Biomedical subjects

Z Wang

Publications and source records attributed to Z Wang.

At least 19 recordsLinked to original sources

PubMed2007

Respiratory syncytial virus nephropathy in rats.

The pathogenesis of minimal change nephrotic syndrome (MCNS) remains unclear. Respiratory tract viruses could contribute to MCNS, and respiratory syncytial virus (RSV) is the most common one. In this study, we planned to investigate the effects of RSV on the proteinuria and glomerular structure of rats and to explore the role of RSV in the pathogenesis of MCNS. Rats were inoculated with 6 x 10(2), 10(4), and 10(6) PFU (plaque-forming units) RSV and killed on days 4, 8, 14, 28, and 60 postinoculation (RSV(4), RSV(8), RSV(14), RSV(28), and RSV(60)). The proteinuria and serum parameters were measured; renal histology was observed by light microscopy and electron microscopy; immune complex deposits were detected by immunofluorescence microscopy; and RSV RNA and RSV titer were determined by in situ hybridization and plaque assay, respectively. After inoculation, the proteinuria increased, especially in 6 x 10(6) PFU RSV(14),(28). The serum albumin of 6 x 10(6) PFU RSV(14),(28) and different-titer RSV(60) decreased. Slight hypercellularity in minority glomeruli and swelling in partial tubular epithelial cells were observed in RSV(4),(8), whereas a relief of the above changes and no abnormalities were detected in RSV(14) and RSV(28),(60), respectively, under a light microscope. Extensive foot process effacement was observed in 6 x 10(6) PFU RSV(14),(28),(60) under an electron microscope. No immune complex deposits were detected in the renal tissues. RSV RNA signal and RSV titer of renal tissues, depending on the dose of inoculum, reached their climax on day 8 postinoculation. Our study reports for the first time that RSV can lead to nephropathy in rats on days 14-60 postinoculation, especially in 6 x 10(6) PFU RSV-inoculated rats, which may be a new exploration of the pathogenesis of MCNS.

Animals↗

PubMed2007

Function of cardiac M3 receptors.

1. Since the initial identification of the M3 subtype of muscarinic acetylcholine receptors (M3-mAChR) in the heart, there have been increasing interest and advances in studies on the pathophysiological roles of M3-mAChR in the heart. Recent studies from several laboratories have provided compelling and solid evidence in support of the important roles of M3-mAChR in regulation and maintenance of cardiac function and in generation and progression of heart disease as well. 2. The functions of the cardiac M3-mAChR revealed thus far include (i) M3-mAChR regulation of heart rate and cardiac repolarization, (ii) modulation of inotropic effects, (iii) cytoprotection against ischaemic injuries of myocardium, (iv) regulation of cell-to-cell communication, and (v) participation in generation and maintenance of atrial fibrillation. 3. Signal transduction mechanisms underlying these pathophysiological functions have also been studied, which have allowed us to get insight into the following mechanistic aspects. (i) M3-mAChR activates a delayed rectifying K+ current I(KM3) to participate in cardiac repolarization, negative chronotropic actions, and anti-dysrhythmic (suppresses ischaemic dysrhythmias) as well as pro-dysrhythmic (facilitates atrial fibrillation) actions. (ii) M3-mAChR interacts with gap-junctional channel connexin 43 to maintain cell-cell communication and excitation propagation. (iii) M3-mAChR regulates intracellular phosphoinositide hydrolysis to improve cardiac contraction and haemodynamic function. (iv) M3-mAChR activate anti-apoptotic signalling molecules, enhances endogenous antioxidant capacity, and diminishes intracellular Ca2+ overload, all of which contribute to protecting the heart against ischaemic injuries. 4. This article provides an overview of the potential roles of the M3-mAChR in parasympathetic control of heart function under normal physiological conditions and in the setting of a variety of pathological processes including heart failure, myocardial ischaemia and dysrhythmias.

