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1.  Molecular Mechanism of the Cell Death Induced by the Histone Deacetylase Pan Inhibitor LBH589 (Panobinostat) in Wilms Tumor Cells 
PLoS ONE  2015;10(7):e0126566.
Wilms tumor (WT) is an embryonic kidney cancer, for which histone acetylation might be a therapeutic target. LBH589, a novel targeted agent, suppresses histone deacetylases in many tumors. This study investigated the antitumor activity of LBH589 in SK-NEP-1 and G401 cells.
SK-NEP-1 and G401 cell growth was assessed by CCK-8 and in nude mice experiments. Annexin V/propidium iodide staining followed by flow cytometry detected apoptosis in cell culture. Gene expressions of LBH589-treated tumor cells were analyzed using an Arraystar Human LncRNA Array. The Multi Experiment View cluster software analyzed the expression data. Differentially expressed genes from the cluster analyses were imported into the Ingenuity Pathway Analysis tool.
LBH589 inhibited cell proliferation of SK-NEP-1 and G401 cells in a dose-dependent manner. Annexin V, TUNEL and Hochest 33342 staining analysis showed that LBH589-treated cells showed more apoptotic features compared with the control. LBH589 treatment inhibited the growth of SK-NEP-1 xenograft tumors in nude mice. Arraystar Human LncRNA Array analysis of genes and lncRNAs regulated by LBH589 identified 6653 mRNAs and 8135 lncRNAs in LBH589-treated SK-NEP-1 cells. The most enriched gene ontology terms were those involved in nucleosome assembly. KEGG pathway analysis identified cell cycle proteins, including CCNA2, CCNB2, CCND1, CCND2, CDK4, CDKN1B and HDAC2, etc. Ingenuity Pathway Analysis identified important upstream molecules: HIST2H3C, HIST1H4A, HIST1A, HIST1C, HIST1D, histone H1, histone H3, RPRM, HSP70 and MYC.
LBH589 treatment caused apoptosis and inhibition of cell proliferation of SK-NEP-1and G401 cells. LBH589 had a significant effect and few side effects on SK-NEP-1 xenograft tumors. Expression profiling, and GO, KEGG and IPA analyses identified new targets and a new “network” of genes responding to LBH589 treatment in SK-NEP-1 cells. RPRM, HSP70 and MYC may be important regulators during LBH589 treatment. Our results provide new clues to the proapoptotic mechanism of LBH589.
PMCID: PMC4503685  PMID: 26176219
2.  Early B-cell factor 3 (EBF3) is a novel tumor suppressor gene with promoter hypermethylation in pediatric acute myeloid leukemia 
Pediatric acute myeloid leukemia (AML) comprises up to 20% of all childhood leukemia. Recent research shows that aberrant DNA methylation patterning may play a role in leukemogenesis. The epigenetic silencing of the EBF3 locus is very frequent in glioblastoma. However, the expression profiles and molecular function of EBF3 in pediatric AML is still unclear.
Twelve human acute leukemia cell lines, 105 pediatric AML samples and 30 normal bone marrow/idiopathic thrombocytopenic purpura (NBM/ITP) control samples were analyzed. Transcriptional level of EBF3 was evaluated by semi-quantitative and real-time PCR. EBF3 methylation status was determined by methylation specific PCR (MSP) and bisulfite genomic sequencing (BGS). The molecular mechanism of EBF3 was investigated by apoptosis assays and PCR array analysis.
EBF3 promoter was hypermethylated in 10/12 leukemia cell lines. Aberrant EBF3 methylation was observed in 42.9% (45/105) of the pediatric AML samples using MSP analysis, and the BGS results confirmed promoter methylation. EBF3 expression was decreased in the AML samples compared with control. Methylated samples revealed similar survival outcomes by Kaplan-Meier survival analysis. EBF3 overexpression significantly inhibited cell proliferation and increased apoptosis. Real-time PCR array analysis revealed 93 dysregulated genes possibly implicated in the apoptosis of EBF3-induced AML cells.
In this study, we firstly identified epigenetic inactivation of EBF3 in both AML cell lines and pediatric AML samples for the first time. Our findings also showed for the first time that transcriptional overexpression of EBF3 could inhibit proliferation and induce apoptosis in AML cells. We identified 93 dysregulated apoptosis-related genes in EBF3-overexpressing, including DCC, AIFM2 and DAPK1. Most of these genes have never been related with EBF3 over expression. These results may provide new insights into the molecular mechanism of EBF3-induced apoptosis; however, further research will be required to determine the underlying details.
Our findings suggest that EBF3 may act as a putative tumor suppressor gene in pediatric AML.
PMCID: PMC4311429  PMID: 25609158
Early B-cell factor 3; Pediatric acute myeloid leukemia; Methylation; Tumor suppressor; Real-time PCR array
3.  Molecular Targeting of the Oncoprotein PLK1 in Pediatric Acute Myeloid Leukemia: RO3280, a Novel PLK1 Inhibitor, Induces Apoptosis in Leukemia Cells 
Polo-like kinase 1 (PLK1) is highly expressed in many cancers and therefore a biomarker of transformation and potential target for the development of cancer-specific small molecule drugs. RO3280 was recently identified as a novel PLK1 inhibitor; however its therapeutic effects in leukemia treatment are still unknown. We found that the PLK1 protein was highly expressed in leukemia cell lines as well as 73.3% (11/15) of pediatric acute myeloid leukemia (AML) samples. PLK1 mRNA expression was significantly higher in AML samples compared with control samples (82.95 ± 110.28 vs. 6.36 ± 6.35; p < 0.001). Kaplan-Meier survival analysis revealed that shorter survival time correlated with high tumor PLK1 expression (p = 0.002). The 50% inhibitory concentration (IC50) of RO3280 for acute leukemia cells was between 74 and 797 nM. The IC50 of RO3280 in primary acute lymphocytic leukemia (ALL) and AML cells was between 35.49 and 110.76 nM and 52.80 and 147.50 nM, respectively. RO3280 induced apoptosis and cell cycle disorder in leukemia cells. RO3280 treatment regulated several apoptosis-associated genes. The regulation of DCC, CDKN1A, BTK, and SOCS2 was verified by western blot. These results provide insights into the potential use of RO3280 for AML therapy; however, the underlying mechanisms remain to be determined.
PMCID: PMC4307303  PMID: 25574601
RO3280; pediatric acute myeloid leukemia (AML); polo-like kinase 1 (PLK1); apoptosis; oncogene target
4.  Relationship between fine particulate matter, weather condition and daily non-accidental mortality in Shanghai, China: A Bayesian approach 
PLoS ONE  2017;12(11):e0187933.
