Biomedical subjects

Xiaodong Zhou

Publications and source records attributed to Xiaodong Zhou.

At least 19 recordsLinked to original sources

PubMed2006

Pretreatment photosensitizer dosimetry reduces variation in tumor response.

PURPOSE: To compensate for photosensitizer uptake variation in photodynamic therapy (PDT), via control of delivered light dose through photodynamic dose calculation based on online dosimetry of photosensitizer in tissue before treatment. METHODS AND MATERIALS: Photosensitizer verteporfin was quantified via multiple fluorescence microprobe measurements immediately before treatment. To compensate individual PDT treatments, photodynamic doses were calculated on an individual animal basis, by matching the light delivered to provide an equal photosensitizer dose multiplied by light dose. This was completed for the lower quartile, median, and upper quartile of the photosensitizer distribution. PDT-induced tumor responses were evaluated by the tumor regrowth assay. RESULTS: Verteporfin uptake varied considerably among tumors and within a tumor. The coefficient of variation in the surviving fraction was found significantly decreased in groups compensated to the lower quartile (CL-PDT), the median (CM-PDT), and the upper quartile (CU-PDT) of photosensitizer distribution. The CL-PDT group was significantly less effective compared with NC-PDT (Noncompensated PDT), CM-PDT, and CU-PDT treatments. No significant difference in effectiveness was observed between NC-PDT, CM-PDT, and CU-PDT treatment groups. CONCLUSIONS: This research suggests that accurate quantification of tissue photosensitizer levels and subsequent adjustment of light dose will allow for reduced subject variation and improved treatment consistency.

Algorithms↗

PubMed2006

Attenuation of collagen production with small interfering RNA of SPARC in cultured fibroblasts from the skin of patients with scleroderma.

OBJECTIVE: Recently, it was observed that SPARC (secreted protein, acidic and rich in cysteine) is overexpressed in the fibroblasts of skin biopsy specimens obtained from patients with systemic sclerosis (SSc; scleroderma), and that specific inhibition of SPARC expression in normal human fibroblasts attenuated the profibrotic effect of transforming growth factor beta (TGFbeta). The purpose of this study was to examine whether inhibition of SPARC with small interfering RNA (siRNA) can be used to ameliorate the overproduction of major extracellular matrix components in SSc fibroblasts. METHODS: Fibroblasts obtained from biopsy specimens of the unaffected skin of 3 patients with diffuse SSc and 3 age- and sex-matched healthy controls were cultured and transfected with SPARC siRNA. Before and after transfection, real-time quantitative reverse transcription-polymerase chain reaction, immunostaining, and Western blotting were used to examine the transcription and/or protein levels of SPARC, connective tissue growth factor (CTGF), type I collagen, type II collagen, TGFbeta receptor 1 (TGFbetaR1), and Smad3. Student's paired t-tests were used to determine the significance of the results. RESULTS: SSc fibroblasts showed overexpression of SPARC, COL1A2, COL3A1, and CTGF, which is consistent with an activated fibroblast phenotype. Upon inhibition of SPARC with siRNA, these activated SSc fibroblasts showed decreased gene expression of COL1A2, COL3A1, and CTGF (43%, 54%, and 58%, respectively). In addition, the overproduction of type I collagen protein in SSc fibroblasts was inhibited and was shown to parallel levels of SPARC expression. In contrast, the expression of TGFBR1 and Smad3 did not change significantly nor was the level of phosphorylation of Smad3 reduced upon SPARC siRNA silencing in unstimulated cultured SSc fibroblasts. CONCLUSION: Overproduction of collagens in SSc skin fibroblasts can be attenuated through SPARC silencing. This inhibition may be associated either with direct interaction between SPARC and collagens or with inhibition of CTGF, which is a downstream effector of TGFbeta signaling. However, SPARC silencing in SSc fibroblasts appears not to be associated with TGFBR1- and Smad3-dependent processes. Application of SPARC silencing represents a potential therapeutic approach to SSc.

