Biomedical subjects

Hua Yang

Publications and source records attributed to Hua Yang.

At least 19 recordsLinked to original sources

PubMed2025

Genome imbalance modulates the expression of long non-coding RNAs in maize.

Genome imbalance, resulting from varying the dosage of individual chromosomes (aneuploidy), has a more detrimental effect than changes in complete sets of chromosomes (haploidy/polyploidy). This imbalance is likely due to disruptions in stoichiometry and interactions among macromolecular assemblies. Previous research has shown that aneuploidy causes global modulation of protein-coding genes (PCGs), microRNAs, and transposable elements (TEs), affecting both the varied chromosome (cis-located) and unvaried genome regions (trans-located) across various taxa. While long non-coding RNAs (lncRNAs) are important gene expression regulators, their roles in the context of genomic imbalance remain largely unexplored. In this study, we analyzed and compared the impact of aneuploidy and haploidy/polyploidy on lncRNA expression using RNA-seq data from maize mature leaf tissue. Our results indicate that cis-located lncRNAs are modulated from dosage compensation to a gene dosage effect, while trans-located lncRNAs exhibit trends ranging from an inverse effect to a positive correlation with chromosomal dosage. Remarkably, the ploidy series showed a lesser degree of lncRNA modulation. LncRNAs and TEs display a similar trend of inverse modulation but exhibit greater sensitivity to dosage changes compared to PCGs. The construction of cis-acting and trans-acting lncRNA co-expression networks indicates that lncRNAs likely function as dosage-sensitive regulators of gene expression under conditions of genomic imbalance. Overall, this study not only elucidates the dosage effect of plant lncRNAs but also serves as a valuable resource for exploring potential regulators of PCGs that play significant biological functions.

Zea mays↗

PubMed2024

Identification of miRNA expression profile in middle ear cholesteatoma using small RNA-sequencing.

BACKGROUND: The present study aims to identify the differential miRNA expression profile in middle ear cholesteatoma and explore their potential roles in its pathogenesis. METHODS: Cholesteatoma and matched normal retroauricular skin tissue samples were collected from patients diagnosed with acquired middle ear cholesteatoma. The miRNA expression profiling was performed using small RNA sequencing, which further validated by quantitative real-time PCR (qRT-PCR). Target genes of differentially expressed miRNAs in cholesteatoma were predicted. The interaction network of 5 most significantly differentially expressed miRNAs was visualized using Cytoscape. Further Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway enrichment analyses were processed to investigate the biological functions of miRNAs in cholesteatoma. RESULTS: The miRNA expression profile revealed 121 significantly differentially expressed miRNAs in cholesteatoma compared to normal skin tissues, with 56 upregulated and 65 downregulated. GO and KEGG pathway enrichment analyses suggested their significant roles in the pathogenesis of cholesteatoma. The interaction network of the the 2 most upregulated (hsa-miR-21-5p and hsa-miR-142-5p) and 3 most downregulated (hsa-miR-508-3p, hsa-miR-509-3p and hsa-miR-211-5p) miRNAs identified TGFBR2, MBNL1, and NFAT5 as potential key target genes in middle ear cholesteatoma. CONCLUSIONS: This study provides a comprehensive miRNA expression profile in middle ear cholesteatoma, which may aid in identifying therapeutic targets for its management.

Humans↗

PubMed2024

Enhanced transgene expression from single-stranded AAV vectors in human cells in vitro and in murine hepatocytes in vivo.

We identified that distal 10 nucleotides in the D-sequence in AAV2 inverted terminal repeat (ITR) share partial sequence homology to 1/2 binding site of glucocorticoid receptor-binding element (GRE). Here, we describe that (1) purified GR binds to AAV2 D-sequence, and the D-sequence competes with GR binding to its cognate binding site; (2) dexamethasone-mediated activation of GR pathway significantly increases the transduction efficiency of AAV2 vectors in human cells; (3) human osteosarcoma cells, U2OS, which lack expression of GR, are poorly transduced by AAV2 vectors, but stable transfection with a GR expression plasmid restores vector-mediated transgene expression; (4) replacement of the distal 10 nucleotides in the D-sequence of the AAV2 ITR with a full-length GRE consensus sequence significantly enhances transgene expression in human cells in vitro and in murine hepatocytes in vivo; and (5) none of the ITRs in AAV1, AAV3, AAV4, AAV5, and AAV6 genomes contains the GRE 1/2 binding site, and insertion of a full-length GRE consensus sequence in the AAV6-ITR also significantly enhances transgene expression from AAV6 vectors, both in vitro and in vivo. These novel vectors, termed generation Y AAV vectors, which are serotype, transgene, or promoter agnostic, should be useful in human gene therapy.