There are concerns that the reported association of ambient fine particulate matter (PM2.5) with mortality might be a mixture of PM2.5 and weather conditions. We evaluated the effects of extreme weather conditions and weather types on mortality as well as their interactions with PM2.5 concentrations in a time series study. Daily non-accidental deaths, individual demographic information, daily average PM2.5 concentrations and meteorological data between 2012 and 2014 were obtained from Shanghai, China. Days with extreme weather conditions were identified. Six synoptic weather types (SWTs) were generated. The generalized additive model was set up to link the mortality with PM2.5 and weather conditions. Parameter estimation was based on Bayesian methods using both the Jeffreys’ prior and an informative normal prior in a sensitivity analysis. We estimate the percent increase in non-accidental mortality per 10 μg/m3 increase in PM2.5 concentration and constructed corresponding 95% credible interval (CrI). In total, 336,379 non-accidental deaths occurred during the study period. Average daily deaths were 307. The results indicated that per 10 μg/m3 increase in daily average PM2.5 concentration alone corresponded to 0.26–0.35% increase in daily non-accidental mortality in Shanghai. Statistically significant positive associations between PM2.5 and mortality were found for favorable SWTs when considering the interaction between PM2.5 and SWTs. The greatest effect was found in hot dry SWT (percent increase = 1.28, 95% CrI: 0.72, 1.83), followed by warm humid SWT (percent increase = 0.64, 95% CrI: 0.15, 1.13). The effect of PM2.5 on non-accidental mortality differed under specific extreme weather conditions and SWTs. Environmental policies and actions should take into account the interrelationship between the two hazardous exposures.
PMCID: PMC5679525  PMID: 29121092
5.  Interaction between RNA helicase ROOT INITIATION DEFECTIVE 1 and GAMETOPHYTIC FACTOR 1 is involved in female gametophyte development in Arabidopsis 
Journal of Experimental Botany  2016;67(19):5757-5768.
RID1 interacts with GFA1 to direct and regulate the splicing and expression of the genes required for female gametophyte development in Arabidopsis.
ROOT INITIATION DEFECTIVE 1 (RID1) is an Arabidopsis DEAH/RHA RNA helicase. It functions in hypocotyl de-differentiation, de novo meristem formation, and cell specification of the mature female gametophyte (FG). However, it is unclear how RID1 regulates FG development. In this study, we observed that mutations to RID1 disrupted the developmental synchrony and retarded the progression of FG development. RID1 exhibited RNA helicase activity, with a preference for unwinding double-stranded RNA in the 3′ to 5′ direction. Furthermore, we found that RID1 interacts with GAMETOPHYTIC FACTOR 1 (GFA1), which is an integral protein of the spliceosome component U5 small nuclear ribonucleoprotein (snRNP) particle. Substitution of specific RID1 amino acids (Y266F and T267I) inhibited the interaction with GFA1. In addition, the mutated RID1 could not complement the seed-abortion phenotype of the rid1 mutant. The rid1 and gfa1 mutants exhibited similar abnormalities in pre-mRNA splicing and down-regulated expression of some genes involved in FG development. Our results suggest that an interaction between RID1 and the U5 snRNP complex regulates essential pre-mRNA splicing of the genes required for FG development. This study provides new information regarding the mechanism underlying the FG developmental process.
PMCID: PMC5066494  PMID: 27683728
Arabidopsis; development; female gametophyte; GFA1; RID1; RNA splicing; U5 snRNP.
6.  Strong Manual Acupuncture Stimulation of “Huantiao” (GB 30) Reduces Pain-Induced Anxiety and p-ERK in the Anterior Cingulate Cortex in a Rat Model of Neuropathic Pain 
Persistent neuropathic pain is associated with anxiety. The phosphorylation of extracellular signal-regulated kinase (p-ERK) in the anterior cingulate cortex (ACC) plays an important role in pain-induced anxiety. Acupuncture is widely used for pain and anxiety. However, little is known about which acupuncture technique is optimal on pain-induced anxiety and the relationship between acupuncture effect and p-ERK. The rat model was induced by L5 spinal nerve ligation (SNL). Male adult SD rats were randomly divided into control, SNL, strong manual acupuncture (sMA), mild manual acupuncture (mMA), and electroacupuncture (EA) group. Bilateral “Huantiao” (GB 30) were stimulated by sMA, mMA, and EA, respectively. The pain withdrawal thresholds (PWTs) and anxiety behavior were measured, and p-ERK protein expression and immunoreactivity cells in ACC were detected. PWTs increased significantly in both sMA and EA groups. Meanwhile, anxiety-like behavior was improved significantly in the sMA and mMA groups. Furthermore, the overexpression of p-ERK induced by SNL was downregulated by strong and mild manual acupuncture. Therefore, strong manual acupuncture on bilateral “Huantiao” (GB 30) could be a proper therapy relieving both pain and pain-induced anxiety. The effect of different acupuncture techniques on pain-induced anxiety may arise from the regulation of p-ERK in ACC.
PMCID: PMC4681793  PMID: 26770252
7.  Hypermethylation of the GATA binding protein 4 (GATA4) promoter in Chinese pediatric acute myeloid leukemia 
BMC Cancer  2015;15:756.
Acute myeloid leukemia (AML) is the second-most common form of leukemia in children. Aberrant DNA methylation patterns are a characteristic feature of AML. GATA4 has been suggested to be a tumor suppressor gene regulated by promoter hypermethylation in various types of human cancers although the expression and promoter methylation of GATA4 in pediatric AML is still unclear.
Transcriptional expression levels of GATA4 were evaluated by semi-quantitative and real-time PCR. Methylation status was investigated by methylation-specific PCR (MSP) and bisulfate genomic sequencing (BGS). The prognostic significance of GATA4 expression and promoter methylation was assessed in 105 cases of Chinese pediatric acute myeloid leukemia patients with clinical follow-up records.
MSP and BGS analysis showed that the GATA4 gene promoter is hypermethylated in AML cells, such as the HL-60 and MV4-11 human myeloid leukemia cell lines. 5-Aza treatment significantly upregulated GATA4 expression in HL-60 and MV4-11 cells. Aberrant methylation of GATA4 was observed in 15.0 % (3/20) of the normal bone marrow control samples compared to 56.2 % (59/105) of the pediatric AML samples. GATA4 transcript levels were significantly decreased in AML patients (33.06 ± 70.94; P = 0.011) compared to normal bone marrow/idiopathic thrombocytopenic purpura controls (116.76 ± 105.39). GATA4 promoter methylation was correlated with patient leukocyte counts (WBC, white blood cells) (P = 0.035) and minimal residual disease MRD (P = 0.031). Kaplan-Meier survival analysis revealed significantly shorter overall survival time in patients with GATA4 promoter methylation (P = 0.014).
Epigenetic inactivation of GATA4 by promoter hypermethylation was observed in both AML cell lines and pediatric AML samples; our study implicates GATA4 as a putative tumor suppressor gene in pediatric AML. In addition, our findings imply that GATA4 promoter methylation is correlated with WBC and MRD. Kaplan-Meier survival analysis revealed significantly shorter overall survival in pediatric AML with GATA4 promoter methylation but multivariate analysis shows that it is not an independent factor. However, further research focusing on the mechanism of GATA4 in pediatric leukemia is required.
