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Biomedical subjects

Yan Jin

Publications and source records attributed to Yan Jin.

At least 91 records · Page 5Linked to original sources
PubMed2005

[Application research on dextran-based hydrogel and its drug controlled release].

OBJECTIVE: To introduce the development of dextran-based hydrogel and its drug delivery system in drug sustained and/or controlled release, and to investigate their application in tissue engineering. METHODS: Related literature was extensively reviewed and comprehensively analyzed. RESULTS: In recent years, great progress was made in the studies of dextran-based hydrogels and study on dextran-based intelligent materials became an investigative hotspot especially in tissue engineering. CONCLUSION: Dextran-based hydrogel is considered to be a good potential material in field of drug delivery and tissue engineering. Endowed with new characteristics, a series of intelligent biomaterials can be derived from dextran-based hydrogels, which can be widely used in biomedicine. Further study should be done on the industrialization of its interrelated production.

Absorbable Implants↗
PubMed2005

[Preparation of enamel matrix proteins controlled release microspheres and their biological effects on the proliferation and differentiation of human periodontal ligament cells in vitro].

OBJECTIVE: To prepare enamel matrix proteins (EMPs) loaded dextran-based hydrogel microspheres (EMPs-dex-MPs), and to evaluate their EMPs controlled release property and their biological effects on the proliferation and differentiation of human periodontal ligament cells (PDLCs) in vitro. METHODS: Using dimethylbenzene as the oil phase, EMPs-dex-MPs were achieved by emulsion-chemical crosslinking technique. The process of the recombination preparation was optimized by orthogonal factorization method. The configuration and size of EMPs-dex-MPs were determined by scanning electron microscope. The EMPs loading content and encapsulation rate of EMPs-dex-MPs, and their biodegradation characteristic were studied by routine analysis methods. Dynamic dialysis method was used to determine the release characteristic of EMPs-dex-MPs in vitro and its influencing factors. The proliferation of cultured PDLCs was measured by MTF method and the differentiation of PDLCs was measured by their alkaline phosphatase (ALP) activities. RESULTS: The results showed that EMPs-dex-MPs were homogenous and stable with the average diameter 25 microm, and the EMPs loading content was (32.8 +/- 1.2)%, the encapsulation rate was (78.9 +/- 1.0)%. Under 9% physiological saline solution contained a very thimbleful quantity of dextranase EMPs-dex-MPs could be biodegraded completely during about 40 days. The in vitro experiments showed that about 80% of EMPs could be released out in 20 days. Using EMPs-dex-MPs could enhance the proliferation responses and ALP activities of PDLCs more than 12 days. CONCLUSION: As a new sustained release system of growth factors, the dex-MPs is stable, workable and biodegradable. EMPs-dex-MPs, whose drug release can be controlled by preparation technique, may be more effective in promoting periodontal tissue regeneration.

Cell Differentiation↗
PubMed2005

[Treatment of rabbit corneal with skin epidermal stem cells].

OBJECTIVE: To construct artificial rabbit corneas with autologous skin epidermal stem cells and allogenic stromal cells in vitro and promote healing of corneal wounds. METHODS: Skin epidermal stem cells were isolated from autologous skin samples. Keratocytes were isolated from newborn cornea biopsies. The cells were combined with acellular porcine corneal stroma scaffold to construct artificial corneas. Then the constructed artificial corneas were used to repair severe vision loss caused by complete loss of corneal epithelial stem cells. RESULTS: Cultured skin epidermal stem cells and keratocytes were in good growth conditions. Cultured artificial corneas consisted of multiplayer epithelial cells growing on stroma equivalent consisting of stromal matrix with incorporated keratocytes. The in vitro constructed artificial corneas were histologically similar to normal rabbit corneas. Three months after transplantation, the cornea wounds were healed and the rabbit cornea became transparent. CONCLUSION: The artificial corneas were constructed successfully in vitro and can be used to repair severe vision loss caused by complete loss of corneal epithelial stem cells.

Animals↗
PubMed2005

[16S rDNA-RFLP analysis of actinomycetes associated with marine sponge Hymeniacidon perleve].