AAV vectors↗

PubMed2007

Palladin regulates cell and extracellular matrix interaction through maintaining normal actin cytoskeleton architecture and stabilizing beta1-integrin.

Cell and extracellular matrix (ECM) interaction plays an important role in development and normal cellular function. Cell adhesion and cell spreading on ECM are two basic cellular behaviors related to cell-ECM interaction. Here we show that palladin, a novel actin cytoskeleton-associated protein, is actively involved in the regulation of cell-ECM interaction. It was found that palladin-deficient mouse embryonic fibroblasts (MEFs) display decreased cell adhesion and compromised cell spreading on various ECMs. Disorganized actin cytoskeleton architecture characterized by faint stress fibers, less lamellipodia and focal adhesions can account for the weakened cell-ECM interaction in palladin(-/-) MEFs. Furthermore, decreased polymerized filament actin and increased globular actin can be observed in palladin(-/-) MEFs, strongly suggesting that palladin is essential for the formation or stabilization of polymerized filament actin. Elevated phospho-cofilin level and proper responses in cofilin phosphorylation to either Rho signal agonist or antagonist in palladin(-/-) MEFs indicate that disrupted stress fibers in palladin(-/-) MEFs is not associated with cofilin phosphorylation. More interestingly, the protein level of ECM receptor beta1-integrin is dramatically decreased in MEFs lacking palladin. Down-regulation of beta1-integrin protein can be restored by proteasome inhibitor MG-132 treatment. All these data implicate that palladin is essential for cell-ECM interaction through maintaining normal actin cytoskeleton architecture and stabilizing beta1-integrin protein.

Actins↗

PubMed2007

Dendritic cell-expanded, islet-specific CD4+ CD25+ CD62L+ regulatory T cells restore normoglycemia in diabetic NOD mice.

Most treatments that prevent autoimmune diabetes in nonobese diabetic (NOD) mice require intervention at early pathogenic stages, when insulitis is first developing. We tested whether dendritic cell (DC)-expanded, islet antigen-specific CD4+ CD25+ suppressor T cells could treat diabetes at later stages of disease, when most of the insulin-producing islet beta cells had been destroyed by infiltrating lymphocytes. CD4+ CD25+ CD62L+ regulatory T cells (T reg cells) from BDC2.5 T cell receptor transgenic mice were expanded with antigen-pulsed DCs and IL-2, and were then injected into NOD mice. A single dose of as few as 5x10(4) of these islet-specific T reg cells blocked diabetes development in prediabetic 13-wk-old NOD mice. The T reg cells also induced long-lasting reversal of hyperglycemia in 50% of mice in which overt diabetes had developed. Successfully treated diabetic mice had similar responses to glucose challenge compared with nondiabetic NOD mice. The successfully treated mice retained diabetogenic T cells, but also had substantially increased Foxp3+ cells in draining pancreatic lymph nodes. However, these Foxp3+ cells were derived from the recipient mice and not the injected T reg cells, suggesting a role for endogenous T reg cells in maintaining tolerance after treatment. Therefore, inoculation of DC-expanded, antigen-specific suppressor T cells has considerable efficacy in ameliorating ongoing diabetes in NOD mice.

Animals↗

PubMed2007

Intestinal epithelial cell proliferation is dependent on the site of massive small bowel resection.