Electronic supplementary material
The online version of this article (doi:10.1186/s12885-015-1760-5) contains supplementary material, which is available to authorized users.
PMCID: PMC4618362  PMID: 26490736
GATA binding protein 4; Pediatric acute myeloid leukemia; Methylation; Tumor suppressor
8.  Analyzing the gene expression profile of anaplastic histology Wilms’ tumor with real-time polymerase chain reaction arrays 
Wilms’ tumor (WT) is one of the most common malignant neoplasms of the urinary tract in children. Anaplastic histology (unfavorable histology) accounts for about 10% of whole WTs, and it is the single most important histologic predictor of treatment response and survival in patients with WT; however, until now the molecular basis of this phenotype is not very clearly.
A real-time polymerase chain reaction (PCR) array was designed and tested. Next, the gene expression profile of pediatric anaplastic histology WT and normal adjacent tissues were analyzed. These expression data were anlyzed with Multi Experiment View (MEV) cluster software further. Datasets representing genes with altered expression profiles derived from cluster analyses were imported into the Ingenuity Pathway Analysis Tool (IPA).
88 real-time PCR primer pairs for quantitative gene expression analysis of key genes involved in pediatric anaplastic histology WT were designed and tested. The gene expression profile of pediatric anaplastic histology WT is significantly different from adjacent normal controls; we identified 15 genes that are up-regulated and 16 genes that are down-regulated in the former. To investigate biological interactions of these differently regulated genes, datasets representing genes with altered expression profiles were imported into the IPA for further analysis, which revealed three significant networks: Cancer, Hematological Disease, and Gene Expression, which included 27 focus molecules and a significance score of 43. The IPA analysis also grouped the differentially expressed genes into biological mechanisms related to Cell Death and Survival 1.15E−12, Cellular Development 2.84E−11, Cellular Growth and Proliferation 2.84E-11, Gene Expression 4.43E−10, and DNA Replication, Recombination, and Repair 1.39E−07. The important upstream regulators of pediatric anaplastic histology WT were TP53 and TGFβ1 signaling (P = 1.15E−14 and 3.79E−13, respectively).
Our study demonstrates that the gene expression profile of pediatric anaplastic histology WT is significantly different from adjacent normal tissues with real-time PCR array. We identified some genes that are dysregulated in pediatric anaplastic histology WT for the first time, such as HDAC7, and IPA analysis showed the most important pathways for pediatric anaplastic histology WT are TP53 and TGFβ1 signaling. This work may provide new clues into the molecular mechanisms behind pediatric anaplastic histology WT.
Electronic supplementary material
The online version of this article (doi:10.1186/s12935-015-0197-x) contains supplementary material, which is available to authorized users.
PMCID: PMC4486424  PMID: 26136641
Pediatric anaplastic histology Wilms’ tumor; Real-time PCR array; Ingenuity pathway analysis; HDAC7; TP53; TGFβ1
9.  Zinc finger protein 382 is downregulated by promoter hypermethylation in pediatric acute myeloid leukemia patients 
Acute myeloid leukemia (AML) is the second-most common form of leukemia in children. Aberrant DNA methylation patterns are characteristic of AML. Zinc finger protein 382 (ZNF382) has been suggested to be a tumor suppressor gene possibly regulated by promoter hypermethylation in various types of human cancer. However, ZNF382 expression and methylation status in pediatric AML is unknown. In the present study, ZNF382 transcription levels were evaluated by quantitative reverse-transcription PCR. Methylation status was investigated by methylation-specific (MSP) PCR and bisulfate genomic sequencing (BGS). The prognostic significance of ZNF382 expression and promoter methylation was assessed in 105 cases of pediatric AML. The array data suggested that the ZNF382 promoter was hypermethylated in the AML cases examined. MSP PCR and BGS analysis revealed that ZNF382 was hypermethylated in leukemia cell lines. Furthermore, treatment with 5-aza-2′-deoxycytidine (5-Aza) upregulated ZNF382 expression in the selected leukemia cell lines. The aberrant methylation of ZNF382 was observed in 10% (2/20) of the control samples compared with 26.7% (28/105) of the AML samples. ZNF382 expression was significantly decreased in the 105 AML patients compared with the controls. Patients with ZNF382 methylation showed lower ZNF382 transcript levels compared with patients exhibiting no methylation. There were no significant differences in clinical characteristics or cytogenetic analysis between the patients with or without ZNF382 methylation. ZNF382 methylation correlated with minimal residual disease (MRD). Kaplan-Meier survival analysis revealed similar survival times in the samples with ZNF382 methylation, and multivariate analysis revealed that ZNF382 methylation was not an independent prognostic factor in pediatric AML. The epigenetic inactivation of ZNF382 by promoter hypermethylation can be observed in AML cell lines and pediatric AML samples. Therefore, our study suggests that ZNF382 may be considered a putative tumor suppressor gene in pediatric AML. However, further studies focusing on the mechanisms responsible for ZNF382 downregulation in pediatric leukemia are required.
PMCID: PMC4214337  PMID: 25319049
zinc finger protein 382; pediatric acute myeloid leukemia; methylation; tumor suppressor
10.  Metallothionein III (MT3) is a putative tumor suppressor gene that is frequently inactivated in pediatric acute myeloid leukemia by promoter hypermethylation 
Acute myeloid leukemia (AML) is the second most common form of leukemia in children. Aberrant DNA methylation patterns are a characteristic feature in various tumors, including AML. Metallothionein III (MT3) is a tumor suppresser reported to show promoter hypermethylated in various cancers. However, the expression and molecular function of MT3 in pediatric AML is unclear.
Eleven human leukemia cell lines and 41 pediatric AML samples and 20 NBM/ITP (Norma bone marrow/Idiopathic thrombocytopenic purpura) control samples were analyzed. Transcription levels of MT3 were evaluated by semi-quantitative and real-time PCR. MT3 methylation status was determined by methylation specific PCR (MSP) and bisulfite genomic sequencing (BSG). The molecular mechanism of MT3 was investigated by apoptosis assays and PCR array analysis.
The MT3 promoter was hypermethylated in leukemia cell lines. More CpG’s methylated of MT3 was observed 39.0% pediatric AML samples compared to 10.0% NBM controls. Transcription of MT3 was also significantly decreased in AML samples compared to NBM/ITP controls (P < 0.001); patients with methylated MT3 exhibited lower levels of MT3 expression compared to those with unmethylated MT3 (P = 0.049). After transfection with MT3 lentivirus, proliferation was significantly inhibited in AML cells in a dose-dependent manner (P < 0.05). Annexin V assay showed that apoptosis was significantly upregulated MT3-overexpressing AML cells compared to controls. Real-time PCR array analysis revealed 34 dysregulated genes that may be implicated in MT3 overexpression and apoptosis in AML, including FOXO1.