Activin Receptors, Type I↗

PubMed2005

A systems biology approach to genetic studies of complex diseases.

Revealing mechanisms underlying complex diseases poses great challenges to biologists. The traditional linkage and linkage disequilibrium analysis that have been successful in the identification of genes responsible for Mendelian traits, however, have not led to similar success in discovering genes influencing the development of complex diseases. Emerging functional genomic and proteomic ('omic') resources and technologies provide great opportunities to develop new methods for systematic identification of genes underlying complex diseases. In this report, we propose a systems biology approach, which integrates omic data, to find genes responsible for complex diseases. This approach consists of five steps: (1) generate a set of candidate genes using gene-gene interaction data sets; (2) reconstruct a genetic network with the set of candidate genes from gene expression data; (3) identify differentially regulated genes between normal and abnormal samples in the network; (4) validate regulatory relationship between the genes in the network by perturbing the network using RNAi and monitoring the response using RT-PCR; and (5) genotype the differentially regulated genes and test their association with the diseases by direct association studies. To prove the concept in principle, the proposed approach is applied to genetic studies of the autoimmune disease scleroderma or systemic sclerosis.

Genomics↗

PubMed2005

Autoantibodies to fibrillin-1 activate normal human fibroblasts in culture through the TGF-beta pathway to recapitulate the "scleroderma phenotype".

Fibroblasts from patients with systemic sclerosis (SSc) are activated producing excessive amounts of extracellular matrix (ECM) components. Recently, we identified a new SSc-specific autoantibody against portions of fibrillin-1, a major component of ECM microfibrils and regulator of TGF-beta1 signaling. To examine a potential pathogenic role of anti-fibrillin-1 autoantibodies, normal human fibroblasts were treated with affinity-purified autoantibodies isolated from SSc sera and then examined for alterations in gene and protein expression levels using microarrays, quantitative RT-PCR, immunoblots, and immunofluorescence. Compared with fibroblasts cultured in normal medium or in medium containing normal human IgG, anti-fibrillin-1 autoantibody-treated normal dermal fibroblasts showed increased expression of COL and several other ECM components characteristically overexpressed in SSc fibroblasts. This was accompanied by phosphorylation and nuclear translocation of Smad3. Neutralization of TGF-beta1 with anti-TGF-beta1 Abs significantly diminished the activation of fibroblasts by anti-fibrillin-1 autoantibodies. These data indicate that anti-fibrillin-1 autoantibodies can induce the activation of normal dermal fibroblasts into a profibrotic phenotype resembling that of SSc by potentially causing the release of sequestered TGF-beta1 from fibrillin-1-containing microfibrils in the ECM.

Active Transport, Cell Nucleus↗

PubMed2005

Solvothermal synthesis of hollow ZnS spheres.

Mono-dispersed semiconductor ZnS hollow spheres with the diameter of 300-500 nm and the shell thickness of about 100-150 nm have been synthesized successfully by solvothermal method from ethanol solution in the presence of a special surfactant-quaternary ammonium salt of 2-undecyl-1-dithioureido-ethyl-imidazoline (SUDEI) made in our lab. The mono-dispersed ZnS hollow spheres are characterized by XRD, size distribution investment, UV-vis, TEM, and SEM, respectively. The UV-vis measurement indicates that there is a broad absorption at 210-280 nm, which is likely to be caused by "hollow-effect." A growth mechanism of ZnS hollow spheres has also been put forward and discussed.

Journal Article↗

PubMed2005

The fabrication and characterization of a formaldehyde odor sensor using molecularly imprinted polymers.

The fabrication and characterization of odor sensors based on molecularly imprinted polymers is reported as the first case of imprinting formaldehyde. A quartz crystal microbalance is employed as a sensitive apparatus of a sensor for the determination of odor formaldehyde. An equation is deduced to characterize the interaction between molecularly imprinted films and the template. A linear relationship between the frequency shifts and the concentration of analyte in the range of 1.25 to 14.25 microM is found. The detection limit is about 20.5 microM. The sensor can selectively distinguish gaseous formaldehyde. It is envisaged that this novel and handy method could be employed to determine formaldehyde gas in the atmosphere.

