide N-termini were located in the interior hydrocarbon region of the membrane. SSNMR on multilayers of ditetradecylphosphatidyl choline at P/Ls of 1/10, 1/20 and 1/30 showed that the peptide formed multimers that affected the motion of the lipid chains and disrupted the lipid alignment. We suggest that these aggregates may be relevant to the membrane-fusing and lytic activities of FPI and that they are worthy of further study.

Amino Acid Sequence↗
PubMed1999

Effect of lidocaine on improving cerebral protection provided by retrograde cerebral perfusion: a neuropathologic study.

OBJECTIVE: To determine whether lidocaine can improve the neuropathologic results in canine brains after retrograde cerebral perfusion (RCP). DESIGN: Randomized, blinded, experimental study. SETTING: University animal laboratory. PARTICIPANTS: Mongrel dogs. INTERVENTIONS: Fourteen mongrel dogs were placed on 120 minutes of hypothermic (20 degrees C) RCP. Following the RPC, they then resumed cardiopulmonary bypass and rewarming for 60 minutes. In the lidocaine group (n = 8), lidocaine was administered continuously; in the control group (n = 6), normal saline was administered. Cerebral perfusion fixation was performed at the end of the experiment. MEASUREMENTS AND MAIN RESULTS: The number of ischemic cells in 200 neurons was counted in the parietal cortex, CA1 sector of the hippocampus, CA3 sector of the hippocampus, ventral posterolateral nucleus of the thalamus, and Purkinje cells of the cerebellar cortex. Those in the parietal cortex, CA1 sector of the hippocampus, and ventral posterolateral nucleus of the thalamus were significantly less in the lidocaine group than in the control group (25.8+/-17.3 v 53.7+/-12.0; p < 0.01; 17.0+/-8.5 v 54.7+/-22.1; p < 0.01; and 16.9+/-17.8 v 49.7+/-28.4; p < 0.05, respectively). The total number of ischemic cells in the five examined regions was also significantly less in the lidocaine group than in the control group (89.5+/-19.4 v 219.5+/-45.5; p < 0.01). CONCLUSION: Continuous lidocaine significantly alleviated the ischemic neuropathologic injury after RCP and thus possibly improved cerebral protection.

Anesthetics, Local↗
PubMed1999

Bone marrow transplantation attenuates murine IgA nephropathy: role of a stem cell disorder.

BACKGROUND: The pathogenesis of IgA nephropathy is still obscure. The aim of this study was to investigate whether the fundamental pathogenesis of IgA nephropathy lies in bone marrow stem cells (BMCs). METHODS: We used donors of two different strains for bone marrow transplantation (BMT) into mice with a high content of serum IgA (ddY strain, HIGA mice), a murine model of IgA nephropathy. One group (B6-->HIGA, N = 5) received BMCs of C57BL/6j (B6) mice, and the other (HIGA-->HIGA, N = 8) were reconstituted with BMCs of HIGA mice. RESULTS: Twenty-six weeks after BMT, in B6-->HIGA mice, mesangial deposits of IgA and C3 were statistically milder than those in HIGA-->HIGA mice. Light microscopic observations disclosed that glomerular sclerosis and mesangial matrix expansion in B6-->HIGA mice were decreased compared with those in HIGA-->HIGA mice. These B6-->HIGA mice also excreted less urinary albumin than HIGA-->HIGA mice. Furthermore, serum levels of IgA in B6-->HIGA mice were markedly lower than those in HIGA-->HIGA mice. Size analysis of serum IgA revealed that macromolecular IgA were notably lower in B6-->HIGA mice than in HIGA-->HIGA mice. CONCLUSIONS: Our results suggest that qualitative and quantitative changes of serum IgA are determined at the level of stem cells, and that BMT from normal donors can attenuate glomerular lesions in HIGA mice. This approach may offer a new avenue to study the pathogenesis of IgA nephropathy.

Age Factors↗
PubMed1999

Patterns of instability of expanded CAG repeats at the ERDA1 locus in general populations.