MT3 may be a putative tumor suppressor gene in pediatric AML. Epigenetic inactivation of MT3 via promoter hypermethylation was observed in both AML cell lines and pediatric AML samples. Overexpression of MT3 may inhibit proliferation and induce apoptosis in AML cells. FOXO1 was dysregulated in MT3-overexpressing cells, offering an insight into the mechanism of MT3-induced apoptosis. However, further research is required to determine the underlying molecular details.
PMCID: PMC4082423  PMID: 24962166
Metallothionein III; Pediatric acute myeloid leukemia; Methylation; Tumor suppressor
11.  Genome-wide association study in Han Chinese identifies four new susceptibility loci for coronary artery disease 
Nature genetics  2012;44(8):890-894.
We performed a meta-analysis of 2 genome-wide association studies of coronary artery disease comprising 1,515 cases with coronary artery disease and 5,019 controls, followed by de novo replication studies in 15,460 cases and 11,472 controls, all of Chinese Han descent. We successfully identified four new loci for coronary artery disease reaching genome-wide significance (P < 5 × 10−8), which mapped in or near TTC32-WDR35, GUCY1A3, C6orf10-BTNL2 and ATP2B1. We also replicated four loci previously identified in European populations (PHACTR1, TCF21, CDKN2A/B and C12orf51). These findings provide new insights into biological pathways for the susceptibility of coronary artery disease in Chinese Han population.
PMCID: PMC3927410  PMID: 22751097
12.  The diploid genome sequence of an Asian individual 
Nature  2008;456(7218):60-65.
Here we present the first diploid genome sequence of an Asian individual. The genome was sequenced to 36-fold average coverage using massively parallel sequencing technology. We aligned the short reads onto the NCBI human reference genome to 99.97% coverage, and guided by the reference genome, we used uniquely mapped reads to assemble a high-quality consensus sequence for 92% of the Asian individual's genome. We identified approximately 3 million single-nucleotide polymorphisms (SNPs) inside this region, of which 13.6% were not in the dbSNP database. Genotyping analysis showed that SNP identification had high accuracy and consistency, indicating the high sequence quality of this assembly. We also carried out heterozygote phasing and haplotype prediction against HapMap CHB and JPT haplotypes (Chinese and Japanese, respectively), sequence comparison with the two available individual genomes (J. D. Watson and J. C. Venter), and structural variation identification. These variations were considered for their potential biological impact. Our sequence data and analyses demonstrate the potential usefulness of next-generation sequencing technologies for personal genomics.
PMCID: PMC2716080  PMID: 18987735
13.  Clinical symptoms and related risk factors in pulmonary embolism patients and cluster analysis based on these symptoms 
Scientific Reports  2017;7:14887.
Pulmonary embolism (PE) remains largely underdiagnosed due to nonspecific symptoms. This study aims to evaluate typical symptoms of PE patients, their related predictors, and to differentiate typical clusters of patients and principal components of PE symptoms. Clinical data from a total of 551 PE patients between January 2012 and April 2016 were retrospectively reviewed. PE was diagnosed according to the European Society of Cardiology Guidelines. Logistic regression models, system clustering method, and principal component analysis were used to identify potential risk factors, different clusters of the patients, and principal components of PE symptoms. The most common symptoms of PE were dyspnea, cough, and tachypnea in more than 60% of patients. Some combined chronic conditions, laboratory and clinical indicators were found to be related to these clinical symptoms. Our study also suggested that PE is associated with a broad list of symptoms and some PE patients might share similar symptoms, and some PE symptoms were usually cooccurrence. Based on ten symptoms generated from our sample, we classified the patients into five clusters which represent five groups of PE patients during clinical practice, and identified four principal components of PE symptoms. These findings will improve our understanding of clinical symptoms and their potential combinations which are helpful for clinical diagnosis of PE.
PMCID: PMC5668424  PMID: 29097743
14.  Dual roles of parathyroid hormone related protein in TGF-β1 signaling and fibronectin up-regulation in mesangial cells 
Bioscience Reports  2017;37(5):BSR20171061.
Little is known about the cross-talk between parathyroid hormone (PTH) related protein (PTHrP) and TGF-β1 in mesangial cells (MCs). Our results showed that PTHrP treatment (≤3 h) induced internalization of PTH1R (PTH/PTHrP receptor)–TβRII (TGF-β type 2 receptor) complex and suppressed TGF-β1-mediated Smad2/3 activation and fibronectin (FN) up-regulation. However, prolonged PTHrP treatment (12–48 h) failed to induce PTH1R–TβRII association and internalization. Total protein levels of PTH1R and TβRII were unaffected by PTHrP treatment. These results suggest that internalization of PTH1R and TβRII after short PTHrP treatment might not lead to their proteolytic destruction, allowing the receptors to be recycled back to the plasma membrane during prolonged PTHrP exposure. Receptor re-expression at the cell surface allows PTHrP to switch from its initial inhibitory effect to promote induction of FN. Our study thus demonstrates the dual roles of PTHrP on TGF-β1 signaling and FN up-regulation for the first time in glomerular MCs. These data also provided new insights to guide development of therapy for diabetic kidney disease (DKD).
PMCID: PMC5665616  PMID: 28954822
diabetic kidney disease; extracellular matrix; parathyroid hormone-related protein; TGF-β1
15.  Comparison of twelve single-drug regimens for the treatment of type 2 diabetes mellitus 
Oncotarget  2017;8(42):72700-72713.
We performed a network meta-analysis to compare the efficacy of 12 single-drug regimens (Glibenclamide, Glimepiride, Pioglitazone, Rosiglitazone, Repaglinide, Metformin, Sitaglitin, Exenatide, Liraglutide, Acarbose, Benfluorex, and Glipizide) in the treatment of type 2 diabetes mellitus (T2DM). Fifteen relevant randomized controlled trials (RCTs) were included; direct and indirect evidence from these studies was combined, and weighted mean difference (WMD) and surface under the cumulative ranking curves (SUCRAs) were examined to evaluate the monotherapies. Liraglutide was more effective than Glimepiride, Pioglitazone, Sitaglitin, Exenatide, and Glipizide at reducing glycated hemoglobin (HbA1c) levels. In contrast, Acarbose was less effective than Glibenclamide, Glimepiride, Pioglitazone, Rosiglitazone, Repaglinide, Metformin, and Liraglutide at decreasing HbA1c levels. Reductions in fasting plasma glucose (FPG) levels were similar after all treatments. Rosiglitazone was less effective than Glibenclamide and Repaglinide at reducing total cholesterol (TC) levels. High density lipoprotein (HDL), low density lipoprotein (LDL), and triglyceride levels did not differ after treatment with any of the monotherapies. HbA1c and FPG SUCRA values were highest for Liraglutide, while HbA1c and FPG values were lowest for Acarbose, and TC and LDL values were lowest for Rosiglitazone. These results suggest that Liraglutide may be most effective, and Acarbose least effective, at reducing blood glucose levels, while Glibenclamide, Repaglinide, and Metformin may be most effective, and Rosiglitazone least effective, at reducing lipoidemia, in T2DM patients.
