Jinhua Xu

Fudan University, Shanghai, Shanghai Shi, China

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Publications (17)44.53 Total impact

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    ABSTRACT: Cyclin D1 is a member of the G1 cyclin family that regulates the transition through the G1 phase of the cell cycle and is involved in the neoplastic transformation of certain tumors. This study was designed to investigate the expression of cyclin D1 in Bowen's disease (BD) and cutaneous squamous cell carcinoma (SCC). Biopsies of 30 cases with BD and 24 cases with SCC confirmed by histopathology were obtained from the Department of Dermatology of Huashan Hospital, Shanghai, China. EnVision immunohistochemical technology with a semiquantitative immunohistochemical score was applied to detect the expression of cyclin D1. Of the 24 specimens with SCC, cyclin D1 was found to be positive in 17 (70.8%), whereas of the 30 specimens with BD, cyclin D1 was found to be positive in 13 (43.3%). The expression of cyclin D1 was significantly higher in the SCC compared to that in the BD group. We did not observe a significant association of cyclin D1 expression with different pathological grades of SCC. In conclusion, cyclin D1 plays a significant role as a diagnostic marker in skin tumors and its overexpression was not found to be correlated with the degree of differentiation of SCC.
    Molecular and clinical oncology. 07/2014; 2(4):545-548.
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    ABSTRACT: Icariin is the major active ingredient of Herba Epimedii. Icaritin (ICT) is a hydrolytic product of Icariin. In the present study, we investigated the protective role of ICT against cigarette smoke extract (CSE)-mediated oxidative stress in human lung epithelial A549 cells. As demonstrated by the WST-8 assay, exposure to CSE (2.5%, 5%, and 10%) reduced the cell viability of A549 cells (84%, 64% and 53%) in a dose-dependent manner and treatment with ICT10μM dramatically attenuated CSEinduced cytotoxicity (73% and 64%). The MFI data suggested that CSE induced oxidative stress by generating ROS(230)and 10μM ICT treatment attenuated CSE-induced ROS production(90). 10μM ICT treatment resulted in significant AKT activation, Nrf2 nuclear translocation, increased GCL transcription and GSH levels, as compared with CSE exposure alone. However, ICT-mediated upregulation of GCL transcription in CSE-treated cells were lost in Nrf2 siRNA-transfected cells. Furthermore, inhibition of PI3K/AKT signaling by LY294002 partially prevents ICT-induced nuclear translocation of Nrf2 and GCL transcription. These findings suggest that ICT attenuates CS-induced oxidative stress by quenching ROS and also by upregulating GSH via a PI3K-AKT-Nrf2-dependent mechanism. Further studies are required to confirm that a similar protective effect of ICT occurs in the lungs in vivo in response to CS exposure.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 12/2013; · 2.99 Impact Factor
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    ABSTRACT: Improvements in skin cancer treatment are likely to derive from novel agents targeting the molecular pathways that promote tumor cell growth and survival. Icariside II (IS) is a metabolite of icariin, which is derived from Herba Epimedii. The aim of the present study was to evaluate the antitumor effects of IS and to determine the mechanism of apoptosis in A431 human epidermoid carcinoma cells. A431 cells were treated with IS (0‑100 µM) for 24 or 48 h and cell viability was detected using the WST‑8 assay. Apoptosis was measured by the Annexin‑V/propidium iodide (PI) flow cytometric assay. Western blot analysis was used to measure the expression of cleaved caspase‑9, cleaved poly ADP ribose polymerase (PARP), phosphorylated signal transducer and activator of transcription 3 (P‑STAT3), phosphorylated extracellular signal-regulated kinase (P‑ERK), and P‑AKT. A431 cells were also pretreated with IS (0‑100 µM) 2 h prior to treatment with epidermal growth factor (EGF; 100 ng/ml) for 10 min. Phosphorylated EGF receptor (P‑EGFR), P‑STAT3, P‑ERK and P‑AKT were detected by western blot analysis. The results demonstrated that IS inhibited the cell viability of the A431 cells in a dose‑dependent manner. Pretreatment with LY294002 [a phosphatidylinositol 3-kinase (PI3K) inhibitor], EGF (an EGFR agonist) and AG1478 (an EGFR inhibitor) partially reversed IS‑induced decreases in cell viability. Treatment with 50 µm IS resulted in an increased number of apoptotic cells mirrored by increases in cleaved caspase‑9 and cleaved PARP. In addition, treatment with 50 µM IS significantly inhibited the activation of the Janus kinase (JAK)‑STAT3 and mitogen‑activated protein kinase (MAPK)‑ERK pathways, but promoted the activation of the PI3K‑AKT pathway. Furthermore, IS effectively inhibited the EGF-induced activation of the EGFR pathways. In conclusion, IS inhibited the cell viability of the A431 cells through the regulation of apoptosis. These effects were mediated, at least in part, by inhibiting the activation of the EGFR pathways.