Air Pollution↗

PubMed2005

Effect of tumor host microenvironment on photodynamic therapy in a rat prostate tumor model.

PURPOSE: Tumor host microenvironment plays an important role in tumor growth, metastasis, and response to cancer therapy. In this study, the influence of tumor host environment on tumor pathophysiology, photosensitizer distribution, and photodynamic therapy (PDT) treatment effect was examined in the metastatic at lymph node and lung (MatLyLu) rat prostate tumor. EXPERIMENTAL DESIGN: MatLyLu tumors implanted in different host environment [i.e., orthotopically (in the prostate) or s.c.] were compared for difference in vessel density, average vessel size, vascular permeability, tumor vascular endothelial growth factor production, and tumor oxygenation. Uptake of photosensitizer verteporfin in tumors in both sites was determined by fluorescence microscopy. To compare tumor response to PDT, both orthotopic and s.c. MatLyLu tumors were given the same doses of verteporfin and laser light treatment, and PDT-induced tumor necrotic area was measured histologically. RESULTS: Orthotopic MatLyLu tumors were found to grow faster, have higher vessel density and more permeable vasculature, have higher vascular endothelial growth factor protein levels, and have lower tumor hypoxic fraction than the s.c. tumors. Uptake of photosensitizer verteporfin in the orthotopic tumor was higher than in the s.c. tumors at 15 minutes after injection (1 mg/kg, i.v.), and became similar at 3 hours after injection. For the vascular targeting PDT treatment (0.25 mg/kg verteporfin, 50 J/cm(2) at 50 mW/cm(2), 15 minutes drug-light interval), there was no significant difference in PDT-induced tumor necrotic area between the orthotopic and s.c. tumors, with 85% to 90% necrosis in both types of tumors. However, tumor necrosis induced by the cellular targeting PDT (1 mg/kg verteporfin, 50 J/cm(2) at 50 mW/cm(2), 3 hours drug-light interval) was significantly different in the orthotopic (64%) versus the s.c. (29%) tumors. CONCLUSIONS: Tumor host environment can significantly affect photosensitizer verteporfin distribution and PDT treatment effect. Verteporfin-PDT regimen targeting tumor cells is more sensitive to such influence than the vascular targeting PDT. Our study showed the importance of tumor host environment in determining tumor physiologic properties and tumor response to PDT. To obtain clinically relevant information, orthotopic tumor model should be used in the experimental studies.

Animals↗

PubMed2005

Small interfering RNA inhibition of SPARC attenuates the profibrotic effect of transforming growth factor beta1 in cultured normal human fibroblasts.

OBJECTIVE: SPARC (secreted protein, acidic and rich in cysteine), or osteonectin, is a matricellular protein. Recently, it was observed to be overexpressed in fibroblasts obtained from the skin of patients with scleroderma, as well as in different tissues from patients with several other fibrotic disorders. Moreover, a genetic polymorphism in SPARC has been associated with susceptibility to scleroderma. Transforming growth factor beta1 (TGFbeta1) is a profibrotic cytokine that stimulates excessive collagen production in patients with scleroderma or other fibrotic diseases. The purpose of this study was to examine whether specific inhibition of SPARC can influence the expression of type I collagen and ameliorate the profibrotic activity of TGFbeta1 on normal human fibroblasts. METHODS: Fibroblasts obtained from the skin of 4 healthy individuals were cultured and transfected with SPARC small interfering RNA (siRNA). TGFbeta was used as a fibrosis stimulus in cultured fibroblasts. Real-time quantitative reverse transcriptase-polymerase chain reaction and Western blotting were used to measure transcription and protein levels of SPARC and type I collagen, respectively. RESULTS: The fibroblasts transfected with SPARC siRNA showed decreased expression of both SPARC and type I collagen. Exogenous TGFbeta1 induced increased expression of both SPARC and type I collagen in cultured normal human fibroblasts, but this response was significantly blunted in the fibroblasts transfected with SPARC siRNA. CONCLUSION: TGFbeta1 can induce increased expression of both SPARC and type I collagen. Specific inhibition of SPARC led to decreased expression of type I collagen and attenuated the profibrotic effect of TGFbeta1 in cultured normal human fibroblasts. Use of siRNA to silence SPARC represents a potential therapeutic approach to fibrotic disorders such as scleroderma.