Animals↗

PubMed2006

Diabetes is related to cerebral infarction but not to AD pathology in older persons.

OBJECTIVE: To examine the potential relation of diabetes to common neuropathologic causes of dementia, cerebral infarction and Alzheimer disease (AD) neuropathology. METHODS: Subjects were 233 older Catholic clergy in the Religious Orders Study, who underwent detailed annual evaluations, including neuropsychological testing, and brain autopsy at time of death (mean age 86 years, 45% men). Diabetes was identified by annual direct medication inspection and history. Cognitive function proximate to death was summarized into five cognitive domains, based on 19 neuropsychological tests. Macroscopic cerebral infarctions were recorded from 1 cm coronal slabs. Neuritic plaques, diffuse plaques, and neurofibrillary tangles were counted in Bielschowsky silver-stained sections and summarized to yield composite measures of neuritic plaques, diffuse plaques, tangles, and overall AD pathology. We also used immunohistochemistry with antibodies to amyloid-beta and PHF-tau to obtain quantitative measures of amyloid burden and neurofibrillary tangle density. Multiple logistic and linear regression analyses were used to examine the relation of diabetes to cerebral infarctions and AD pathology, controlling for age, sex, and education. RESULTS: AD pathology was related to all five cognitive domains (p < 0.01) and infarctions were related to perceptual speed (p < 0.001). Diabetes (present in 15% subjects) was associated with an increased odds of infarction (OR = 2.47, 95% CI: 1.16, 5.24). Diabetes was not related to global AD pathology score, or to specific measures of neuritic plaques, diffuse plaques or tangles, or to amyloid burden or tangle density. CONCLUSION: We found a relation between diabetes and cerebral infarction but not between diabetes and Alzheimer disease pathology in older persons.

Aged↗

PubMed2006

CD8 blockade promotes the expansion of antigen-specific CD4+ FOXP3+ regulatory T cells in vivo.

Treatment with a cocktail of CD4 and CD8-specific monoclonal antibodies (mAb) induces long-term transplantation tolerance and regulatory CD4(+) T cells that induce tolerance in non-tolerant T cells. In contrast, treatment with a CD4-specific mAb alone fails to induce long-term tolerance. The current study was designed to test the hypothesis that CD8 blockade plays a role in promoting the development of CD4(+) regulatory T cells. Using the DO11.10 CD4(+) TCR transgenic mouse model we show that treatment with a CD4/CD8-specific mAb cocktail induces antigen-specific tolerance to OVA, measured by a significant decrease in OVA-specific IgG, on challenge with antigen. Although treatment with OVA and the CD4-specific mAb alone also induces a significant decrease in OVA-specific antibody, the number of DO11.10 cells is significantly greater in mice treated with the CD4/CD8-specific mAb cocktail, and this is associated with a significant increase in proliferation of DO11.10 cells in response to specific antigen. DO11.10 cells sorted from mice made tolerant to OVA with the CD4/CD8-specific mAb cocktail promote an OVA-specific IgG1 (Th2-type) response but not an OVA-specific IgG3 (Th1-type) response on transfer into new syngeneic recipients, suggesting their ability to regulate the type of antigen-specific immune response that ensues after priming with antigen. In addition, DO11.10 cells from tolerant mice express markers that are characteristic of CD4(+) regulatory cells, including FOXP3, GITR and CTLA4, but not CD25. Taken as a whole, these data suggest that CD8 blockade promotes CD4(+) FOXP3(+) regulatory CD4(+) T cells by promoting their proliferation in tolerant mice.

Animals↗

PubMed2006

Transgenic animal production and animal biotechnology.

Considerable progress has been made in methods for production of transgenic livestock; beginning with pronuclear microinjection over 20 years ago. New methods, including the use of viral vectors, sperm-mediated gene transfer and somatic cell cloning, have overcome many of the limitations of pronuclear microinjection. It is now possible to not only readily make simple insertional genetic modifications, but also to accomplish, more complex, homozygous gene targeting and artificial chromosome transfer in livestock.