106 culturable symbiotic actinomycetes strains were isolated from intertidal marine sponge Hymeniacidon perleve collected from Chinese Yellow Sea. The 16S rDNA sequences of these strains were amplified and RFLP patterns were analyzed by digestion of 16S rDNA fragments with Hha I. 11 different patterns were identified, with confirmation by the RFLP analysis using Vector NTI simulation. Using Hha I RFLP patterns, the actinomycetes could be identified at the genus level. Phylogentic trees using 16S rDNA sequences were constructed. Majority of actinomycetes belonged to Streptomycetes (78). The other strains belonged to Nocardiopsis (18), Pseudonocardia (3), Nocardia (3), Micromonospora (2), Rhodococcus (1), Actinoalloteichus (1). Strain 177 is the candidate for new species of Actinalloteichus.

Actinobacteria↗
PubMed2004

Inhibition of TGFbeta signaling potentiates the FGF-2-induced stimulation of cardiomyocyte DNA synthesis.

OBJECTIVE: Added transforming growth factor beta (TGFbeta) inhibits the proliferation of immature cardiomyocytes. We have now examined the hypothesis that suppression of endogenous TGFbeta signaling will boost the proliferative response (DNA synthesis) of cardiac myocytes to serum and/or to the mitogenic factor fibroblast growth factor-2 (FGF-2). METHODS AND RESULTS: Overexpression of a kinase-deficient TGFbeta type II receptor (TGFbetaRIIDeltaKD) resulted in a 2.8-fold increase in cardiomyocyte DNA synthesis in serum-rich cultures, an effect requiring active FGFR-1 since it was not observed in the presence of excess kinase-deficient FGFR-1. This finding suggested that endogenous TGFbeta-TGFbetaRII suppressed endogenous FGFR-1-mediated signals that stimulate or are permissive for DNA synthesis. TGFbeta had no effect, however, on the FGF-2-induced acute stimulation of extracellular signal regulated kinase1/2. FGF-2, added in the absence or presence of TGFbeta inhibition, elicited a 3- or a 13-fold stimulation of DNA synthesis, respectively, pointing to a synergistic effect. CONCLUSION: Inhibition of TGFbetaRII-transduced signaling upregulates the proliferative response of cardiomyocytes to serum, and greatly potentiates the stimulatory effect of FGF-2. A combinatorial strategy including activation of FGF-2 and inhibition of TGFbeta-triggered signal transduction may be required for maximal stimulation of immature cardiomyocyte DNA synthesis.

Animals↗
PubMed2004

The effects of tamoxifen and its metabolites on platelet function and release of reactive oxygen intermediates.

Tamoxifen is effective in the prevention and treatment of breast cancer, but its use is associated with an increased risk of thrombosis. The mechanism for this effect is unknown. Reactive oxygen intermediates enhance platelet-dependent thrombosis, and in oncological studies, tamoxifen has been shown to increase production of reactive oxygen species. Therefore, the effects of tamoxifen and its bioactive metabolites on platelet activity and platelet reactive oxygen species were determined. Platelets were incubated with tamoxifen or the metabolites 4-hydroxy-tamoxifen (4-OH), N-desmethyl tamoxifen, or 4-hydroxy-N-desmethyl tamoxifen (endoxifen). Tamoxifen metabolites have been previously shown to possess enhanced bioactivity, and consistent with this observation, tamoxifen metabolites but not tamoxifen modestly increased platelet aggregation. These effects were similar with platelets isolated from male or female subjects. Platelet nitric oxide release or cGMP levels were not altered by incubation with tamoxifen or any of its metabolites. Incubation with tamoxifen metabolites increased stimulation-dependent platelet superoxide release [8.1 +/- 1.6 arbitrary units (a.u.) for control versus 15.2 +/- 3.5 a.u. for 4-OH; P < 0.01]. Coincubation with a superoxide dismutase mimetic eliminated the tamoxifen metabolite-induced enhancement of platelet aggregation. Corresponding to increased superoxide release, incubation with tamoxifen metabolites enhanced the functional activation of NADPH oxidase as determined by phosphorylation of its subunits p47(phox) and p67(phox). In summary, incubation of platelets with the active metabolites of tamoxifen increases stimulation-dependent superoxide release through a NADPH oxidase-dependent mechanism. This results in modest changes in platelet function and seems to be consistent with previous oncological studies demonstrating tamoxifen-dependent increase in reactive oxygen species generation.