PMCID: PMC5641162
type 2 diabetes mellitus; single-drug regimen; effects; randomized controlled trials; network meta-analysis
16.  PIM-1 kinase inhibitor SMI-4a exerts antitumor effects in chronic myeloid leukemia cells by enhancing the activity of glycogen synthase kinase 3β 
Molecular Medicine Reports  2017;16(4):4603-4612.
The development of targeted tyrosine kinase inhibitors (TKIs) has succeeded in altering the course of chronic myeloid leukemia (CML). However, a number of patients have failed to respond or experienced disease relapse following TKI treatment. Proviral integration site for moloney murine leukemia virus-1 (PIM-1) is a serine/threonine kinase that participates in regulating apoptosis, cell cycle, signal transduction and transcriptional pathways, which are associated with tumor progression, and poor prognosis. SMI-4a is a selective PIM-1 kinase inhibitor that inhibits PIM-1 kinase activity in vivo and in vitro. The present study aimed to explore the mechanism underlying the antitumor effect of SMI-4a in K562 and imatinib-resistant K562 (K562/G) cell lines. It was demonstrated that SMI-4a inhibited the proliferation of K562 and K562/G cells using a WST-8 assay. The Annexin V-propidium iodide assay demonstrated that SMI-4a induced apoptosis of K562 and K562/G cells in a dose-, and time-dependent manner. Furthermore, Hoechst 33342 staining was used to verify the apoptosis rate. The clone formation assay revealed that SMI-4a significantly inhibited the colony formation capacity of K562 and K562/G cells. Western blot analysis demonstrated that SMI-4a decreased phosphorylated (p)-Ser9-glycogen synthase kinase (GSK) 3β/pGSK3β and inhibited the translocation of β-catenin. In addition, the downstream gene expression of apoptosis regulator Bax and poly(ADP-ribose) polymerase-1 was upregulated, and apoptosis regulator Bcl-2 and Myc proto-oncogene protein expression levels were downregulated. Immunofluorescence results demonstrated changes in the expression level of β-catenin in the plasma and nucleus. The results of the present study suggest that SMI-4a is an effective drug to use in combination with current chemotherapeutics for the treatment of imatinib-resistant CML.
PMCID: PMC5647015  PMID: 28849186
SMI-4a; chronic myeloid leukemia; cell apoptosis; cell cycle; GSK 3β
17.  Wider geographic distribution and higher diversity of hexaploids than tetraploids in Carassius species complex reveal recurrent polyploidy effects on adaptive evolution 
Scientific Reports  2017;7:5395.
Polyploidy roles on adaptive evolution and ecological novelty have been extensively studied in plants but remained unclear in vertebrates owing to the rare polyploidy incidences. Here, a huge number of 3105 specimens in Carassius species complex including 2211 hexaploids and 894 tetraploids were sampled from 34 locations through mainland China. And hexaploids had wider geographic distribution than tetraploids especially in the areas with high altitude, high latitude and low annual precipitation. Then, an approximate 1050 bp transferrin (tf) fragments were amplified from all the samples, and 526 tf alleles were identified from a total of 37260 sequences at last. Intriguingly, higher nucleotide diversity of tf alleles in hexaploids than in tetraploids was revealed. Moreover, via phylogenetic analysis of tf alleles, potential origin center of Carassius species complex was deduced to be Yangtze River basin and hexaploids should undergo multiple independent polyploidy origins from sympatric tetraploids. These findings indicate that the hexaploids might possess stronger environmental adaptation and ecological novelty than the tetraploids, which provide an association paradigm of recurrent polyploidy and ecological context in polyploid vertebrates.
PMCID: PMC5511294  PMID: 28710383
18.  Efficient Characterization and Classification of Contrast Sensitivity Functions in Aging 
Scientific Reports  2017;7:5045.
The contrast sensitivity function (CSF), delineating contrast sensitivity over a wide range of spatial frequencies, provides a comprehensive characterization of spatial vision and a sensitive test for many physiological and pathological processes. A precise CSF measurement tool for the aging population is of great theoretical and practical importance. In the current study, we tested whether the assumptions of the newly developed quick CSF method were valid and whether it can rapidly, reliably, and effectively evaluate CSFs in the aging population. The quick CSF method combines Bayesian adaptive inference with an information gain strategy to directly estimate four parameters that define the observer’s CSF. Eighteen young and twenty-five old observers participated in the evaluation of the quick CSF method. All observers were screened for ophthalmological and mental diseases. Our results showed that the CSFs derived from the quick CSF method well matched with those from the traditional Ψ method, with excellent test-retest reliability. More importantly, the quick CSF method can accurately detect the difference of CSFs between the young and old groups. Aging significantly degrades contrast sensitivity. The quick CSF method demonstrates great potentials for both laboratory research and clinical applications in the aging population.
PMCID: PMC5505956  PMID: 28698553
19.  Burden on caregivers of ventilator-dependent patients 
Medicine  2017;96(27):e7396.
Caring for prolonged mechanical ventilation (PMV) patients imposes heavy psychological, physical, social, and financial burdens on caregivers. Currently, studies regarding the burden on caregivers of PMV patients are scant; therefore, the present study investigated the burden on caregivers of PMV patients.
This cross-sectional study was approved by the Institutional Review Board of Zuoying Armed Forces General Hospital. A survey was conducted among the caregivers of PMV patients who were admitted to a chronic respiratory care ward (RCW) or were receiving home care from June to December 2010. The survey included basic demographic information of PMV patients and their caregivers and the Burden Assessment Scale scores for 4 domains comprising a total of 21 questions (physical burden, n = 5; psychological burden, n = 6; social burden, n = 6; financial burden, n = 4). Statistical analyses were conducted using the t test, 1-way analysis of variance with the Scheffé post hoc test, and the chi-square test, and P < .05 was considered statistically significant.
A total of 160 caregivers (age, 50–53 years) were recruited (n = 80 each in the home care and RCW groups), and most of these caregivers were married women. Due to insufficient sleep, physical exhaustion, back pain, and caregiving, home caregivers had significantly higher physical burden levels than RCW caregivers (P < .01).
Home caregivers experienced higher physical burden levels than RCW caregivers. Therefore, clinical and professional support must be provided to home caregivers of PMV patients.
PMCID: PMC5502166  PMID: 28682893
burden; Burden Assessment Scale; caregivers; home care; prolonged mechanical ventilation; respiratory care ward
20.  The efficacy and toxicity of afatinib in advanced EGFR-positive non-small-cell lung cancer patients after failure of first-generation tyrosine kinase inhibitors: a systematic review and meta-analysis 
Journal of Thoracic Disease  2017;9(7):1980-1987.
The first generation epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs), gefitinib and erlotinib, have become the standard first-line treatment for non-small-cell lung cancer (NSCLC) patients with EGFR mutation. However, there was no pooled analysis focused on the usage of the second-generation TKI, afatinib, in advanced EGFR-positive NSCLC patients after failure of first generation TKIs. Therefore, a meta-analysis was conducted to solve the above question.