    Molecular Medicine Reports 06/2013; · 1.17 Impact Factor
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    ABSTRACT: BACKGROUND: CD4+ T cells DNA hypomethylation is involved in the pathogenesis of systemic lupus erythematosus (SLE). Recent studies showed that ultraviolet B (UVB, 290-320nm) might induce the exacerbation of SLE by decreasing the DNA methylation level. However, the role of DNA methyltransferase 1 (DNMT1) in the UVB-induced CD4+ T cells DNA hypomethylation remains unclear. OBJECTIVE: To elucidate the role of DNMT1 in lupus CD4+ T cells global DNA hypomethylation enhanced by UVB. METHODS: 35 SLE patients and 15 healthy controls were enrolled in the study. CD4+ T cells from SLE patients and healthy controls exposed to different dosages of UVB were analyzed. The global DNA methylation measurement, real-time PCR, Western blotting and DNMT1 catalytic activity detection were employed. RESULTS: The level of global DNA methylation and DNMT1 mRNA expression in CD4+ T cells from SLE patients were significantly lower than those from the control group. DNA methylation was decreased after UVB exposure in a dosage-dependent manner in SLE patients, but not in the control group. DNMT1 mRNA and protein expression level were not affected by UVB exposure in both SLE patients and healthy controls. DNMT1 catalytic activity was significantly decreased in CD4+ T cells from SLE patients after UVB exposure in a dosage-dependent manner. DNMT1 catalytic activity was lower and more sensitive to UVB exposure in CD4+ T cells from active SLE patients that from stable ones. CONCLUSION: UVB enhanced DNA hypomethylation of CD4+ T cells in SLE via inhibiting DNMT1 catalytic activity in a dosage-dependent manner.
    Journal of dermatological science 05/2013; · 3.71 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the effects of ultraviolet B (UVB) exposure on DNA methylation in patients with systemic lupus erythematosus (SLE) and its significance in the pathogenesis of SLE. T cells from 35 SLE patients and 21 healthy individuals were cultured and irradiated with UVB. The global DNA methylation profiles of the T cells obtained from the patients and controls following irradiation with UVB were assessed using specific monoclonal antibodies for 5-methylcytosine and analyzed quantitatively through flow cytometry. Real-time reverse transcription-polymerase chain reaction (RT-PCR) was used to analyze the levels of DNA methyltransferase 1 (DNMT1) and methyl CpG binding domain protein 2 (MBD2) in T cells from the patients and controls following UVB irradiation. Significant global DNA hypomethylation was observed in the SLE patients compared with the controls (P<0.01). The SLE patients also had significantly lower levels of DNMT1 mRNA expression (P<0.01) and significantly higher levels of MBD2 mRNA compared with the controls (P<0.01). DNA methylation was decreased following UVB irradiation at two different dosages and the DNA methylation levels of the patients with active SLE were more sensitive to UVB. The level of DNMT1 mRNA was decreased following UVB irradiation at the higher dosage in the patients with active SLE, but no significant difference was observed in MBD2 mRNA expression. UVB exposure is able to inhibit DNA methylation and DNMT1 mRNA expression, which is subsequently involved in the epigenetic mechanism of SLE. The process by which DNA hypomethylation occurs in patients with SLE is complicated and the multiple factors that are involved in DNA methylation and demethylation events require further study.