Blood Platelets↗
PubMed2004

Structure of a glutamate transporter homologue from Pyrococcus horikoshii.

Glutamate transporters are integral membrane proteins that catalyse the concentrative uptake of glutamate from the synapse to intracellular spaces by harnessing pre-existing ion gradients. In the central nervous system glutamate transporters are essential for normal development and function, and are implicated in stroke, epilepsy and neurodegenerative diseases. Here we present the crystal structure of a eukaryotic glutamate transporter homologue from Pyrococcus horikoshii. The transporter is a bowl-shaped trimer with a solvent-filled extracellular basin extending halfway across the membrane bilayer. At the bottom of the basin are three independent binding sites, each cradled by two helical hairpins, reaching from opposite sides of the membrane. We propose that transport of glutamate is achieved by movements of the hairpins that allow alternating access to either side of the membrane.

Amino Acid Sequence↗
PubMed2004

Monitoring molecular beacon/DNA interactions using atomic force microscopy.

The molecular beacon (MB) is a new fluorescence probe containing a single-stranded oligonucleotide with a probe sequence embedded in complementary sequences that form a hairpin stem. Due to the inherent fluorescent signal transduction mechanism, an MB functions as a sensitive probe with a high signal-to-background ratio for real-time monitoring and provides a variety of exciting opportunities in DNA, RNA, and protein studies. To better understand the properties of MBs, the specific interactions between MB and target DNA (complementary and one-base mismatch) have been directly investigated by atomic force microscopy. The interaction force between a linear DNA probe and the target DNA was also detected and compared to that between MB and target DNA. The results demonstrate the high specificity of the MB/target DNA compared to the linear DNA/target DNA interaction.

DNA↗
PubMed2004

Characterization of the 3a protein of SARS-associated coronavirus in infected vero E6 cells and SARS patients.

Proteomics was used to identify a protein encoded by ORF 3a in a SARS-associated coronavirus (SARS-CoV). Immuno-blotting revealed that interchain disulfide bonds might be formed between this protein and the spike protein. ELISA indicated that sera from SARS patients have significant positive reactions with synthesized peptides derived from the 3a protein. These results are concordant with that of a spike protein-derived peptide. A tendency exists for co-mutation between the 3a protein and the spike protein of SARS-CoV isolates, suggesting that the function of the 3a protein correlates with the spike protein. Taken together, the 3a protein might be tightly correlated to the spike protein in the SARS-CoV functions. The 3a protein may serve as a new clinical marker or drug target for SARS treatment.

Animals↗
PubMed2004

Transcriptional regulation of FGF-2 gene expression in cardiac myocytes.