Animals↗

PubMed2006

Nodular fasciitis in the orofacial region.

Nodular fasciitis (NF) is a benign, reactive proliferation of fibroblasts in subcutaneous tissues which commonly occurs in the deep fascia. It can only be diagnosed by histopathological examination of a biopsy. A total of 23 orofacial NF patients was analysed, including those reported in the English language literature and six new patients from the files of this hospital. All patients were treated between 1994 and 2005. The reported lesions were located in cheek masseter muscle, parotid gland, upper neck, upper gingiva and body of mandibular. The clinical and histological features and differential diagnoses are discussed. All lesions were removed under general or local anaesthesia and no recurrence of the lesions was found.

Adult↗

PubMed2006

Raf 1 represses expression of the tight junction protein occludin via activation of the zinc-finger transcription factor slug.

Although dysregulation of tight junction (TJ) proteins is observed in epithelial malignancy, their participation in epithelial transformation is poorly understood. Recently we demonstrated that expression of oncogenic Raf 1 in Pa4 epithelial cells disrupts TJs and induces an oncogenic phenotype by downregulating expression of the TJ protein, occludin. Here we report the mechanism by which Raf 1 regulates occludin expression. Raf 1 inhibited occludin transcription by repressing a minimal segment of the occludin promoter in concert with upregulation of the transcriptional repressor, Slug without influencing the well-documented transcriptional repressor, Snail. Overexpression of Slug in Pa4 cells recapitulated the effect of Raf 1 on occludin expression, and depletion of Slug by small interfering RNA abrogated the effect of Raf 1 on occludin. Finally, chromatin immunoprecipitation assays and site-directed mutagenesis demonstrated a direct interaction between Slug and an E-box within the minimal Raf 1-responsive segment of the occludin promoter. These findings support a role of Slug in mediating Raf 1-induced transcriptional repression of occludin and subsequent epithelial to mesenchymal transition.

Animals↗

PubMed2006

The clinical value of hepatocyte growth factor and its receptor--c-met for liver cancer patients with hepatectomy.

BACKGROUND: To study the dynamic change of hepatocyte growth factor after hepatectomy in patients with primary liver cancer, and to analyse the prognostic value of hepatocyte growth factor and c-met for these patients. METHODS: Thirty-one consecutive patients undergoing partial hepatectomy for liver cancer were studied. Serum hepatocyte growth factor level was determined by using enzyme-linked immunosorbent assay kit before and after operation, respectively. C-met protein and MRNA expressions in cancerous and paracancerous tissues were examined by immunohistochemical and RT-PCR methods, respectively. The correlations between clinical-pathologic parameters and the expressions of hepatocyte growth factor in serum and c-met in cancerous tissues were analysed, respectively. RESULTS: Liver cancer patients had a significantly higher level of serum hepatocyte growth factor than normal controls (1.0424+/-0.498 ng/ml versus 0.685+/-0.115 ng/ml, p=0.008). Serum hepatocyte growth factor level was positively affected by tumour size, node cirrhosis, portal vein tumour thrombi, cholangiocarcinoma (including combined hepatocellular carcinoma), poorly differentiated hepatocellular carcinoma and tumour recurrence or metastases. After hepatectomy, serum hepatocyte growth factor level peaked on the third postoperative day, and then declined, but did not return to normal level on the postoperative day 10. From the preoperative day to postoperative day 10, the level of serum hepatocyte growth factor had a decrease of percent (85.33+/-10.2%) in the group with large tumours (>5 cm), but an elevation of percent (121.9+/-10.3%) in the group with small tumours (<or=5 cm). From the preoperative day to postoperative day 3, the level of serum hepatocyte growth factor had a higher elevation in the group with major resection than in the group with local resection (p=0.016). Moderately or strongly positive expression of c-met protein was observed in 27 cancerous regions (27/31), and only in 5 paracancerous regions. The intensive expression of c-met MRNA was 100% (31/31) detectable in the cancerous tissues, but only 22.6% (7/31) in the paracancerous tissues. C-met protein expression in cancerous tissues was correlated with portal vein tumour thrombi, cholangiocarcinoma and tumour recurrence or metastases, and the expression in paracancerous tissues was correlated with node cirrhosis. No significant correlation was observed between the hepatocyte growth factor in serum and c-met in cancerous tissues. CONCLUSION: The over-expressions of the hepatocyte growth factor and c-met indicates an adverse prognosis for patients with liver cancer. The sustained high level of serum hepatocyte growth factor after hepatectomy may be a factor related to early tumour recurrence and metastasis. Liver regeneration may be a main factor leading to high level of serum hepatocyte growth factor in early postoperative stage.