Cells, Cultured↗

PubMed2005

Classification analysis of the transcriptosome of nonlesional cultured dermal fibroblasts from systemic sclerosis patients with early disease.

OBJECTIVE: To compare the transcriptosome of early-passage nonlesional dermal fibroblasts from systemic sclerosis (SSc) patients with diffuse disease and matched normal controls in order to gain further understanding of the gene activation patterns that occur in early disease. METHODS: Total RNA was isolated from early-passage fibroblasts obtained from nonlesional skin biopsy specimens from 21 patients with diffuse SSc (disease duration <5 years in all but 1) and 18 healthy controls who were matched to the cases by age (+/-5 years), sex, and race. Array experiments were performed on a 16,659-oligonucleotide microarray utilizing a reference experimental design. Supervised methods were used to select differentially expressed genes. Quantitative polymerase chain reaction (PCR) was used to independently validate the array results. RESULTS: Of the 8,324 genes that passed filtering criteria, classification analysis revealed that <5% were differentially expressed between SSc and normal fibroblasts. Individually, differentially expressed genes included COL7A1, COL18A1 (endostatin), DAF, COMP, and VEGFB. Using the panel of genes discovered through classification analysis, a set of model predictors that achieved reasonably high predictive accuracy was developed. Analysis of 1,297 gene ontology (GO) classes revealed 35 classes that were significantly dysregulated in SSc fibroblasts. These GO classes included anchoring collagen (30934), extracellular matrix structural constituent (5201), and complement activation (6958, 6956). Validation by quantitative PCR demonstrated that 7 of 7 genes selected were concordant with the array results. CONCLUSION: Fibroblasts cultured from nonlesional skin of patients with SSc already have detectable abnormalities in a variety of genes and cellular processes, including those involved in extracellular matrix formation, fibrillogenesis, complement activation, and angiogenesis.

Dermis↗

PubMed2005

Monozygotic twins clinically discordant for scleroderma show concordance for fibroblast gene expression profiles.

OBJECTIVE: Fewer than 5% of monozygotic (MZ) and dizygotic (DZ) twin pairs are clinically concordant for systemic sclerosis (SSc), yet the majority of MZ twins are concordant for antinuclear antibodies. To discover genetic versus nongenetic molecular pathways important to the pathogenesis of SSc, we compared global gene expression patterns in twins discordant for SSc. METHODS: Total RNA from dermal fibroblasts of 15 discordant twin pairs (10 MZ and 5 DZ) and 5 normal controls were used in microarray analysis. Aberrantly expressed genes were confirmed using quantitative real-time reverse transcriptase-polymerase chain reaction. RESULTS: Lesional and nonlesional fibroblasts from SSc patients showed no significant differences in gene expression, while SSc patients had gene profiles that were significantly different from those of unaffected DZ twins and normal controls. Unaffected MZ twins, however, were not significantly different from SSc patients. Unsupervised hierarchical clustering segregated the fibroblast samples as originating from 2 major groups. Group A contained 5 discordant MZ twin pairs, 3 affected MZ twins, and 3 affected DZ twins. Group B contained all 5 normal population controls, all 5 healthy DZ twins, 2 discordant MZ twins, and 2 discordant DZ twin pairs. Normal fibroblasts incubated with serum from an SSc-affected patient or with serum from her unaffected MZ twin sister developed the increased expression of COL1A2, SPARC, and CTGF typically seen in SSc fibroblasts. CONCLUSION: These results demonstrate that dermal fibroblasts from SSc patients and from 40-50% of their genetically identical but clinically unaffected MZ twins exhibit a similar gene expression pattern which can be induced in normal fibroblasts by sera from both. Thus, a stronger genetic predisposition to SSc (than can be detected clinically) is apparent at the molecular level in skin fibroblasts.