Early intestinal adaptation after massive small bowel resection (SBR) is driven by increased epithelial cell (EC) proliferation. There is a clear clinical difference in the post-operative course of patients after the loss of proximal (P) compared to distal (D) small bowel. This study examined the effects of the site of SBR on post-resectional intestinal adaptation, and investigated the potential mechanisms involved. C57BL/6J mice (n = 7/group) underwent: (1) 60% P-SBR, (2) 60% D-SBR, (3) 60% mid (M)-SBR and (4) SHAM-operation (transection/reanastomosis). Mice were sacrificed at 7 days after surgery and ECs and adjacent mucosal lymphocytes (IELs) isolated. Adaptation was assessed in both jejunum and ileum by quantification of villus height, crypt depth, villus cell size, crypt cell size (microns), goblet cell number, and EC proliferation (%BrdU incorporation). Proliferation signalling pathways including keratinocyte growth factor (KGF)/KGFR(1), IL-7/IL-7R, and epidermal growth factor receptor (EGFR) were measured by RT-PCR. Expression of IL-7 was further analysed by immunofluorescence. Data were analyzed using ANOVA. All three SBR models led to significant increases in villus height, crypt depth, goblet cell numbers and EC proliferation rate when compared to respective SHAM groups. The strongest morphometric changes were found for jejunal segments after M-SBR and for ileal segments after P-SBR. Furthermore, morphometric analysis showed that at 1-week post-resection a tremendous increase in EC numbers occurred in jejunal villi (cell hyperplasia), whereas a significant increase in EC size predominated in ileal villi (cell hypertrophy). mRNA expression of KGF, KGFR(1), IL-7R, and EGFR showed a significant increase only after D-SBR, whereas IL-7 increased significantly after SBR in all investigated models, and this was confirmed by immunofluorescence studies. Early intestinal adaptation shows distinct differences depending on the site of SBR, and is predominately driven by cell hyperplasia in jejunal villi and cell hypertrophy in ileal villi. However, the exact mechanisms, which guide these signalling pathways are still unclear.

Adaptation, Physiological↗

PubMed2007

Influences of polycyclic aromatic hydrocarbons (PAHs) on soil microbial community composition with or without vegetation.

Uptake of three polycyclic aromatic hydrocarbons (PAHs), naphthalene (NAP), phenanthrene (PHN), and pyrene (PYR), from soils by ryegrass, white clover and soybean were investigated in an 8-week pot experiment. The microbial phospholipid-fatty-acid (PLFA) patterns in PAHs-contaminated soil were analyzed. Contamination with PAHs inhibited the soil microbial activity. In non-vegetated soils, the total PLFA showed 87% reduction on the addition of PAHs after an 8-week incubation compared to the PAH-free soil; the concentrations of NAP, PHN, and PYR in soils showed 19.4%, 25.5% and 24.3% reduction, respectively, due mainly to the evaporative loss and microbial degradation. In vegetated soils, the reduction of added NAP and PHN levels was not related to the plant biomass nor to the total PLFA. However, the reduction in PYR concentrations in soil mediated by soybean growth was much pronounced than those by ryegrass or white clover growth, but thisis not related to the total microbial biomass as revealed by PLFAs. The principal-component analysis (PCA) of the PLFA signatures revealed significant changes in the PLFA pattern in PAH-spiked soils when different vegetations were planted. Using the PLFA as a biomarker, it was found that the Gram-negative bacteria were more sensitive to PAHs than Gram-positive bacteria and fungi.

Plant Development↗

PubMed2007

Ultrastructural changes of the cochlea after oral and maxillofacial firearm wounds.

BACKGROUND: There have been reports that maxillofacial firearm wounds could induce hearing loss. The effects on the ultrastructure of the cochlea and cochlear nerves after oral and maxillofacial firearm wounds are still unclear. This experiment investigates the ultrastructural changes of the cochlea and cochlear nerve after oral and maxillofacial firearm wounds. METHODS: Twenty dogs were wounded by steel spheres or detonators to establish animal models of oral and maxillofacial firearms wound. At different times after trauma, the wounds were examined and the specimens of the cochlea and cochlear nerve were taken to study the ultrastructural changes. RESULTS: The ultrastructural changes of the cochlea and cochlear nerve at 1 hour after trauma were cilia disorganization, edema of the nerve, and mitochondrial denaturalization. At 6 hours, there was extensive degeneration in the cochlea and cochlear nerve, cilia falling off of hair cells, and dissolution of the nerve sheath structure. CONCLUSIONS: The ultrastructure of the cochlea and cochlear nerve after injury is severe, but in the early period the injury is reversible.