OBJECTIVE: Fibroblast growth factor-2 (FGF-2) exerts its cardioprotective effect through cell surface receptor signaling and may play a role in the normal maintenance of a healthy myocardium. One mechanism of FGF-2 release from contracting cardiomyocytes is through transient sarcolemmal disruption, with accumulation in the extracellular matrix. Continuous FGF-2 release would require a link to synthesis and, thus, we examined regulation of FGF-2 promoter activity in cardiomyocytes as a potential target for optimizing cardioprotection. METHODS AND RESULTS: To investigate autoregulation, neonatal rat cardiomyocytes, (NRCM), were transfected with approximately 1 or 0.1 kb of rat FGF-2 promoter sequences linked to luciferase, -1058FGF-2p.luc and -110FGF-2p.luc, and treated with or without FGF-2. FGF-2 promoter activity was significantly increased approximately 2.5-fold with both genes. The proximal promoter region of rat FGF-2 contains putative binding sites for the early growth response-1 (Egr-1) and stimulating protein 1 (Sp1) transcription factors. Overexpression of Egr-1 and Sp1 increased -1058FGF-2p.luc expression by 4.4- and 8.7-fold, respectively. Mutation of Egr-1 and overlapping Sp1 sites did not blunt the response of -110FGF-2p.luc to FGF-2 treatment but did significantly reduce basal promoter activity. Transgenic mice expressing -1058FGF-2p.luc were treated with isoproterenol (IsP) to increase heart rate and endogenous FGF-2 release. FGF-2 promoter activity was stimulated significantly at 6 h, and increases in both FGF-2 and its receptor mRNA levels were also detected. In contrast, no effect of IsP was seen on -1058FGF-2p.luc or -110FGF-2p.luc in transfected NRCMs. CONCLUSIONS: FGF-2 released from cardiomyocytes may act to regulate its own synthesis at the transcriptional level. The mechanism does not appear to require an intact Egr-1 site in the proximal promoter region. This may, however, reflect redundancy in the control of FGF-2 promoter activity as our data support a stimulatory role for Egr-1 and Sp1.

Adrenergic beta-Agonists↗
PubMed2004

Phosphorylation of serine 262 in the gap junction protein connexin-43 regulates DNA synthesis in cell-cell contact forming cardiomyocytes.

Mitogenic stimulation of cardiomyocytes is associated with decreased gap junction coupling and protein kinase C (PKC)-mediated phosphorylation of the gap junction protein connexin43 (Cx43). Identification of and interference with the amino acid(s) that becomes phosphorylated in response to stimulation are important steps towards defining the relationship between Cx43 phosphorylation and cell cycle. Using immunoblotting and phosphospecific antibodies we were able to show that serine-262 (S262) on Cx43 becomes phosphorylated in response to growth factor or PKC stimulation of cardiomyocytes. To examine the effect of Cx43, S262 phosphorylation and cell-cell contact (and/or coupling) on DNA synthesis, we overexpressed wild-type (wt) or mutant Cx43, carrying a S262-to-alanine (S262A, simulating the unphosphorylated state) or a S262-to-aspartate (S262D, simulating constitutive phosphorylation) substitutions in cultures of cell-cell contact forming or isolated cardiomyocytes. Overexpression of wt-Cx43 caused a significant decrease in DNA synthesis irrespective of the presence of cell-cell contact. In cell-cell contact forming cultures, the S262D mutation reversed while the S262A mutation increased the inhibitory effect of Cx43. In the absence of cell-cell contact, the S262-Cx43 mutations had no significant effect on Cx43 inhibition of DNA synthesis. Dye-coupling, evaluated by scrape-loading, indicated increased gap junction permeability in S262A (compared to wt or S262D) overexpressing myocytes. We conclude that Cx43 inhibits cardiomyocyte DNA synthesis irrespectively of cell-cell contact or coupling. Cell-cell contact, and possibly gap junction-mediated communication is required, however, in order to reverse Cx43 inhibition of DNA synthesis by S262 phosphorylation.

Animals↗
PubMed2004

The province of Alberta, Canada avoids the hospitalization epidemic for congestive heart failure patients.

BACKGROUND: We assessed the incidence and prevalence of congestive heart failure (CHF) in patients diagnosed at the time of hospitalization and patients diagnosed in specialists offices without prior hospitalization in order to compare the trends in Canada with previously published trends in the USA and other industrialized countries. METHODS: Administrative data for Alberta, Canada from 1 April 1994 to 31 March 2000. RESULTS: There was a small but statistically significant decline in the age-sex incident and prevalent hospitalization rates for CHF between 1994/1995 (incidence per 1000 of 1.59; 99% CI 1.51, 1.66: prevalence per 1000 of 2.31; 99% CI 2.22, 2.40) and the year 1999/2000 (incidence per 1000 of 1.24; 99% CI 1.18, 1.30: prevalence per 1000 of 1.97; 99% CI 1.89, 2.05). Crude hospitalization rate per 1000 also demonstrated a small but statistically significant decline between 1994/1995 (2.98; 99% CI 2.88, 3.08) and 1999/2000 (2.55; 99% CI 2.46, 2.64). The age-sex incident rates of ambulatory diagnosis of CHF were similar throughout the 1994/1995-1999/2000 time period (0.88; 99% CI 0.82, 0.94 during 1994/1995 and 0.84; 99% CI 0.79, 0.89 during 1999/2000). The crude mortality percentage for incident hospitalization for CHF were similar throughout the 1994/1995-1999/2000 time period (31.0%; 99% CI 28.7, 33.3 during 1994/1995 and 28.6%; 99% CI 26.3, 30.9 during 1999/2000). CONCLUSIONS: We noted a small decrease in the incident, prevalent, and total hospitalizations for CHF in the time period 1994/1995-1999/2000. The decrease was not the result of a substituted increase in ambulatory diagnosis for CHF.