Adult↗

PubMed2004

Gene expression profiling of pediatric acute myelogenous leukemia.

Contemporary treatment of pediatric acute myeloid leukemia (AML) requires the assignment of patients to specific risk groups. To explore whether expression profiling of leukemic blasts could accurately distinguish between the known risk groups of AML, we analyzed 130 pediatric and 20 adult AML diagnostic bone marrow or peripheral blood samples using the Affymetrix U133A microarray. Class discriminating genes were identified for each of the major prognostic subtypes of pediatric AML, including t(15;17)[PML-RARalpha], t(8;21)[AML1-ETO], inv(16) [CBFbeta-MYH11], MLL chimeric fusion genes, and cases classified as FAB-M7. When subsets of these genes were used in supervised learning algorithms, an overall classification accuracy of more than 93% was achieved. Moreover, we were able to use the expression signatures generated from the pediatric samples to accurately classify adult de novo AMLs with the same genetic lesions. The class discriminating genes also provided novel insights into the molecular pathobiology of these leukemias. Finally, using a combined pediatric data set of 130 AMLs and 137 acute lymphoblastic leukemias, we identified an expression signature for cases with MLL chimeric fusion genes irrespective of lineage. Surprisingly, AMLs containing partial tandem duplications of MLL failed to cluster with MLL chimeric fusion gene cases, suggesting a significant difference in their underlying mechanism of transformation.

Adult↗

PubMed2004

cDNA microarrays reveal distinct gene expression clusters in idiopathic inflammatory myopathies.

BACKGROUND: Polymyositis (PM) and dermatomyositis (DM) are complex human diseases of autoimmune origin which cause progressive skeletal muscle weakness in adults and children. Histopathological studies of affected muscles suggest that cytotoxic T cell-induced injury predominates in PM, while humoral immune mechanisms seem more likely in DM. Early expression of MHC class I molecules on myocytes is a striking feature of both disorders. This study was to use gene microarray analysis of muscle biopsies from PM and DM patients to obtain a comprehensive view of molecules participating in disease pathogenesis. MATERIAL/METHODS: Muscle biopsies from 10 patients (6 PM and 4 DM) and 5 controls were selected for gene expression profiles. Microarray filters containing 4000 known human genes were used to hybridize with RNAs from muscle biopsies. Real-time RT-PCR assays were used to confirmed selected genes that showed changes in expression levels in PM and DM from microarray data. The t-statistic was used to measure any differences in the amount of gene expression in the normal versus myositis biopsies. RESULTS: Forty genes clustering into two major groups showed significantly altered expression levels in PM/DM compared to normal biopsies. One cluster of over-expressed genes was primarily of immune origin and included HLA-class I and II, interferon-inducible proteins, natural killer (NK) protein, immunoglobulins and complement. The other cluster of under-expressed genes were of muscle origin, especially those involved in the fast twitch response. PM and DM gene profiles appeared similar. CONCLUSIONS: PM and DM muscle biopsies show similar gene expression profiles despite reported differences in histopathological changes. Altered gene expressions of immune regulation and myofibrillar proteins are prominent in muscle biopsies of myositis.

Adult↗

PubMed2004

Genetic signatures of pre-expansion bottleneck in the Choctaw population of Oklahoma.