Animals↗

PubMed2007

Intestinal epithelial cell-derived interleukin-7: A mechanism for the alteration of intraepithelial lymphocytes in a mouse model of total parenteral nutrition.

Total parenteral nutrition (TPN), with the absence of enteral nutrition, results in profound changes to both intestinal epithelial cells (EC) as well as the adjacent intraepithelial lymphocyte (IEL) population. Intestinal EC are a rich source of IL-7, a critical factor to support the maintenance of several lymphoid tissues, and TPN results in marked EC changes. On this basis, we hypothesized that TPN would diminish EC-derived IL-7 expression and that this would contribute to the observed changes in the IEL population. Mice received enteral food and intravenous crystalloid solution (control group) or TPN. TPN administration significantly decreased EC-derived IL-7 expression, along with significant changes in IEL phenotype; decreased IEL proliferation; and resulted in a marked decrease in IEL numbers. To better determine the relevance of TPN-related changes in IL-7, TPN mice supplemented with exogenous IL-7 or mice allowed ad libitum feeding and treated with exogenous administration of anti-IL-7 receptor (IL-7R) antibody were also studied. Exogenous IL-7 administration in TPN mice significantly attenuated TPN-associated IEL changes, whereas blocking IL-7R in normal mice resulted in several similar changes in IEL to those observed with TPN. These findings suggest that a decrease in EC-derived IL-7 expression may be a contributing mechanism to account for the observed TPN-associated IEL changes.

Animals↗

PubMed2006

Mitochondrial targeting with antioxidant peptide SS-31 prevents mitochondrial depolarization, reduces islet cell apoptosis, increases islet cell yield, and improves posttransplantation function.

Apoptotic cell death is a defined pathway for islet cell demise, and mitochondrial dysfunction contributes to islet cell apoptosis. The hypothesis that the novel peptide D-Arg-2', 6'-dimethyltyrosine-Lys-Phe-NH2 (SS-31), previously shown to target inner mitochondrial membrane and prevent oxidative damage of neuronal cells and other cell types, optimizes pancreatic islet isolation and improves posttransplantation function in recipients with diabetes was investigated. Herein is demonstrated that SS-31 readily penetrates intact mouse islets, preserves mitochondrial polarization, reduces islet cell apoptosis, and increases islet cell yield. Optimization of islet isolation is demonstrable after SS-31 pretreatment of islet (pancreas) donor mice and with the addition of SS-31 to reagents that are used in the isolation of mouse islets. The supplementation of in vitro culture medium with SS-31 reduced islet cell apoptosis and increased the viability of human islets, as ascertained by dual-parameter flow cytometry analysis. In a stringent marginal islet cell mass transplantation model (200 mouse islets transplanted under the renal capsule of syngeneic diabetic mice) and using islets that were derived from old mice (>24 wk), SS-31 treatment was associated with prompt and sustained normoglycemia, whereas the untreated islet graft recipients remained diabetic. Our data suggest a novel strategy to optimize islet isolation and reduce the need for multiple pancreata to achieve insulin independence in the recipient with type 1 diabetes. Because SS-31 was effective with "extended" islet donors, it is hypothesized that the antioxidant SS-31 may serve to increase the pool of eligible organ donors.

Animals↗

PubMed2006

Aurora-A induces cell survival and chemoresistance by activation of Akt through a p53-dependent manner in ovarian cancer cells.