Adult↗

PubMed2006

Regulation of adiponectin receptors in hepatocytes by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone.

AIMS/HYPOTHESIS: Adiponectin is an adipocyte-derived hormone that plays a critical role in the development of type 2 diabetes via interaction with adiponectin receptors 1 (ADIPOR1) and 2 (ADIPOR2). Rosiglitazone is a peroxisome proliferator-activated receptor-gamma (PPARG) agonist that is widely used in the treatment of type 2 diabetes. We hypothesised that rosiglitazone regulates lipid and glucose metabolism through modulation of the expression of adiponectin receptors in the liver. METHODS: The expression of ADIPOR1 and ADIPOR2 was analysed in HepG2 hepatocytes. The promoters of adiponectin receptors were isolated and used to analyse the transcriptional regulation. The expression of adiponectin receptors in the liver was determined in mice treated with rosiglitazone. RESULTS: Rosiglitazone elevated the mRNA and protein levels of ADIPOR2 and stimulated ADIPOR2 promoter in HepG2 cells. Analysis with the ADIPOR2 promoter revealed a putative rosiglitazone-responsive region that contained a glucocorticoid receptor (GR)-binding element. The GR agonist dexamethasone synergised with rosiglitazone to stimulate the ADIPOR2 promoter wheras the GR antagonist RU486 abolished this stimulation. Treatment of mice with rosiglitazone elevated the expression of ADIPOR2 in the liver. CONCLUSIONS/INTERPRETATION: This study indicates that rosiglitazone can elevate the expression of ADIPOR2 in hepatocytes. Our data also suggest that the PPARG agonist rosiglitazone can interact functionally with a GR element in the ADIPOR2 promoter to mediate stimulation of transcription. This study thus reveals a new paradigm underlying the therapeutic effect of PPARG activators in the treatment of type 2 diabetes.

Base Sequence↗

PubMed2006

Treatment of a high-strength sulphate-rich alkaline leachate using an anaerobic filter.

The research looks at the feasibility of treating an alkaline sulphate-rich leachate arising from the co-disposal of municipal solid waste with cement kiln dust by means of an anaerobic filter (AF). This type of leachate with a high sulphate concentration is commonly prohibited for discharge to sewer and requires an on-site treatment solution. The AF used had a working volume of 4l and contained reticulated polyurethane foam as the biomass support material. The filters were operated over a 152 day experimental period during which the COD loading onto the filter was increased from 0.76 to 7.63kgCODm(-3)d(-1). In the early stages of operation at low loading, soluble sulphides accumulated that inhibited methanogenic activity. This was restored by dosing FeCl(3) to the reactor. The continued dosing allowed efficient COD removal of between 75% and 90% until the nominal retention time in the reactor was 3 days, at which point reactor performance declined significantly. The main mechanism for COD removal was by sulphate-reducing bacteria, which also resulted in up to 88% sulphate removal from the leachate. The average methane generation rate was 0.10lg(-1) COD removed. The results indicate the potential for using this approach as a pre-treatment that could significantly reduce the COD load to a second stage treatment process, but problems associated with the implementation of the technology at a larger scale have been identified.