    Experimental and therapeutic medicine 04/2013; 5(4):1219-1225. · 0.34 Impact Factor
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    ABSTRACT: The anti-tumor effect of aconitine in melanoma cell line B16 has been studied in this paper. We found that B16 cells showed significantly reduced growth rates and increased apoptotic effects in the presence of aconitine. Furthermore, aconitine inhibited the PI3K/AKT and MAPK/ERK1/2 signaling pathways, thus regulating the levels of protein and mRNA of PCNA and apoptotic related signaling molecules. Above all, we found that aconitine showed an anti-melanoma effect in suppressing tumor growth in vivo. In conclusion, we show that aconitine may be a useful anticancer drug in the future.
    Molecules 01/2013; 18(1):757-67. · 2.43 Impact Factor
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    ABSTRACT: This study evaluated the antitumor effects of icariside II (IS), isolated from Herba Epimedii, on in vitro and in vivo models of melanoma and determined its mechanism of apoptosis. Mouse (B16) and human (A375, SK-MEL-5) melanoma cell lines were treated with IS at different concentrations (0-100 μM). Cell viability and proliferation was detected by WST-1 assay and with the xCELLigence system, respectively. Apoptosis was measured by the annexin-V/PI flow cytometric assay. Western blot was used to measure cleaved caspase 3, survivin, P-STAT3, P-ERK and P-AKT. B16 and A375 cells were injected subcutaneously into C57BL/6J and BALB/c-nu mice, respectively. After 1 wk, IS solution at (50 mg/kg, 100 mg/kg) was administered by intraperitoneal injection 3 times for a week. Tumor size was measured with an electronic digital caliper. IS inhibited the proliferation of melanoma cells in a dose- and time-dependent manner. Treatment of A375 cells with IS resulted in an increased number of apoptotic cells ranging from 5.6% to 26.3% mirrored by increases in cleaved caspase-3 and a decrease in survivin expression. IS significantly inhibited the activation of the JAK-STAT3 and MAPK pathways but promoted an unsustained activation peak of the PI3K-AKT pathway. IS administration (50 mg/kg) resulted in a 47.5% decreased tumor volume in A375 bearing mice. Furthermore, IS administration (50 mg/kg, 100 mg/kg) resulted in 41% and 49% decreased tumor volume in B16 bearing mice, respectively. IS dramatically inhibited the proliferation of melanoma cells in vivo and in vitro through the regulation of apoptosis. These effects demonstrate the ability of IS to effectively overcome the survival signals of tumor cells, which support further preclinical evaluation of IS in cancer as a new potential chemotherapeutic agent.
    Nutrition and Cancer 01/2013; 65(1):110-117. · 2.70 Impact Factor
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    ABSTRACT: BACKGROUND: The mechanism of DNA hypomethylation in systemic lupus erythematosus (SLE) has not been fully elucidated. Recent studies showed that miR-29b could regulate DNA methylation by targeting the DNA methylation machinery. However, the role of miR-29b in T cell aberrant DNA hypomethylation of SLE still remains unclear. OBJECTIVE: In this study, we asked whether miR-29b regulate DNA methylation in lupus CD4+ T cells. METHODS: The miR-29b expression was analyzed by quantitative polymerase chain reaction (qPCR). Sp1, DNMT1, CD11a and CD70 mRNA and protein levels were determined by qPCR, Western-blotting and flow cytometry, respectively. The global DNA methylation levels were evaluated by the Methyflash™ DNA Methylation Quantification Kit. CD11a and CD70 promoter methyaltion levels were detected by bisulfate modification and methylation-sensitive high resolution melting analysis. RESULTS: In SLE patients, the miR-29b levels were up-regulated as compared to healthy donors and its degree of overexpression was negatively correlated with sp1 and DNMT1 protein levels, respectively. Overexpression of miR-29b resulted in significant reduction of sp1 and DNMT1 expression. Further analysis demonstrated that overexpression of miR-29b in CD4+ T cells from healthy donors led to the DNA hypomethylation and up-regulation of genes encoding CD11a and CD70, and inhibition of miR-29b expression in CD4+ T cells from patients with lupus caused reverse effects. CONCLUSION: Our study suggests that miR-29b negatively regulates DNMT1 expression by targeting sp1 in T cells. The overexpression of miR-29b contributes to the reduction of DNMT1 levels and thereby DNA hypomethylation in SLE. This finding provides potential novel strategies for therapeutic interventions.