A highly polymorphic CAG repeat locus, ERDA1, was recently described on human chromosome 17q21.3, with alleles as large as 50-90 repeats and without any disease association in the general population. We have studied allelic distribution at this locus in five human populations and have characterized the mutational patterns by direct observation of 731 meioses. The data show that large alleles (>/=40 CAG repeats) are generally most common in Asian populations, less common in populations of European ancestry, and least common among Africans. We have observed a high intergenerational instability (46. 3%+/-5.1%) of the large alleles. Although the mutation rate is not dependent on parental sex, paternal transmissions have predominantly resulted in contractions, whereas maternal transmissions have yielded expansions. Within this class of large alleles, the mutation rate increases concomitantly with increasing allele size, but the magnitude of repeat size change does not depend on the size of the progenitor allele. Sequencing of specific alleles reveals that the intermediate-sized alleles (30-40 repeats) have CAT/CAC interruptions within the CAG-repeat array. These results indicate that expansion and instability of trinucleotide repeats are not exclusively disease-associated phenomena. The implications of the existence of massively expanded alleles in the general populations are not yet understood.

Alleles↗
PubMed1999

HICLAS: a taxonomic database system for displaying and comparing biological classification and phylogenetic trees.

MOTIVATION: Numerous database management systems have been developed for processing various taxonomic data bases on biological classification or phylogenetic information. In this paper, we present an integrated system to deal with interacting classifications and phylogenies concerning particular taxonomic groups. RESULTS: An information-theoretic view (taxon view) has been applied to capture taxonomic concepts as taxonomic data entities. A data model which is suitable for supporting semantically interacting dynamic views of hierarchic classifications and a query method for interacting classifications have been developed. The concept of taxonomic view and the data model can also be expanded to carry phylogenetic information in phylogenetic trees. We have designed a prototype taxonomic database system called HICLAS (HIerarchical CLAssification System) based on the concept of taxon view, and the data models and query methods have been designed and implemented. This system can be effectively used in the taxonomic revisionary process, especially when databases are being constructed by specialists in particular groups, and the system can be used to compare classifications and phylogenetic trees. AVAILABILITY: Freely available at the WWW URL: http://aims.cps.msu.edu/hiclas/ CONTACT: pramanik@cps.msu.edu; lotus@wipm.whcnc.ac.cn

Classification↗
PubMed1999

Select 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors vary in their ability to reduce egg yolk cholesterol levels in laying hens through alteration of hepatic cholesterol biosynthesis and plasma VLDL composition.

The inability to markedly attenuate cholesterol levels in chicken eggs has led to speculation that cholesterol is essential for yolk formation and that egg production would cease when yolk cholesterol deposition was inadequate for embryonic survival. However, this critical level hypothesis remains unproven. Here, we determine the relative responsiveness of laying hens to three select inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), the rate-limiting enzyme of cholesterol biosynthesis. A control diet, either alone or supplemented with one of two dietary levels (0.03 or 0.06%) of atorvastatin, lovastatin, or simvastatin, was fed to White Leghorn hens for 5 wk. Liver cholesterol concentrations (mg/g tissue) were decreased (P </= 0.05) by each HMGR inhibitor; however, total liver cholesterol (mg) did not differ among treatments. Microsomal hepatic HMGR activities were increased one- to twofold in all HMGR inhibitor-treated groups, while HMGR mRNA levels were unaffected. Diameters of plasma VLDL particles, the main cholesterol-carrying yolk precursor macromolecules, were reduced (P </= 0.05) only in hens fed 0.06% atorvastatin, and the particles contained 38% less total cholesterol (P </= 0.05) than controls. Plasma total cholesterol concentrations were lowered (P </= 0.05) by both doses of atorvastatin (-56, -63%) and simvastatin (-36,-45%). Egg cholesterol contents were maximally reduced by 46% (P </= 0.05), 7% (P > 0.05), and 22% (P </= 0.05) in hens fed the 0.06% level of atorvastatin, lovastatin, and simvastatin, respectively, while overall egg production [-19% (P </= 0.05), +4% (P > 0.05), and -3% (P > 0.05)], was much less affected. We concluded that cholesterol per se may not be an obligatory component for yolk formation in chickens and, as such, may be amenable to further pharmacological manipulation

Animals↗
PubMed1999

Rate and directionality of mutations and effects of allele size constraints at anonymous, gene-associated, and disease-causing trinucleotide loci.