Aged↗
PubMed2004

Outcomes and costs among seniors requiring hospitalization for community-acquired pneumonia in Alberta.

OBJECTIVES: To determine the age-specific rates of hospital discharge, cost per day, and overall in-hospital 1- and 4-year mortality for seniors who required hospitalization for the treatment of community-acquired pneumonia (CAP). DESIGN: Retrospective analysis of two administrative health service databases. SETTING: Province of Alberta, Canada. PARTICIPANTS: Residents of Alberta aged 18 and older. MEASUREMENTS: Hospital abstracts and vital statistics from April 1, 1994, to March 31, 1999, were analyzed, and mortality and cost outcomes statistically modeled by regression. RESULTS: There were 8,500 annual hospital discharges for CAP costing more than $40 million per year. The overall in-hospital all-cause mortality rate was 12%, and the 1-year mortality rate was 26%. The mean age of pneumonia cases increased (P<.000) from 62.8 in 1994/1995 to 67.2 in 1998/1999. The proportion of hospital discharges in those aged 85 and older was 13% in 1994/1995, increasing to 18% in 1998/1999 (P<.000). The age-specific hospital discharge rate and length of hospitalization increased with age. After adjustment for other factors using modeling, it was found that the relative risk (RR) of in-hospital and 1-year mortality increased with age, the RR of using special medical care and higher-than-average daily hospital cost decreased with age, and the RR of greater-than-average daily hospital cost was not associated with an increase in comorbidity. Total costs per hospital stay were similar in patients aged 85 and older to those in patients aged 65 to 74, despite a one-third longer length of stay, which was consistent with reduced use of special medical care in those aged 85 and older. CONCLUSION: The increased use of hospital resources for CAP in the setting of an aging population may have been partially avoided because of limitations in care provided for seniors aged 85 and older.

Aged↗
PubMed2004

Home care before and after hospitalization for acute myocardial infarction in Alberta, Canada.

UNLABELLED: Home care services are provided to about 10% of those admitted to hospital for acute myocardial infarction and about 20% of those discharged from hospital. The use of home care in patients with an acute myocardial infarction is growing in Alberta over the brief time span of this four year study. Those that received home care prior to a hospitalization for acute myocardial infarction were "old and frail" with a high mortality rate during and after hospitalization. The provision of home care after hospitalization selected those patients that stay in hospital longer and required more hospital care. BACKGROUND: The use of home care before and after hospitalization for acute myocardial infarction is described. METHODS: Hospital discharge abstracts were used to identify patients hospitalized in alberta, canada for acute myocardial infarction which were then linked to home care administrative data. RESULTS: There were 12,648 patients with acute myocardial infarction from April 1, 1995 until March 31, 1999. Home care within 60 days prior to hospitalization was provided for 8.7% of patients with acute myocardial infarctions (n = 1097) which significantly (p = 0.023) increased from 7.6% in the fiscal year 1995/6 to 9.5% in the fiscal year 1998/9. Home care within 60 days after hospitalization was provided to 16.4% of patients with acute myocardial infarctions (n = 2076) which significantly (p < 0.000) increased from 14.1% in the fiscal year 1995/6 to 18.1% in fiscal year 1998/9. Recipients of home care were significantly older, had more comorbidities, and greater severity of illness, but were less likely to undergo coronary artery revascularization during hospitalization. After multivariate adjustment, length of hospital stay, 60 day re-admissions, and mortality were higher in those receiving home care post hospitalization. Nearly half of those receiving home care prior to hospitalization died within one year. 80% of those receiving home care prior to admission also received home care services after hospitalization. CONCLUSION: Those patients who received home care prior to a hospitalization for acute myocardial infarction were "old and frail" with a high mortality rate during and after hospitalization. The provision of home care after hospitalization selected those patients that stay in hospital longer and required more hospital care.