    Journal of dermatological science 10/2012; · 3.71 Impact Factor
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    ABSTRACT: Psoriasis is a common, chronic, intractable skin disease that affects approximately 2% of the world's population. Transcriptional regulation is one of the most fundamental processes in psoriasis. However, high-throughput functional analysis of multiple transcription factors and their target genes in psoriasis is still rare. Thus, the objective of our study was to interpret the mechanisms of psoriasis through the regulation network construction using the GSE14905 microarray data. The results showed E2F transcription factor 1 (E2F1), jun proto-oncogene (JUN), nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (NF-κB1), signal transducer and activator of transcription 1 (STAT1), STAT3 and SP3 were hinge points in our transcriptome network. Importantly, JUN may regulate activating transcription factor 3 expression to involve cell proliferation process; STAT1 and STAT3 can inhibit tissue inhibitor of metalloproteinases-3 expression to modulate the cell adhesion molecule pathway; NF-κB and E2F1 can downregulate cyclin D1, but upregulate proliferating cell nuclear antigen expression to promote the cell cycle pathway. In addition, the regulation network between transcription factors and pathways revealed that NF-κB1 could promote the Toll-like receptor signaling pathway and that SP3 may inhibit the steroid hormone biosynthesis pathway in psoriasis. This transcriptional regulation analysis may provide a better understanding of molecular mechanism and some potential therapeutic targets in the treatment of human psoriasis.
    The Journal of Dermatology 10/2012; · 1.77 Impact Factor
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    ABSTRACT: Extramammary Paget's disease (EMPD) is a rare cutaneous malignant neoplasm. The genetic alterations underlying its pathogenesis have less been described. Therefore, we analyzed the possible mutations in the KRAS, HRAS, NRAS, BRAF, ARAF, RAF1, PIK3CA, AKT1, CTNNB1 and APC genes as well as methylation and expression of CDH1 in 144 EMPD cases and 42 matched normal skin tissues. A distinct mutation profile was identified in EMPDs with 27 (19%) cases mutant for RAS and RAF genes and 50 (35%) cases harboring oncogenic mutations in PIK3CA and AKT1. Moreover, a mutually exclusive pattern was observed in the genetic variants in these two signaling pathways. No mutation was detected in CTNNB1 and APC genes. High prevalence of low expression and hypermethylation of CDH1 gene was detected in 33 and 48% of the EMPD cases, respectively. Furthermore, PIK3CA and AKT1 mutations were significantly correlated with CDH1 hypermethylation which could explain why the majority of EMPD cases with mutant PIK3CA and AKT1 were invasive. Our study demonstrates that genetic variants associated with constitutive activation of RAS/RAF and PI3K/AKT pathways are involved in the pathogenesis of EMPD. This may represent novel therapeutic targets for this skin cancer.