Aurora-A is frequently altered in epithelial malignancies. Overexpressing Aurora-A induces centrosome amplification and G2/M cell cycle progression. We have previously shown elevated level of Aurora-A in ovarian cancer and activation of telomerase by Aurora-A in human mammary and ovarian epithelia. Here we report that Aurora-A protects ovarian cancer cells from apoptosis induced by chemotherapeutic agent and activates Akt pathway in a p53-dependent manner. Ectopic expression of Aurora-A renders cells resistant to cisplatin (CDDP), etoposide and paclitaxel-induced apoptosis and stimulates Akt1 and Akt2 activity in wild-type p53 but not p53-null ovarian cancer cells. Aurora-A inhibits cytochrome C release and Bax conformational change induced by CDDP. Knockdown of Aurora-A by RNAi sensitizes cells to CDDP-induced apoptosis and decreases phospho-Akt level in wild-type p53 cells. Reintroduction of p53 decreases Akt1 and Akt2 activation and restores CDDP sensitivity in p53-null but not p53-null-Aurora-A cells. Inhibition of Akt by small molecule inhibitor, API-2, overcomes the effects of Aurora-A-on cell survival and Bax mitochondrial translocation. Taken collectively, these data indicate that Aurora-A activates Akt and induces chemoresistance in a p53-dependent manner and that inhibition of Akt may be an effective means of overcoming Aurora-A-associated chemoresistance in ovarian cancer cells expressing wild-type p53.

Antineoplastic Agents↗

PubMed2006

Prevalence of age-related maculopathy in the adult population in China: the Beijing eye study.

OBJECTIVE: To evaluate the prevalence of age-related maculopathy (ARM) in adult Chinese living in rural or urban regions of mainland China. DESIGN: Population-based prevalence study. METHODS: The study included 4439 subjects (aged 40 or more years) out of 5324 subjects invited to participate (response rate 83.4%). It was held in rural and urban regions of Greater Beijing. The participants underwent a detailed ophthalmic examination including fundus photography. All fundus photographs were graded by the Wisconsin Age-Related Maculopathy Grading System. RESULTS: Fundus photographs were available for 4376 (98.6%) subjects. Early ARM was present in 122 (1.4%) of 8655 (95% confidence interval [CI] 1.16% to 1.66%) eyes or 63 (1.4%) of 4376 (95% CI 1.09% to 1.79%) subjects, late ARM in 12 (0.14%) of 8655 (95% CI 0.06% to 0.22%) eyes or seven (0.2%) of 4376 (95% CI 0.04% to 0.28%) subjects, and exudative ARM as part of late ARM in seven (0.1%) of 8655 (95% CI 0.02% to 0.14%) eyes or six (0.1%) of 4376 (95% CI 0.03% to 0.25%) subjects. The prevalence of early ARM, late ARM, and exudative ARM, respectively, increased from 0.61%, 0.07%, and 0.07% in the 40-to-44-year age group, to 1.66%, 0.26%, and 0.26% in the 55-to-59-year group, and to 2.99%, 0.90%, and 0.60% in the group aged 75 years and older. ARM was causative for visual impairment (best-corrected visual acuity in the better eye, <20/60 and > or =20/400) or blindness (visual acuity <20/400) in one subject (0.023%). CONCLUSIONS: Visual impairment due to ARM was relatively uncommon in the adult Chinese population in rural and urban regions.

Adult↗

PubMed2006

Searching for interpretable rules for disease mutations: a simulated annealing bump hunting strategy.

BACKGROUND: Understanding how amino acid substitutions affect protein functions is critical for the study of proteins and their implications in diseases. Although methods have been developed for predicting potential effects of amino acid substitutions using sequence, three-dimensional structural, and evolutionary properties of proteins, the applications are limited by the complication of the features and the availability of protein structural information. Another limitation is that the prediction results are hard to be interpreted with physicochemical principles and biological knowledge. RESULTS: To overcome these limitations, we proposed a novel feature set using physicochemical properties of amino acids, evolutionary profiles of proteins, and protein sequence information. We applied the support vector machine and the random forest with the feature set to experimental amino acid substitutions occurring in the E. coli lac repressor and the bacteriophage T4 lysozyme, as well as to annotated amino acid substitutions occurring in a wide range of human proteins. The results showed that the proposed feature set was superior to the existing ones. To explore physicochemical principles behind amino acid substitutions, we designed a simulated annealing bump hunting strategy to automatically extract interpretable rules for amino acid substitutions. We applied the strategy to annotated human amino acid substitutions and successfully extracted several rules which were either consistent with current biological knowledge or providing new insights for the understanding of amino acid substitutions. When applied to unclassified data, these rules could cover a large portion of samples, and most of the covered samples showed good agreement with predictions made by either the support vector machine or the random forest. CONCLUSION: The prediction methods using the proposed feature set can achieve larger AUC (the area under the ROC curve), smaller BER (the balanced error rate), and larger MCC (the Matthews' correlation coefficient) than those using the published feature sets, suggesting that our feature set is superior to the existing ones. The rules extracted by the simulated annealing bump hunting strategy have comparable coverage and accuracy but much better interpretability as those extracted by the patient rule induction method (PRIM), revealing that the strategy is more effective in inducing interpretable rules.