Adult↗
PubMed2004

Enhancement of phenanthrene solubilization and biodegradation by trehalose lipid biosurfactants.

Effects of trehalose lipid biosurfactants produced by Rhodococcus erythropolis on the solubilization and biodegradation of phenanthrene (PHE) were investigated. Based on surface tension measurements, the average critical micelle concentration (CMC) of trehalose lipids was determined to be approximately 16 mg total organic carbon (TOC)/L. In solubilization assays, the addition of biosurfactants at 20-fold the CMC increased the apparent solubility of PHE by more than 30-fold. Using a known PHE degrader (isolate P5-2), batch PHE biodegradation experiments were conducted, with and without trehalose lipids, in three systems: Water (devoid of soil solids), soil (Kenansville loamy sand having 0.72% organic matter), and soil-water slurry. Addition of trehalose lipids at 10-fold the CMC enhanced both the rate and the extent of PHE mineralization by isolate P5-2 in the liquid culture. The addition of biosurfactant (32.2 mg TOC/kg soil) to the soil system also increased both the initial rate (by more than twofold) and the extent of PHE mineralization. Biosurfactants increased the rate, but not the extent, of PHE mineralization in the soil-water slurry. The results obtained in the present study indicate that the trehalose lipid biosurfactants produced by R. erythropolis have good solubilization capacity for hydrophobic organic compounds and great potential for applications in bioremediation of sites contamination with polycyclic aromatic hydrocarbons.

Biodegradation, Environmental↗
PubMed2004

Acute myocardial infarction in Alberta: temporal changes in outcomes, 1994 to 1999.

BACKGROUND: The current survival trends in patients with acute myocardial infarction (AMI) are not known. A population-based study using administrative data to examine the short and long term survival of patients after AMI in Alberta between 1994 and 1999 was conducted. METHODS: AMI patients were identified from hospital discharge data. Temporal changes in the adjusted (age, sex, AMI anatomical location and comorbidities) fatality rate were analyzed in 19,928 AMI patients. RESULTS: The age- and sex-adjusted incidence of hospitalization for AMI in Alberta significantly declined from 169.6 per 100,000 population in 1994 to 160.8 per 100,000 in 1999 (P=0.03). The risk-adjusted in-hospital case fatality rate from all causes was 11.4% (95% CI 10.6% to 12.3%) in 1994 versus 9.2% (8.4% to 10.1%) in 1999; the 30-day case fatality rate was 12.6% (11.7% to 13.6%) in 1994 versus 10.1% (9.1% to 11.0%) in 1999; and the one-year case fatality rate was 19.0% (17.8% to 20.1%) in 1994 versus 14.9% (13.8% to 16.0%) in 1999. The percentage of hospitalized AMI patients who underwent coronary angiography within one year after admission rose from 48.2% in 1994 to 52.4% in 1999; percutaneous transluminal coronary angioplasty increased from 25.5% to 35.0% and coronary artery bypass surgery increased from 9.7% to 12.6%. Prescriptions for pharmacological drugs at discharge increased from 1994 to 1999 among patients aged 65 and older: from 29.5% in 1994 to 41.0% in 1999 for beta-blockers, from 5.2% to 18.7% for lipid lowering agents and from 14.0% to 20.5% for angiotensin-converting enzyme inhibitors. INTERPRETATION: There was a modest improvement in patient survival after AMI between 1994 and 1999. The improvements may be associated with increasing use of revascularization and pharmacological therapy provided in the management of AMI.

Adrenergic beta-Antagonists↗