Anaerobiosis↗

PubMed2006

Thioredoxin-interacting protein (txnip) is a glucocorticoid-regulated primary response gene involved in mediating glucocorticoid-induced apoptosis.

Glucocorticoid hormones induce apoptosis in lymphoid cells. This process is transcriptionally regulated and requires de novo RNA/protein synthesis. However, the full spectrum of glucocorticoid-regulated genes mediating this cell death process is unknown. Through gene expression profiling we discovered that the expression of thioredoxin-intereacting protein (txnip) mRNA is significantly induced by the glucocorticoid hormone dexamethasone not only in the murine T-cell lymphoma line WEHI7.2, but also in normal mouse thymocytes. This result was confirmed by Northern blot analysis in multiple models of dexamethasone-induced apoptosis. The induction of txnip mRNA by dexamethasone appears to be mediated through the glucocorticoid receptor as it is blocked in the presence of RU486, a glucocorticoid receptor antagonist. Deletion and mutation analysis of the txnip promoter identified a functional glucocorticoid response element in the txnip promoter. Reporter assays demonstrated that this glucocorticoid response element was necessary and sufficient for induction of txnip by dexamethasone. Expression of a GFP-TXNIP fusion protein was sufficient to induce apoptosis in WEHI7.2 cells, and repression of endogenous txnip by RNA interference inhibited dexamethasone-induced apoptosis in WEHI7.2 cells. Together, these findings indicate that txnip is a novel glucocorticoid-induced primary target gene involved in mediating glucocorticoid-induced apoptosis.

Anti-Inflammatory Agents↗

PubMed2006

Effect of dendritic cell vaccine against a tongue squamous cell cancer cell line (Tca8113) in vivo and in vitro.

Dendritic cells (DCs), as primary antigen-presenting cells with the capacity to activate naïve T lymphocytes, are considered to be promising adjuvants for immunity against cancer. In this study, the effect of T lymphocyte-mediated immunity induced by a DC vaccine against Tca8113 cells in vivo and in vitro was evaluated. DCs were from human peripheral blood monocytes cultured in the presence of granulocyte-macrophage colony stimulating factor, interleukin 4 and/or tumour necrosis factor alpha, and stimulated with Tca8113 cell lysate prepared by the freeze-thaw method. The autologous T cells activated by these DCs were used in an in vitro MTT assay to detect their tumouricidal activity and investigated for their anti-tumour effect in vivo by administration to nude mice with implanted tumours (Tca8113). An adequate number of DCs were successfully generated from the monocytes. The T cells activated by the DC-based vaccine killed Tca8113 cells in vitro (P<0.01), postponed tumour doubling time of the implanted tumours in nude mice (P<0.01) and inhibited the growth of the tumours (P<0.05). These results show that DCs from monocytes induce a lymphocyte-mediated immune response against tongue squamous carcinoma, and could be used as a vehicle for tumour antigens.

Animals↗

PubMed2006

Tenotomy does not affect saccadic velocities: support for the "small-signal" gain hypothesis.

We investigated the effects of four-muscle tenotomy on saccadic characteristics in infantile nystagmus syndrome (INS) and acquired pendular nystagmus (APN). Eye movements of 10 subjects with INS and one with APN were recorded using infrared reflection, magnetic search coil, or high-speed digital video. The expanded nystagmus acuity function (NAFX) quantified tenotomy-induced foveation changes in the INS. Saccadic characteristics and peak-to-peak nystagmus amplitudes were measured. Novel statistical tests were performed on the saccadic data. Six out of the 10 INS subjects showed no changes in saccadic duration, peak velocity, acceleration, or trajectory. In the other four, the differences were less than in peak-to-peak amplitudes (from 14.6% to 39.5%) and NAFX (from 22.2% to 162.4%). The APN subject also showed no changes despite a 50% decrease in peak-to-peak amplitude and a 34% increase in NAFX. The "small-signal" changes (peak-to-peak nystagmus amplitude and NAFX) were found to far exceed any "large-signal" changes (saccadic). Tenotomy successfully reduced INS and APN, enabling higher visual acuity without adversely affecting saccadic characteristics. These findings support the peripheral, small-signal gain reduction (via proprioceptive tension control) hypothesis. Current linear plant models, limited to normal steady-state muscle tension levels, cannot explain the effects of the tenotomy.