    International Journal of Cancer 07/2012; · 6.20 Impact Factor
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    ABSTRACT: Combination therapy of paclitaxel (taxol) with natural anti-tumor agents that are capable of inhibiting survival signals may provide a rational molecular basis for novel chemotherapeutic strategies. Our previous study showed that icariside II (IS), derived from Herba Epimedii, inhibited the proliferation of melanoma cells in vivo and in vitro through the regulation of apoptosis. In this report, the combination effects of paclitaxel and IS were investigated in human melanoma A375 cells. As compared to the treatment with paclitaxel alone, the co-administration of IS and paclitaxel resulted in an enhancement of apoptosis as revealed by WST-8 and PI assays. Meanwhile, Western blot analysis showed that the co-administration of IS and paclitaxel resulted in increases of cleaved caspase-3, one of the terminal pro-apoptotic proteins. In melanoma, IL-8 and VEGF are positively correlated with disease stage and a high probability of progression. We demonstrated that treatment of A375 cells with IS in combination with paclitaxel resulted in a significant decrease in the production of IL-8 and VEGF, compared with paclitaxel alone. Recent studies suggest that TLR4-MyD88-ERK signaling may be a novel target for reversing chemoresistance to paclitaxel. Our flow cytometry and Western blot data showed that paclitaxel activated TLR4-MyD88-ERK signaling and that IS treatment could effectively inhibit this paclitaxel-induced activation of TLR4-MyD88-ERK signaling. In conclusion, this study demonstrated for the first time that IS could potentiate paclitaxel-induced apoptosis in melanoma cells. These effects were mediated, at least in part, by inhibiting the activation of the TLR4 signal transduction pathways. These findings support further preclinical evaluation of IS as a new potential anti-tumor agent.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 06/2012; 50(9):3019-24. · 2.99 Impact Factor
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    ABSTRACT: Extramammary Paget's disease is a rare cutaneous malignant neoplasm. The genetic and epigenetic mechanisms underlying its pathology remain unknown. In this study, we investigated the expression levels, and mutation and methylation status of a common tumor suppressor gene, deleted in liver cancer 1 (DLC1), and an oncogene, PIK3CA, in tumor (n=132) and normal tissues (n=20) from unrelated patients. The presence of epigenetic and genetic lesions was then correlated to the patient pathology data to determine the potential role of these genes in extramammary Paget's disease etiology and progression. The DLC1 gene was found to be downregulated in 43 (33%) tumors, as compared with immunohistochemistry results from normal tissues. Methylation-sensitive, high-resolution melting analysis indicated that the DLC1 promoter was hypermethylated in 51 (39%) extramammary Paget's disease tumors. This hypermethylation was associated with significantly decreased DLC1 levels (P=0.011), and had a strong positive correlation with advanced age (P=0.002). PIK3CA mutations were detected by direct sequencing in 32 (24%) tumors, the majority of which were invasive. Furthermore, PIK3CA mutations significantly correlated with DLC1 hypermethylation. Thus, aberrant DLC1 methylation and PIK3CA mutations may have important roles in extramammary Paget's disease pathogenesis, and may represent potential molecular targets for therapy.
    Modern Pathology 04/2012; 25(8):1160-8. · 5.25 Impact Factor
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    ABSTRACT: Atopic dermatitis (AD) is a common inflammatory and chronically relapsing disorder with increasing prevalence. However, little is known about its prevalence in Shanghai, the top metropolitan of China. This study will estimate and compare the prevalence of AD in urban and rural areas in representative samples of 3 to 6-year-old children in Shanghai. A descriptive cross-sectional study was performed. Pre-school children were obtained by cluster sampling from 8 communities in different districts in Shanghai. The main instrument was the core questionnaire module for AD used in the U.K. Working Party's study. All the data were statistically analyzed by EpiData 3.1 and SPSS16.0. A total of 10,436 children completed the study satisfactorily, with a response rate of 95.8%. The prevalence of AD in 3 to 6-year-old children was 8.3% (Male: 8.5%, Female: 8.2%). The prevalence in urban areas of Shanghai was gradiently and significantly higher than that in rural areas. The highest prevalence was in the core urban area (10.2% in Xuhui Tianping) vs. the lowest far from the urban areas (4.6% in Chongming Baozhen). The prevalence of AD was 8.3% (95%CI: 7.6%-9.1%) in children aged 3 to 6 in Shanghai. The prevalence of AD decreased from the center to the rural areas in Shanghai.