Previous research showed that the Choctaw Indians of Oklahoma exhibit considerable linkage disequilibria (LD) in a number of regions of the genome that has allowed genetic fine mapping for potential susceptibility genes for the autoimmune connective tissue disease scleroderma, or systemic sclerosis (SSc). In principle, such enhanced background LD in the Choctaws could be caused by population bottleneck event(s) followed by recent population expansion. This investigation utilizes genome-scan data on 175 dinucleotide loci from 76 Choctaw individuals to seek genetic evidence of the demographic history of the Choctaw Nation. Of the 175 loci examined, 105 are in Hardy-Weinberg equilibrium. The average unbiased homozygosity over the 105 loci for the Choctaws (29.3%) is significantly higher than that in the European descent group (20.9%); and when adjusted for sample-size differences, the Choctaw also exhibit a significantly smaller number of segregating alleles (6.65 vs. 8.14) at these loci. Both of these observations are consistent with the trend expected in an isolated population. Comparison of the allele size variance and gene diversity yields an imbalance index (lnbeta) of 0.811 in the Choctaw. Of the 105 loci examined, 93 exhibit excess expected homozygosity in comparison to the expectations of a stepwise mutation model in a population of constant size. Taken together, these observations are consistent with a signature of the recent population size expansion of the Choctaws, preceded by bottleneck event(s).

Female↗

PubMed2004

Analysis of effective molecular diffusion rates for verteporfin in subcutaneous versus orthotopic Dunning prostate tumors.

Photosensitizer biodistribution change inside tissue is one of the dominant factors in photodynamic therapy efficacy. In this study, the pharmacokinetics of a benzoporphyrin derivative (BPD), delivered in verteporfin for injection formulation, have been quantified in the rat Dunning prostate tumor MAT-LyLu model, using both subcutaneous and orthotopic sites. Blood plasma sampling indicated that BPD had a bi-exponential metabolic lifetime in vivo, with the two lifetimes being 9.6 min and 8.3 h. The spatial distributions in the tumor were quantified as a function of distance from the perfused blood vessels, using fluorescence histologic images of the tumor. A fluorescent vascular marker was used to obtain locations and shapes of perfused capillaries at a wavelength of emission different from that of BPD and to allow colocalized images to be acquired of vessel and BPD locations. Using the BPD fluorescence images obtained 15 min after intravenous administration, a forward finite-element solution to the diffusion equation was used to predict the drug distribution by matching the fluorescence intensity images observed microscopically. An inverse solver was used to minimize the root mean square error between the image of simulated diffusion and the experimental image, resulting in estimation of the diffusion coefficient of BPD in the tumor models. Effective diffusion coefficients were 0.88 and 1.59 microm2/s for the subcutaneous and orthotopically grown tumors, respectively, indicating that orthotopic tumors have significantly higher vascular extravasation rates as compared with subcutaneous tumors. This analysis supports the hypothesis that leakage rates of the photosensitizer vary considerably. Thus, although varying the time between injection and optical irradiation may be used to vary the targeting between vascular and less vascular areas, the precise time of treatment will depend on the nature of the permeability of the vasculature in the tissue being treated.

Animals↗

PubMed2003

Classification of pediatric acute lymphoblastic leukemia by gene expression profiling.

Contemporary treatment of pediatric acute lymphoblastic leukemia (ALL) requires the assignment of patients to specific risk groups. We have recently demonstrated that expression profiling of leukemic blasts can accurately identify the known prognostic subtypes of ALL, including T-cell lineage ALL (T-ALL), E2A-PBX1, TEL-AML1, MLL rearrangements, BCR-ABL, and hyperdiploid karyotypes with more than 50 chromosomes. As the next step toward developing this methodology into a frontline diagnostic tool, we have now analyzed leukemic blasts from 132 diagnostic samples using higher density oligonucleotide arrays that allow the interrogation of most of the identified genes in the human genome. Nearly 60% of the newly identified subtype discriminating genes are novel markers not identified in our previous study, and thus should provide new insights into the altered biology underlying these leukemias. Moreover, a proportion of the newly selected genes are highly ranked as class discriminators, and when incorporated into class-predicting algorithms resulted in an overall diagnostic accuracy of 97%. The performance of an array containing the identified discriminating genes should now be assessed in frontline clinical trials in order to determine the accuracy, practicality, and cost effectiveness of this methodology in the clinical setting.