Acceleration↗

PubMed2006

Tumor-suppression function of transcription factor USF2 in prostate carcinogenesis.

Although the transcription factor USF2 has been implicated in the regulation of cellular growth and proliferation, it is unknown whether alterations in USF2 contribute to tumorigenesis and tumor development. We examined the role of USF2 in prostate tumorigenesis. Western blot analysis revealed markedly decreased USF2 levels in three androgen-independent prostate cancer cell lines, PC-3, DU145, and M12, as compared to nontumorigenic prostate epithelial cells or the androgen-dependent cell line, LNCaP. Ectopic expression of USF2 in PC-3 cells did not affect the cell proliferation rate of PC-3 cells on plastic surfaces. However, it dramatically decreased anchorage-independent growth of PC-3 cells in soft agar (90-98% inhibition) and the invasion capability (80% inhibition) of PC-3 cells in matrix gel assay. Importantly, expression of USF2 in PC-3 cells inhibited the tumorigenicity of PC-3 cells in an in vivo nude mice xenograft model (80-90% inhibition). These results suggest that USF2 has tumor-suppression function. Consistent with its function in tumor suppression, we found that the USF2 protein is present in normal prostate epithelial cells but absent in 18 of 42 (43%) human prostate cancer tissues (P = 0.015). To further examine the functional role of USF2 in vivo, we generated mice with genetic deletion of USF2 gene. We found that USF2-null mice displayed marked prostate hyperplasia at a young age, suggesting that USF2 is involved in the normal growth and differentiation of prostate. Together, these studies demonstrate that USF2 has tumor-suppressor function and plays a role in prostate carcinogenesis.

Animals↗

PubMed2006

Comparative acute and combinative toxicity of aflatoxin B1 and fumonisin B1 in animals and human cells.

Aflatoxin B(1) (AFB(1)) and fumonisin B(1) (FB(1)) are important food-borne mycotoxins. The co-contamination of food stuffs with these two mycotoxins is well known and has been possibly implicated in the development of human hepatocellular carcinoma in high risk regions around the world. In this study the acute and combinative toxicity of AFB(1) and FB(1) were tested in F-344 rats, mosquitofish (Gambusia affinis), immortalized human hepatoma cells (HepG2) and human bronchial epithelial cells (BEAS-2B). Preliminary experiments were conducted in order to assess the acute toxicity and obtain LD(50), LC(50) and IC(50) values for individual toxins in each model, respectively. This was followed by testing combinations of AFB(1) and FB(1) to obtain LD(50), LC(50) and IC(50) values for the combination in each model. All models demonstrated a significant dose response in relation to toxin treatment. The potency of the mixture was gauged through the determination of the interaction index metric. Results of this study demonstrate that these two toxins interacted to produce alterations in the toxic responses with a strong additive interaction noted in the cases of F344 rats and mosquitofish. It can be gathered that this combination may pose a significant threat to public health and further research needs to be completed addressing alterations in metabolism and detoxification that may influence the toxic manifestations in combination. These results will provide foundational knowledge for future studies on long-term combinative toxic and health effects of these mycotoxins.

Aflatoxin B1↗

PubMed2006

Neurotrophin-3 ameliorates sensory-motor deficits in Er81-deficient mice.