    PLoS ONE 01/2012; 7(5):e36174. · 3.53 Impact Factor
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    ABSTRACT: Fractional exhaled nitric oxide (FeNO) is a non-invasive biomarker of airway inflammation. Our aim was to analyze the interrelationship and differentiate the predicting effects of asthma, allergic rhinitis (AR), and atopic dermatitis (AD) on the FeNO levels in children from mainland China. A case-control study with age- and gender matched 1:1 was designed based on a larger cross-sectional survey on asthma, AR, and AD in Shanghai. A self-administered questionnaire was used to collect information on children's health information. Children with positive reports on physician-diagnosed asthma and/or AR and/or AD were recruited as cases, and children with no report of any of the diseases were designated as controls. The FeNO measurement was performed online, using the NIOX MINO® instrument (Aerocrine AB, Solna, Sweden) at 50 ml/min. A total of 130 subjects (65 cases and 65 controls, average age = 10 years) were recruited in this study. The average FeNO level was significantly higher in the cases (29.8 ± 1.9 ppb) than that in the controls (13.3 ± 1.7 ppb) (p < .001). Using multiple linear regression analysis controlling for confounding factors, including parental asthma/allergic diseases and home exposure, asthma (β = 0.330, p < .001) and AR (β = 0.157, p = .006) showed significant predicting effects for high FeNO levels, whereas AD was not related to the FeNO levels. Both asthma and AR could independently increase the FeNO levels in Chinese schoolchildren. Other diseases besides asthma should be considered when applying FeNO as a screening tool for asthma in Chinese children.
    Journal of Asthma 12/2011; 48(10):1001-6. · 1.85 Impact Factor
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    ABSTRACT: To analyze associations between the patterns of global DNA hypomethylation and expression of DNA methyltransferase (DNMT1, DNMT3A, and DNMT3B) in patients with systemic lupus erythematosus (SLE) and to obtain a deeper understanding of the role that epigenetic mechanism may have on SLE. The global DNA methylation profile in T cells from 34 patients with SLE and 23 healthy controls was assessed by the specific monoclonal antibodies to 5-methylcytosine and was analyzed quantitatively by flow cytometry. Real-time reverse transcription-polymerase chain reaction was applied to analyze DNMTs (DNMT1, DNMT3A, and DNMT3B) mRNA levels in T cells from patients and controls. Patients with SLE had significantly global DNA hypomethylation than that in controls (P = 0.004), and the global DNA methylation was inverse correlated with the SLE Disease Activity Index (P < 0.0005). Patients with SLE had significantly lower levels of DNMT1 mRNA than that in controls (P < 0.0005), and there was no correlation between the level of DNMT1 mRNA and SLE Disease Activity Index, neither the correlation between the levels of DNMT1 mRNA and global DNA methylation. There was no statistical difference in levels of DNMT3A mRNA between the patients with SLE and normal controls. The levels of DNMT3B mRNA were very low, and there was no difference in patients with SLE and normal controls. Global DNA hypomethylation plays an important role in the pathogenesis of SLE. Lower expression of DNMT1 mRNA may play a role in the pathogenesis of SLE, which is not the exclusive regulation factor of global DNA methylation of SLE. The mechanism of global DNA hypomethylation in patients with SLE was complicated. Enzymes that participate in DNA methylation and demethylation events should be studied further.