Amino Acid Sequence↗

PubMed2006

Tandem parallel fragmentation of peptides for mass spectrometry.

Parallel fragmentations of peptides in the source region and in the collision cell of tandem mass spectrometers are sequentially combined to develop parallel collision-induced-dissociation mass spectrometry (p2CID MS). Compared to MS/MS spectra, the p2CID mass spectra show increased signal intensities (2-400-fold) and number of sequence ions. This improvement is attributed to the fact that p2CID MS virtually samples all the ions generated by electrospray ionization, including intact and fragment ions of different charge states from a peptide. We implement the method using a quadrupole time-of-flight tandem mass spectrometer. The instrument is operated in TOF-MS mode that allows the ions from source region broadband-passing the first mass analyzer to enter the collision cell. Cone voltage and collision energy are investigated to optimize the outcome of the two parallel CID processes. In the in-source parallel CID, elevated cone voltage produces singly charged intact peptide ions and large fragment ions, as well as decreases the charge-state distribution of peptide ions mainly to double and single charges. The in-collision-cell parallel CID is optimized to dissociate the ions from the source region to produce small and medium fragment ions. The method of p2CID MS is especially useful for sequencing of large peptides with labile amide bonds and peptides with C-terminal arginine. It has unique potential for de novo sequencing of peptides and proteome analysis, especially for affinity-enriched subproteomes.

Dynorphins↗

PubMed2006

Citation classics in Fertility and sterility, 1975-2004.

The Science Citation Index of the Institute for Scientific Information was searched to identify the 102 most frequently cited articles in the Fertility and Sterility journal for the past 30 years. Identification of the citation classic articles provides resourceful perspectives on the evolution of Fertility and Sterility and reproductive medicine.

Bibliometrics↗

PubMed2006

The zinc finger transcription factor 191 is required for early embryonic development and cell proliferation.

Human zinc finger protein 191 (ZNF191/ZNF24) was cloned and characterized as a SCAN family member, which shows 94% identity to its mouse homologue zinc finger protein 191 (Zfp191). ZNF191 can specifically interact with an intronic polymorphic TCAT repeat (HUMTH01) in the tyrosine hydroxylase (TH) gene. Allelic variations of HUMTH01 have been stated to have a quantitative silencing effect on TH gene expression and to correlate with quantitative and qualitative changes in the binding by ZNF191. Zfp191 is widely expressed during embryonic development and in multiple tissues and organs in adult. To investigate the functions of Zfp191 in vivo, we have used homologous recombination to generate mice that are deficient in Zfp191. Heterozygous Zfp191(+/-) mice are normal and fertile. Homozygous Zfp191(-/-) embryos are severely retarded in development and die at approximately 7.5 days post-fertilization. Unexpectedly, in Zfp191(-/-) and Zfp191(+/-) embryos, TH gene expression is not affected. Blastocyst outgrowth experiments and the RNA interference-mediated knockdown of ZNF191 in cultured cells revealed an essential role for Zfp191 in cell proliferation. In further agreement with this function, no viable Zfp191(-/-) cell lines were obtained by derivation of embryonic stem (ES) cells from blastocysts of Zfp191(+/-) intercrosses or by forced homogenotization of heterozygous ES cells at high concentrations of G418. These data show that Zfp191 is indispensable for early embryonic development and cell proliferation.

Animals↗

PubMed2006

Organic anion recognition of naphthalenesulfonates by steroid-modified beta-cyclodextrins: enhanced molecular binding ability and molecular selectivity.