We studied the patterns of within- and between-population variation at 29 trinucleotide loci in a random sample of 200 healthy individuals from four diverse populations: Germans, Nigerians, Chinese, and New Guinea highlanders. The loci were grouped as disease-causing (seven loci with CAG repeats), gene-associated (seven loci with CAG/CCG repeats and eight loci with AAT repeats), or anonymous (seven loci with AAT repeats). We used heterozygosity and variance of allele size (expressed in units of repeat counts) as measures of within-population variability and GST (based on heterozygosity as well as on allele size variance) as the measure of genetic differentiation between populations. Our observations are: (1) locus type is the major significant factor for differences in within-population genetic variability; (2) the disease-causing CAG repeats (in the nondisease range of repeat counts) have the highest within-population variation, followed by the AAT-repeat anonymous loci, the AAT-repeat gene-associated loci, and the CAG/CTG-repeat gene-associated loci; (3) an imbalance index beta, the ratio of the estimates of the product of effective population size and mutation rate based on allele size variance and heterozygosity, is the largest for disease-causing loci, followed by AAT- and CAG/CCG-repeat gene-associated loci and AAT-repeat anonymous loci; (4) mean allele size correlates positively with allele size variance for AAT- and CAG/CCG-repeat gene-associated loci and negatively for anonymous loci; and (5) GST is highest for the disease-causing loci. These observations are explained by specific differences of rates and patterns of mutations in these four groups of trinucleotide loci, taking into consideration the effects of the past demographic history of the modern human population.

Alleles↗
PubMed1999

Patterns in costs and outcomes for patients with prolonged mechanical ventilation undergoing tracheostomy: an analysis of discharges under diagnosis-related group 483 in New York State from 1992 to 1996.

OBJECTIVE: To analyze the costs and discharge status for patients with prolonged mechanical ventilation undergoing tracheostomy. DESIGN: Retrospective analysis of a statewide database. PATIENTS: All patients (n = 37,573) >18 yrs of age who had prolonged mechanical ventilation (procedure code 96.72) and were discharged from the hospital between 1992 and 1996 with a final DRG code of 483. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Rates of change in discharges and hospital reimbursements and the cost per survivor were examined by case payment groups and discharge year. A direct relation between volume and reimbursement rate was seen over time, although the patient age distributions remained relatively stable. The greatest increase in volume was from 1995 to 1996. For most years, there was a consistent inverse relation between age and survival, with older survivors being more likely to be discharged to residential healthcare facilities and younger patients more likely to be discharged home. There was a consistent direct relation between age and cost per survivor, mainly the result of improved survival rather than decreased reimbursements in later years. CONCLUSIONS: More controlled reimbursements and improved overall survival rates for DRG 483 have contributed to the improved cost per survivor among all age groups over the period. Given the greater proportion of elderly that do not survive or who are placed into residential healthcare facilities, more scrutiny is needed concerning the use of DRG 483 resources so that care is better coordinated for these patients in the inpatient and postacute care settings.

Adult↗
PubMed1999

Transcriptional and posttranscriptional regulation of insulin-like growth factor binding protein-3 by cyclic adenosine 3',5'-monophosphate: messenger RNA stabilization is accompanied by decreased binding of a 42-kDa protein to a uridine-rich domain in the 3'-untranslated region.

The Madin Darby bovine kidney (MDBK) cell line was used to investigate the mechanisms underlying the cAMP regulation of insulin-like growth factor binding protein-3 (IGFBP-3) gene expression. Treatment of confluent monolayers either with forskolin or cAMP produced a 60- to 75-fold induction of IGFBP-3 mRNA and protein levels. This effect did not require new protein synthesis as inhibition of translation by cycloheximide actually caused a 2-fold increase in the cAMP induction. The rates of IGFBP-3 gene transcription, assessed by nuclear run-on assays, increased approximately 15-fold in cells exposed to cAMP. In addition, the half-life of the IGFBP-3 mRNA transcript was increased approximately 3-fold in the presence of cAMP. Gel mobility shift and competition experiments revealed the specific binding of an approximately 42-kDa cytoplasmic protein factor to the 3'-untranslated region (3'-UTR) of the IGFBP-3 mRNA. A 21-nucleotide uridine-rich segment that contained no AUUUA motif was sufficient for the specific binding. The binding activity of this protein was reduced after cAMP treatment but was increased by phosphatase treatment. In conclusion, the cAMP induction of IGFBP-3 mRNA in MDBK cells occurred at both the transcriptional and posttranscriptional levels. The IGFBP-3 mRNA stabilization in MDBK cells probably involved the phosphorylation of a member of the family of U-rich region mRNA-binding proteins and is the first reported member whose RNA-binding activity is reduced by cAMP.