Algorithms↗

PubMed2003

Genome-wide association study for regions of systemic sclerosis susceptibility in a Choctaw Indian population with high disease prevalence.

OBJECTIVE: Systemic sclerosis (SSc) is a complex, multisystem connective tissue disease in which genetic factors contribute to disease susceptibility. The aim of this study was to localize chromosome regions associated with susceptibility to SSc in a relatively isolated and homogeneous population of Choctaw Indians with a high prevalence of SSc. METHODS: A genome-wide microsatellite screen at 10 cM resolution (400 markers) was performed in 20 Choctaw patients with SSc and 76 ethically matched controls. Based on the results of the initial screen, fine-scale microsatellite mapping at < or =1 cM resolution was performed in 10 selected chromosome regions. Allele and marker haplotype frequencies were compared between SSc patients and controls. RESULTS: From the genome-wide screen, 12 markers showed evidence of highly significant associations with SSc in this population (P < 0.01), while 5 other markers showed significant associations (0.01 < P < 0.05). Among these markers, loci D5S410, D6S422, D15S978, and D20S107 are near the SPARC, MHC, FBN1, and TOPOI genes, respectively, confirming the results of our previous studies, which used different markers. D1S2800 and D14S63 have been reported to show linkage to systemic lupus erythematosus (SLE) in family-based studies, and D1S206, D6S422, and D6S264 are loci on 1p21.2, 6p22.3, and 6q23-27, respectively, which are in regions reported as showing linkage to SLE and other autoimmune diseases. Other markers showing unique associations with SSc were D7S510 (7p12-11), D7S661 (7q35), D8S514 (8q24.12), D19S221 (19p13.2), D19S220 (19q13.2), D22S423 (22q13.1), DXS1068 (Xp11.4), and DXS8055 (Xq21-23). Further analysis with fine-scale microsatellite mapping revealed at least 14 potential haplotypes associated with SSc. CONCLUSION: Our findings indicate that a number of genetic loci may contribute to the high prevalence of SSc in the Choctaw and are consistent with the paradigm that some autoimmune rheumatic diseases are likely to share genetic determinants.

Chromosomes, Human↗

PubMed2003

[Nested case-control study on riboflavin levels in blood and urine and the risk of lung cancer].

The present study is designed to explore the relationship between the riboflavin levels in blood and urine and the risk of lung cancer among miners in Yunnan Tin Corporation(YTC) by means of nested case-control design. Cases were patients with lung cancer newly diagnosed from 1992 to 1995. For each case, 2 controls were randomly matched with occupational exposure history, age, the time of collecting blood or urine samples. The indexes for evaluating the riboflavin nutritional status were erythrocyte glutathione reductase activation coefficient (EGR-AC) and the ratio of riboflavin and creatinine in urine. When analyzed as either the continuous or the rank variables, the odds ratios(ORs) used to estimate the relative risk of lung cancer have no statistical significance(P > 0.05) after adjusting the confusing factors. No association of riboflavin indexes in blood and urine with the lung cancer risk among YTC miners were observed in the present study.

Case-Control Studies↗

PubMed2002

Detection of hepatitis B virus by piezoelectric biosensor.

A highly sensitive piezoelectric HBV DNA biosensor has been developed based on the sensitive mass-transducing function of the quartz crystal microbalance and the speciality of nucleic acid hybridization reaction. HBV nucleic acid probe was immobilized onto the gold electrodes of a 9 MHz AT-cut piezoelectric quartz crystal with the polyethyleneimine adhesion, glutaraldehyde cross-linking (PEI-Glu) method or the physical adsorption method. The coated crystal with the PEI-Glu method to immobilized HBV nucleic acid probe showed the better results than the physical adsorption method with respect to sensitivity reproducibility and stability. The frequency shifts of hybridization have better linear relationship with the amount of HBV DNA, when the amount was in range 0.02-0.14 microg/ml. The crystal could be regenerated nearly five times without perceptible decrease of sensitivity.

Biosensing Techniques↗