    International journal of dermatology 06/2011; 50(6):697-704. · 1.18 Impact Factor
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    ABSTRACT: JAK2 V617F, a somatic point mutation that leads to constitutive JAK2 phosphorylation and kinase activation, has been incorporated into the WHO classification and diagnostic criteria of myeloid neoplasms. Although various approaches such as restriction fragment length polymorphism, amplification refractory mutation system and real-time PCR have been developed for its detection, a generic rapid closed-tube method, which can be utilized on routine genetic testing instruments with stability and cost-efficiency, has not been described. Asymmetric PCR for detection of JAK2 V617F with a 3'-blocked unlabeled probe, saturate dye and subsequent melting curve analysis was performed on a Rotor-Gene® Q real-time cycler to establish the methodology. We compared this method to the existing amplification refractory mutation systems and direct sequencing. Hereafter, the broad applicability of this unlabeled probe melting method was also validated on three diverse real-time systems (Roche LightCycler® 480, Applied Biosystems ABI® 7500 and Eppendorf Mastercycler® ep realplex) in two different laboratories. The unlabeled probe melting analysis could genotype JAK2 V617F mutation explicitly with a 3% mutation load detecting sensitivity. At level of 5% mutation load, the intra- and inter-assay CVs of probe-DNA heteroduplex (mutation/wild type) covered 3.14%/3.55% and 1.72%/1.29% respectively. The method could equally discriminate mutant from wild type samples on the other three real-time instruments. With a high detecting sensitivity, unlabeled probe melting curve analysis is more applicable to disclose JAK2 V617F mutation than conventional methodologies. Verified with the favorable inter- and intra-assay reproducibility, unlabeled probe melting analysis provided a generic mutation detecting alternative for real-time instruments.
    PLoS ONE 01/2011; 6(10):e26534. · 3.53 Impact Factor
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    ABSTRACT: Toxic epidermal necrolysis (TEN) and Stevens-Johnson Syndrome (SJS) are drug-induced diseases with no well-established treatments. The application of corticosteroid therapy is controversial. Intravenous immunoglobulin (IVIG) therapy is emerging as a promising new method for the treatment of these two diseases. The efficacy of combination therapy of IVIG and corticosteroid in the treatment of TEN/SJS has seldom been reported. Sixty-five consecutive patients with either TEN or SJS, admitted over a 14-year period from January 1993 to October 2007, were treated with corticosteroid and analyzed retrospectively using SCORTEN, a severity-of-illness scoring system for TEN/SJS prognosis, to evaluate efficacy. For patients admitted after January 2001, additional therapy with a dose of 0.4 g/kg/day of IVIG for 5 days was applied. In the 45 patients with TEN treated without IVIG, 8.63 patients were expected to die based on the SCORTEN system, but 10 deaths were observed. Standardized mortality ratio (SMR) analysis [(Sigmaobserved deaths/Sigmaexpected deaths) x 100] suggested that patients with TEN treated with systemic corticosteroid were 16% more likely to die than those treated with routine therapy (SMR = 1.16; 95% confidence interval, 0.56-2.13). In the further study of combination therapy, 12 patients with TEN and eight patients with SJS were admitted. There were two deaths in the TEN group and one death in the SJS group, with 3.51 deaths expected on the basis of the SCORTEN system. SMR analysis showed that combination therapy had a tendency to reduce the mortality rate of TEN (SMR = 0.85; 95% confidence interval, 0.18-2.50). Nevertheless, in both the TEN and SJS groups, the difference in mortality rate between the two therapies was not statistically significant (P = 0.651 and P = 1, respectively). In patients with TEN, combination therapy also reduced significantly the time of arrested progression (P = 0.019) and the total hospitalization time (P = 0.043), but could not reduce the time to the tapering of corticosteroid (P = 0.96). In SJS patients, the times of arrested progression and hospitalization were also reduced significantly (P = 0.019 and P = 0.0475, respectively). Likewise, the time to the tapering of corticosteroid was not reduced (P = 0.122). Combination therapy with corticosteroid and IVIG exhibited a tendency to reduce the mortality rate in comparison with the solo administration of corticosteroid. The decrease in the mortality rate, however, was not statistically significant. Combination therapy also arrested progression earlier and decreased the hospitalization time, meaning that the total dose of corticosteroid may be reduced. Combination therapy, however, did not lead to earlier tapering of corticosteroid. No severe adverse effects of IVIG were found during treatment.
    International journal of dermatology 10/2009; 48(10):1122-8. · 1.18 Impact Factor