Two factors, the ETS transcription factor ER81 and skeletal muscle-derived neurotrophin-3 (NT3), are essential for the formation of muscle spindles and the function of spindle afferent-motoneuron synapses in the spinal cord. Spindles either degenerate completely or are abnormal, and spindle afferents fail to project to spinal motoneurons in Er81 null mice; however, the interactions between ER81 and NT3 during the processes of afferent neuron and muscle spindle development are poorly understood. To examine if overexpression of NT3 in muscle rescues spindles and afferent-motoneuron connectivity in the absence of ER81, we generated myoNT3;Er81(-/-) double-mutant mice that selectively overexpress NT3 in muscle in the absence of ER81. Spindle reflex arcs in myoNT3;Er81(-/-) mutants differed greatly from Er81 null mice. Muscle spindle densities were greater and more afferents projected into the ventral spinal cord in myoNT3;Er81(-/-) mice. Spindles of myoNT3;Er81(-/-) muscles responded normally to repetitive muscle taps, and the monosynaptic inputs from Ia afferents to motoneurons, grossly reduced in Er81(-/-) mutants, were restored to wild-type levels in myoNT3;Er81(-/-) mice. Thus, an excess of muscle-derived NT3 reverses deficits in spindle numbers and afferent function induced by the absence of ER81. We conclude that muscle-derived NT3 can modulate spindle density and afferent-motoneuron connectivity independently of ER81.

Animals↗

PubMed2006

Plasminogen activator inhibitor-1 promoter polymorphism is not associated with the aggressiveness of disease in prostate cancer.

AIMS: PAI-1 (plasminogen activator inhibitors-1) regulates plasminogen activation, and is related to tumour development. This study aims to test whether the promoter polymorphism in the PAI-1 gene is related to the aggressiveness of disease in prostate cancer. MATERIALS AND METHODS: In the present study, Taqman SNP genotyping assay was used to detect PAI-1 4G/5G polymorphism in DNA from paraffin-embedded tissues of 98 Caucasian patients with prostate cancer. RESULTS: The distribution of the genotypes is in Hardy-Weinberg equilibrium. The genotype had no statistically significant relationship with other prognostic factors. Similar risks for recurrence were seen in individuals with the 4G/4G and 4G/5G genotypes compared to those with 5G/5G genotype (odds ratio [OR] 2.65, 95% CI: 0.41-16.94, P = 0.30; OR = 2.19, 95% CI: 0.38-12.49, P = 0.38). CONCLUSION: We concluded that PAI-1 promoter polymorphism is not associated with the aggressiveness of disease in prostate cancer.

Aged↗

PubMed2006

Whole genome expression profiling using DNA microarray for determining biocompatibility of polymeric surfaces.

There is an ever increasing need to find surfaces that are biocompatible for applications like medical implants and microfluidics-based cell culture systems. The biocompatibility of five different surfaces with different hydrophobicity was determined using gene expression profiling as well as more conventional methods to determine biocompatibility such as cellular growth rate, morphology and the hydrophobicity of the surfaces. HeLa cells grown on polymethylmethacrylate (PMMA) or a SU-8 surface treated with HNO3-ceric ammonium nitrate (HNO3-CAN) and ethanolamine showed no differences in growth rate, morphology or gene expression profiles as compared to HeLa cells grown in cell culture flasks. Cells grown on SU-8 treated with only HNO3-CAN showed almost the same growth rate (36 +/- 1 h) and similar morphology as cells grown in cell culture flasks (32 +/- 1 h), indicating good biocompatibility. However, more than 200 genes showed different expression levels in cells grown on SU-8 treated with HNO3-CAN compared to cells grown in cell culture flasks. This shows that gene expression profiling is a simple and precise method for determining differences in cells grown on different surfaces that are otherwise difficult to find using conventional methods. It is particularly noteworthy that no correlation was found between surface hydrophobicity and biocompatibility.

Biocompatible Materials↗