3' Untranslated Regions↗
PubMed1999

Corticosteroids and glaucoma risk.

Corticosteroids (glucocorticoids), used frequently as potent anti-inflammatory agents, increase the risk of glaucoma by raising the intraocular pressure (IOP) when administered exogenously (topically, periocularly or systemically) and in certain conditions of increased endogenous production (e.g. Cushing's syndrome). Approximately 18 to 36% of the general population are corticosteroid responders. This response is increased to 46 to 92% in patients with primary open-angle glaucoma (POAG). Patients over 40 years of age and with certain systemic diseases (e.g. diabetes mellitus, high myopia) as well as relatives of patients with POAG are more vulnerable to corticosteroid-induced glaucoma. The association of corticosteroid-induced ocular hypertension in other conditions which are considered as risk factors for glaucoma (racial origins, hypertension, migraine, vasospasm) is likely but not fully established. The proposed mechanism of corticosteroid-induced glaucoma includes morphological and functional changes in the trabecular meshwork system and is similar to the pathogenesis of POAG. Trabecular cells exposed to corticosteroids in vitro show endoreplication of nuclei, an increase in cell size and excessive production of an approximately 56kD glycoprotein, identified as myocilin and transcribed by the GLC1A gene. Induction of ocular hypertension after corticosteroid administration depends on the specific drug, the dose, the frequency of administration and the corticosteroid responsiveness of the patient. The risk of corticosteroid-induced glaucoma can be minimised with judicious use of corticosteroids, as well as education of patients and medical practitioners. New treatment modalities include modified steroids and nonsteroidal anti-inflammatory agents that will have less effect on the elevation of IOP.

Glaucoma↗
PubMed1999

Cloning and sequence analysis of an amastin coding gene from Leishmania major Abdou.

OBJECTIVE: To clone a surface protein encoding gene from Leishmania major Abdou parasites. METHODS: Using Trypanosotidae cruzi (T. cruzi) amastin DNA sequence as a reference, computer search was done on Genbank and dbEST data bases with BLASTN path. A Leishmania major Abdou DNA library has been established and screened by in situ colony hybridization. RESULTS: No homology sequence to T. cruzi amastin was found in Genbank, but a 309 nt DNA fragment from Leishmania major (L. major) existed in bEST. Leishmania major Abdou DNA library was screened using specific probes synthesized according to 309 nt DNA sequence of T. cruzi amastin gene, and full-length coding sequence for Leishmania major Abdou amastin was cloned. The coding sequence consisted of 552 nt, and translated into 183 amino acid residues. The homology is 23.5% at amino acid sequence level between Leishmania major Abdou and T. cruzi amastins. CONCLUSION: We have cloned the full length amastin coding DNA for Leishmania major Abdou.

Amino Acid Sequence↗
PubMed1999

[Rat retinal ganglion cells in culture].

OBJECTIVE: To establish a culture system for retinal ganglion cells (RGCs) in order to lay a foundation for the experimental research in vitro. METHODS: The retinae of 16 postnatal 2 - 3 day Sprague-Dawley rats were dissected into cell suspension with trypsin digestion. The cell suspension was implanted in 24 well culture plates with a cover slide 1 cm(2) in size and covered with murine tail collagen preplaced in each well (4 x 10(5) cells/well) and cultured under 37 degree C in an incubator with 5% CO(2). The cells were identified by immunocytochemical method with anti-rat Thy -1.1 monoclonal antibody after culture for 1, 3, 5 days, respectively, and the number of RGCs and its axon-growth percentage were counted in each 10-field high power (HP, 200 x) view under light microscope. RESULTS: The RGCs cultured in murine tail collagen tissue grew very well. Some cells possessed axons and some axons connected in networks. The RGC number and its axon-growth percentage were (401 +/- 9) cells/10 HP and (25.34 +/- 0.72)% in 1-day-culture, (351 +/- 6) cells/10 HP and (35.16 +/- 2.22)% in 3-day-culture, (109 +/- 8) cells/10 HP and (69.84 +/- 0.97)% in 5-day-culture, respectively. CONCLUSION: RGCs can be cultured successfully and the murine tail collagen tissue is a good substratum for RGC survival in vitro.

Animals↗