Two beta-cyclodextrin (beta-CD) derivatives bearing steroid groups (1 and 2) were synthesized by the condensation of mono(6-aminoethylamino-6-deoxy)-beta-CD with cholic acid and deoxycholic acid, respectively, and their original conformations and binding behavior to the organic anion of naphthalenesulfonate derivatives were investigated by using 1H NMR spectroscopy and spectrofluorometric titration in combination with computational methods. The 2D NMR experiments reveal that the steroid groups attached to the beta-CD rim could be deeply embedded in the beta-CD cavity to form the intramolecular (for 1) or intermolecular (for 2) inclusion complexes in aqueous solution. Upon complexation with naphthalenesulfonate derivatives, modified beta-CDs display two obviously different binding modes, that is, the competitive inclusion mode and the induced-fit inclusion mode, which is consistent with the results of molecular modeling study. The two modes and the strict size/shape fitting relationship between the hosts and guests reasonably explain the different binding behaviors and molecular selectivity of host beta-CDs 1 and 2 toward the naphthalenesulfonate guests. Therefore, the cholic acid- or deoxycholic acid-modified beta-CDs could effectively recognize the size/shape of guest molecules as compared with the parent beta-CD, giving good molecular selectivity up to 24.9 for the disodium 2,6-naphthalenedisulfonate/disodium 1,5-naphthalenedisulfonate pair by the host 1.

Anions↗

PubMed2006

Retinal vascular abnormalities in adult Chinese in rural and urban Beijing: the Beijing Eye Study.

OBJECTIVE: To assess retinal vascular abnormalities, including focal and generalized arteriolar narrowing, arteriovenous nicking, and arteriolar sheathing, in adult Chinese in rural and urban Beijing, and their associations with self-reported diagnosis of cardiovascular and cerebrovascular diseases. DESIGN: Population-based cross-sectional cohort study. PARTICIPANTS: The study included 4439 subjects out of 5324 subjects invited to participate (response rate, 83.4%) with an age of > or =40 years. It was divided into a rural part (n = 1973 [44.4%]) and an urban part (n = 2466 [55.6%]). Mean age was 56.2+/-10.6 years (range, 40-101 years). METHODS: Color optic disc photographs were morphometrically examined. One eye of each participant was randomly selected. Generalized and focal arteriolar narrowing, arteriovenous nicking (arteriovenous crossing abnormalities), and arteriolar sheathing were assessed. Self-reported histories of cardiovascular and cerebrovascular diseases and habits of smoking and alcohol drinking were obtained from questionnaires. MAIN OUTCOME MEASURES: Frequency of generalized and focal arteriolar narrowing, arteriovenous nicking, and arteriolar sheathing. RESULTS: Optic disc photographs were available for 4228 (95.2%) subjects. Focal arteriolar narrowing was found in 6.3%, arteriovenous nicking in 6.6%, arteriolar sheathing in 4.8%, and generalized narrowing in 4.3% of the subjects. Abnormalities were more common in the temporal quadrant; they were rare in the inferior nasal quadrant. Frequencies and severities of all retinal microvascular abnormalities examined increased with age (P<0.05). The microvascular abnormalities were detected more frequently in the rural population than in the urban population (P<0.05). After controlling for age, gender, area, and habit of drinking alcohol, generalized arteriolar narrowing (odds ratio [OR], 2.63; 95% confidence interval [CI], 1.64, 4.22), focal arteriolar narrowing (OR, 1.51; 95% CI, 1.00, 2.29), and arteriolar sheathing (OR, 1.71; 95% CI, 1.08, 2.71) were significantly associated with the self-reported diagnosis of arterial hypertension. The microvascular abnormalities were not significantly associated with the self-reported diagnosis of coronary heart disease or stroke. CONCLUSIONS: Retinal vascular abnormalities in adult Chinese increase with age and are more commonly found in people living in rural areas. Retinal vascular abnormalities are associated with the self-reported diagnosis of arterial hypertension, and are not related to self-reported diagnosis of coronary heart disease or previous cerebrovascular events such as stroke.

Adult↗