Electronic databases were searched for eligible literatures. ORR (objective response rate), DCR (disease controlled rate), PFS (progression-free survival), OS (overall survival) and primary grade 3/4 adverse events were pooled with the corresponding 95% confidence interval using R software. Sensitivity analyses and heterogeneity were quantitatively evaluated.
A total of 545 EGFR-positive patients were available for analysis from five studies after detailed screening from 909 relevant studies. The pooled ORR and DCR of afatinib in EGFR-positive patients after failure of the first generation EGFR-TKIs were 0.12 (0.08–0.19) and 0.60 (0.53–0.68), respectively. Besides, the 6 m-PFS rate, 1 y-PFS rate and 6 m-OS rate were 0.26 (0.22–0.30), 0.08 (0.06–0.10) and 0.74 (0.56–0.86). The grade 3/4 rate of diarrhea and that of skin deformity were 0.23 (0.10–0.46) and 0.14 (0.05–0.33), respectively. Sensitivity analyses revealed similar results with lower heterogeneity.
Considering the efficacy, toxicity and current availability, afatinib could be a therapeutic option for advanced EGFR mutated NSCLC patients after the failure of 1st-generation TKIs.
PMCID: PMC5542997
Afatinib; epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs); non-small-cell lung cancer (NSCLC); efficacy; toxicity; meta-analysis
21.  The Effect of Comprehensive Care on the Patients Received Minimally Invasive Percutaneous Nephrolithotomy 
Iranian Journal of Public Health  2017;46(7):923-929.
We analyzed the effect of comprehensive care on the patients who received minimally invasive percutaneous nephrolithotomy (MPCNL).
Patients hospitalized from 2013–2014 in Zhumadian Central Hospital (n=124) were enrolled and divided into two groups on random basis. The control group was treated with routine nursing model while the observation group was given comprehensive care additionally. The surgery time, degree of comfort, complications and successful cases, hospitalization time, sleep quality, nursing satisfaction and changes of systolic pressure, pulse and respiratory at different time were observed and analyzed.
The surgery time of the control group was significantly longer than that of observation group (P<0.05). The observation group felt more comfortable and showed more significant successful cases than the control group. Moreover, the hospitalization time were significantly reduced in observation group when compared with control group (P<0.05). The sleep quality of the observation group was significantly better than that of the control group (P<0.05). Before anesthesia, diastolic blood pressure, systolic blood pressure, pulse and respiration were not significantly different between the two groups. The diastolic blood pressure, systolic blood pressure, pulse and respiration after anesthesia, intraoperative 30 min, postoperative 30 min and other moments were significantly different. The incidence of complications in the control group was significantly higher than that in the observation group. The nursing satisfaction of the observation group was significantly higher than that of the control group.
The comprehensive care on the patients undergoing MPCNL was effective, and it can dramatically shorten surgery time, improve the success rate, improve the sleep quality of patients, keep life sign stable and minimize the complications.
PMCID: PMC5563874
Minimally invasive percutaneous nephrolithotomy; MPCNL; Renal lithiasis
22.  World Congress Integrative Medicine & Health 2017: part two 
Ee, Carolyn | Thuraisingam, Sharmala | Pirotta, Marie | French, Simon | Xue, Charlie | Teede, Helena | Kristoffersen, Agnete E. | Sirois, Fuschia | Stub, Trine | Engler, Jennifer | Joos, Stefanie | Güthlin, Corina | Felenda, Jennifer | Beckmann, Christiane | Stintzing, Florian | Evans, Roni | Bronfort, Gert | Keefe, Daniel | Taberko, Anna | Hanson, Linda | Haley, Alex | Ma, Haiwei | Jolton, Joseph | Yarosh, Lana | Keefe, Francis | Nam, Jung | Evans, Roni | Ojala, Liwanag | Kreitzer, Mary J. | Hanson, Linda | Fink, Careen | Kraft, Karin | Flower, Andrew | Lewith, George | Harman, Kim | Stuart, Beth | Bishop, Felicity L. | Frawley, Jane | Füleki, Lilla | Kiss, Eva | Vancsik, Tamas | Krenacs, Tibor | Funabashi, Martha | Pohlman, Katherine A. | Mior, Silvano | Thiel, Haymo | Hill, Michael D. | Cassidy, David J. | Westaway, Michael | Yager, Jerome | Hurwitz, Eric | Kawchuk, Gregory N. | O’Beirne, Maeve | Vohra, Sunita | Gaboury, Isabelle | Morin, Chantal | Gaertner, Katharina | Torchetti, Loredana | Frei-Erb, Martin | Kundi, Michael | Frass, Michael | Gallo, Eugenia | Maggini, Valentina | Comite, Mattia | Sofi, Francesco | Baccetti, Sonia | Vannacci, Alfredo | Di Stefano, Mariella | Monechi, Maria V. | Gori, Luigi | Rossi, Elio | Firenzuoli, Fabio | Mediati, Rocco D. | Ballerini, Giovanna | Gardiner, Paula | Lestoquoy, Anna S. | Negash, Lily | Stillman, Sarah | Shah, Prachi | Liebschutz, Jane | Adelstein, Pamela | Farrell-Riley, Christine | Brackup, Ivy | Penti, Brian | Saper, Robert | Sampedro, Isabel Giralt | Carvajal, Gilda | Gleiss, Andreas | Gross, Marie M. | Brendlin, Dorothea | Röttger, Jonas | Stritter, Wiebke | Seifert, Georg | Grzanna, Noelle | Stange, Rainer | Guendling, Peter W. | Gu, Wen | Lu, Yan | Wang, Jie | Zhang, Chengcheng | Bai, Hua | He, Yuxi | Zhang, Xiaoxu | Zhang, Zhengju | Wang, Dali | Meng, Fengxian | Hagel, Alexander | Albrecht, Heinz | Vollbracht, Claudia | Dauth, Wolfgang | Hagel, Wolfgang | Vitali, Francesco | Ganzleben, Ingo | Schultis, Hans | Konturek, Peter | Stein, Jürgen | Neurath, Markus | Raithel, Martin | Hagel, Alexander | Vollbracht, Claudia | Raithel, Martin | Konturek, Peter | Krick, Bianka | Haller, Heidemarie | Klose, Petra | Dobos, Gustav | Kümmel, Sherko | Cramer, Holger | Haller, Heidemarie | Saha, Felix J. | Kowoll, Anna | Ebner, Barbara | Berger, Bettina | Dobos, Gustav | Choi, Kyung-Eun | He, Lisha | Wang, Han | He, X. | Gu, C. | Zhang, Y. | Zhao, Linhua | Tong, Xiaolin | He, Lisha | Wang, Han | He, Xinhui | Gu, Chengjuan | Zhang, Ying | Zhao, Linhua | Tong, Xiaolin | He, Lisha | Wang, Han | He, Xinhui | Gu, Chengjuan | Zhang, Ying | Zhao, Linhua | Tong, Xiaolin | Ho, Robin S. T. | Chung, Vincent C. H. | Wu, Xinyin | Wong, Charlene H. L. | Wu, Justin C. Y. | Wong, Samuel Y. S. | Lau, Alexander Y. L. | Sit, Regina W. S. | Wong, Wendy | Holmes, Michelle | Bishop, Felicity | Calman, Lynn | Holmes, Michelle | Bishop, Felicity | Lewith, George | Newell, Dave | Field, Jonathan | Htut, Win L. | Han, Dongwoon | Choi, Da I. | Choi, Soo J. | Kim, Ha Y. | Hwang, Jung H. | Huang, Ching W. | Jang, Bo H. | Chen, Fang P. | Ko, Seong G. | Huang, Wenjing | Jin, De | Lian, Fengmei | Jang, Soobin | Kim, Kyeong H. | Lee, Eun K. | Sun, Seung H. | Go, Ho Y. | Ko, Youme | Park, Sunju | Jang, Bo H. | Shin, Yong C. | Ko, Seong G. | Janik, Hubert | Greiffenhagen, Natalie | Bolte, Jürgen | Kraft, Karin | Jaworski, Mariusz | Adamus, Miroslawa | Dobrzynska, Aleksandra | Jeitler, Michael | Jaspers, Jessica | von Scheidt, Christel | Koch, Barbara | Michalsen, Andreas | Steckhan, Nico | Kessler, Christian | Jin, De | Huang, Wen-jing | Pang, Bing | Lian, Feng-Mei | Jong, Miek | Baars, Erik | Glockmann, Anja | Hamre, Harald | Kainuma, Mosaburo | Murakami, Aya | Kubota, Toshio | Kobayashi, Daisuke | Sumoto, Yasuhiro | Furusyo, Norihiro | Ando, Shin-Ichi | Shimazoe, Takao | Kelber, Olaf | Verjee, S. | Gorgus, Eva | Schrenk, Dieter | Kemper, Kathi | Hill, Ellie | Kemper, Kathi | Rao, Nisha | Gascon, Gregg | Mahan, John | Kienle, Gunver | Dietrich, Jörg | Schmoor, Claudia | Huber, Roman | Kim, Weon H. | Han, Dongwoon | Ahmed, Mansoor | He, Luzhu | Hwang, Jung Hye | Kiss, Eva | Vancsik, Tamas | Meggyeshazi, Nora | Kovago, Csaba | Krenacs, Tibor | Klaus, Anne K. | Zerm, Roland | Pranga, Danilo | Ostermann, Thomas | Reif, Marcus | von Laue, Hans Broder | Brinkhaus, Benno | Kröz, Matthias | Klaus, Anne K. | Zerm, Roland | Pranga, Danilo | Recchia, Daniela Rodrigues | Ostermann, Thomas | Reif, Marcus | von Laue, Hans B. | Brinkhaus, Benno | Kröz, Matthias | Klein-Laansma, Christien T. | Jong, Mats | von Hagens, Cornelia | Jansen, Jean P. | van Wietmarschen, Herman | Jong, Miek C. | Ko, Youme | Sun, Seung-Ho | Go, Ho-Yeon | Jeon, Chan-Yong | Song, Yun-Kyung | Ko, Seong-Gyu | Koch, Anna K. | Rabsilber, Sybille | Lauche, Romy | Kümmel, Sherko | Dobos, Gustav | Langhorst, Jost | Cramer, Holger | Koch, Anna K. | Trifunovic-Koenig, Milena | Klose, Petra | Cramer, Holger | Dobos, Gustav | Langhorst, Jost | Koster, Evi | Baars, Erik | Delnoij, Diana | Kroll, Lena | Weiss, Kathrin | Kubo, Ai | Hendlish, Sarah | Altschuler, Andrea | Connolly, Nancy | Avins, Andy | Lauche, Romy | Recchia, Daniela Rodrigues | Cramer, Holger | Wardle, Jon | Lee, David | Sibbritt, David | Adams, Jon | Ostermann, Thomas | Lauche, Romy | Sibbritt, David | Park, Crystal | Mishra, Gita | Adams, Jon | Cramer, Holger | Lechner, Johann | Lee, Inseon | Chae, Younbyoung | Lee, Jisu | Cho, Seung H. | Choi, Yujin | Lee, Jee Y. | Ryu, Han S. | Yoon, Sung S. | Oh, Hye K. | Hyun, Lyun K. | Kim, Jin O. | Yoon, Seong W. | Lee, Ju-Yeon | Shin, Sang-Hoon | Jang, Min | Müller, Indra | Park, So-Hyun Janson | Lestoquoy, Anna S. | Laird, Lance | Negash, Lily | Mitchell, Suzanne | Gardiner, Paula | Li, Xiaofei | Wang, Yunhui | Zhen, Jianhua | Yu, He | Liu, Tiegang | Gu, Xiaohong | Liu, Hui | Ma, Weiguo | Zhang, Chengcheng | Shang, Xuezheng | Bai, Yu | Meng, Fengxian | Liu, Wei | Rooney, Collin | Smith, Amos | Lopes, Shirlene | Demarzo, Marcelo | do Patrocínio Nunes, Maria | Lorenz, Peter | Gründemann, Carsten | Heinrich, Miriam | Garcia-Käufer, Manuel | Grunewald, Franziska | Messerschmidt, Silke | Herrick, Anja | Gruber, Kim | Beckmann, Christiane | Knödler, Matthias | Huber, Roman | Steinborn, Carmen | Stintzing, Florian | Lu, Taoying | Wang, Lixin | Wu, Darong | Luberto, Christina M | Hall, Daniel L. | Chad-Friedman, Emma | Lechner, Suzanne | Park, Elyse R. | Luberto, Christina M. | Park, Elyse | Goodman, Janice | Luer, Sonja | Heri, Matthias | von Ammon, Klaus | Frei-Erb, Martin | Ma, Weiguo | Meng, Fengxian | Maggini, Valentina | Gallo, Eugenia | Landini, Ida | Lapucci, Andrea | Nobili, Stefania | Mini, Enrico | Firenzuoli, Fabio | McDermott, Clare | Lewith, George | Richards, Selwyn | Cox, Diane | Frossell, Sarah | Leydon, Geraldine | Eyles, Caroline | Raphael, Hilly | Rogers, Rachael | Selby, Michelle | Adler, Charlotte | Allam, Jo | Meng, Fengxian | Gu, Wen | Zhang, Chengcheng | Bai, Hua | Zhang, Zhengju | Wang, Dali | Bu, Xiangwei | Zhang, Honghong | Zhang, Jianpeng | Liu, Hui | Mikolasek, Michael | Berg, Jonas | Witt, Claudia | Barth, Jürgen | Miskulin, Ivan | Lalic, Zdenka | Miskulin, Maja | Dumic, Albina | Sebo, Damir | Vcev, Aleksandar | Mohammed, Nasr A. A. | Han, Dongwoon | Ahmed, Mansoor | Choi, Soo Jeung | Im, Hyea Bin | Hwang, Jung Hye | Mukherjee, Anwesha | Kandhare, Amit | Bodhankar, Subhash | Mukherjee, Anwesha | Kandhare, Amit | Thakurdesai, Prasad | Bodhankar, Subhash | Munk, Niki | Evans, Erica | Froman, Amanda | Kline, Matthew | Bair, Matthew J. | Musial, Frauke | Kristoffersen, Agnete E. | Alræk, Terje | Hamre, Harald J. | Stub, Trine | Björkman, Lars | Fønnebø, Vinjar M. | Pang, Bing | Lian, Feng-mei | Ni, Qing | Tong, Xiao-lin | Li, Xin-long | Liu, Wen-ke | Feng, Shuo | Zhao, Xi-yan | Zheng, Yu-jiao | Zhao, Xue-min | Lin, Yi-qun | Pang, Bing | Lian, Feng-mei | Tong, Xiao-lin | Zhao, Tian-yu | Zhao, Xi-Yan | Phd, Hui Che | Zhang, Chen | Pang, Bing | Liu, Feng | Tong, Xiao-lin | Zhao, Lin-hua | Zhao, Xue-min | Ye, Ru | Gu, Cheng-juan | Pang, Bing | Ni, Qing | Tong, Xiao-lin | Lian, Feng-mei | Zhao, Xi-yan | Jin, De | Zhao, Xue-min | Zheng, Yu-jiao | Lin, Yi-qun | Peng, Wenbo | Lauche, Romy | Sibbritt, David | Adams, Jon | Peng, Wenbo | Wardle, Jon | Cramer, Holger | Mishra, Gita | Lauche, Romy | Pohlman, Katherine A. | Mior, Silvano | Funabashi, Martha | De Carvalho, Diana | El-Bayoumi, Mohamed | Haig, Bob | Kelly, Kimbalin | Wade, Darrell J. | O’Beirne, Maeve | Vohra, Sunita | Portalupi, Emanuela | Gobo, Giampietro | Bellavita, Luigi | Guglielmetti, Chiara | Raak, Christa | Teuber, Myriam | Molsberger, Friedrich | von Rath, Ulrich | Reichelt, Ulrike | Schwanebeck, Uta | Zeil, Sabine | Vogelberg, Christian | Veintimilla, Dolores Rodríguez | Vollbracht, Claudia | Mery, Guerrero Tapia | Villavicencio, Marisol Maldonado | Moran, Sandra Herrera | Sachse, Christian | Gündlin, Peter W | Stange, Rainer | Sahebkarkhorasani, Monirsadat | Azizi, Hoda | Schumann, Dania | Lauche, Romy | Sundberg, Tobias | Leach, Matthew J. | Cramer, Holger | Seca, Susana | Greten, Henry | Selliah, Sugir | Shakya, Anu | Han, Dongwoon | Kim, Ha Yun | Choi, Da I. | Im, Hyea B. | Choi, Soo J. | Sherbakova, Anna | Ulrich-Merzenich, Gudrun | Kelber, Olaf | Abdel-Aziz, Heba | Sibinga, Erica | Webb, Lindsey | Ellen, Jonathan | Skrautvol, Kari | Nåden, Dagfinn | Song, Rhayun | Grabowska, Weronika | Osypiuk, Kamila | Diaz, Gloria V. | Bonato, Paolo | Park, Moonkyoung | Hausdorff, Jeffrey | Fox, Michael | Sudarsky, Lewis R. | Tarsy, Daniel | Novakowski, James | Macklin, Eric A. | Wayne, Peter M. | Song, Rhayun | Hwang, Inok | Ahn, Sukhee | Lee, Myung-Ah | Wayne, Peter M. | Sohn, Min K. | Sorokin, Oleg | Steckhan, Nico | Heydeck, Dagmar | Borchert, Astrid | Hohmann, Christoph-Daniel | Kühn, Harmut | Michalsen, Andreas | Kessler, Christian | Steckhan, Nico | Hohmann, Christoph-Daniel | Cramer, Holger | Michalsen, Andreas | Dobos, Gustav | von Scheidt, Christel | Kirschbaum, Clemens | Stalder, Tobias | Stöckigt, Barbara | Teut, Michael | Suhr, Ralf | Sulmann, Daniela | Brinkhaus, Benno | Streeter, Chris | Gerbarg, Patrica | Silveri, Marisa | Brown, Richard | Jensen, John | Stritter, Wiebke | Rutert, Britta | Eggert, Angelika | Längler, Alfred | Seifert, Georg | Holmberg, Christine | Sun, Jin | Deng, Xin | Li, Wen-Yuan | Wen, Bin | Robinson, Nicola | Liu, Jian-Ping | Sung, Hyun K. | Yang, Narae | Go, Ho Y. | Shin, Seon M. | Jung, Hee | Kim, Young J. | Jung, Woo S. | Park, Tae Y. | Suzuki, Kiyoshi | Ito, Toshinori | Uchida, Seiya | Kamohara, Seika | Ono, Naoya | Takamura, Mitsuyuki | Yokochi, Ayumu | Maruyama, Kazuo | Tapia, Patricio | Thabaut, Katarzyna | Brinkhaus, Benno | Stöckigt, Barbara | Thronicke, Anja | Kröz, Matthias | Steele, Megan | Matthes, Harald | Herbstreit, Cornelia | Schad, Friedemann | Tian, Jiaxing | Lian, Fengmei | Yang, Libo | Tong, Xiaolin | Tian, Tian | Zhang, Hewei | Tian, Xia | Wang, CongCong | Chai, Qian Yun | Zhang, Lijuan | Xia, Ruyu | Huang, Na | Fei, Yutong | Liu, Jianpin | Trent, Natalie | Miraglia, Mindy | Dusek, Jeffrey | Pasalis, Edi | Khalsa, Sat B. | Trifunovic-König, Milena | Klose, Petra | Cramer, Holger | Lauche, Romy | Koch, Anna | Dobos, Gustav | Langhorst, Jost | Uebelacker, Lisa | Tremont, Geoffrey | Gillette, Lee | Epstein-Lubow, Gary | Strong, David | Abrantes, Ana | Tyrka, Audrey | Tran, Tanya | Gaudiano, Brandon | Miller, Ivan | Ullmann, Gerhild | Ullmann, Gerhild | Li, Yuhua | Vaidya, Sujata | Marathe, Vinod | Vale, Ana C. | Motta, Jacquelyne | Donadão, Fabíola | Valente, Angela C. | Valente, Luana C. Carvalho | Ghelman, Ricardo | Vesovic, Dusan | Jevdic, Dragan | Jevdic, Aleksandar | Jevdic, Katarina | Djacic, Mihael | Letic, Dragica | Bozic, Drago | Markovic, Marija | Dunjic, Slobodan | Vesovic, Dusan | Jevdic, Dragan | Jevdic, Aleksandar | Jevdic, Katarina | Djacic, Mihael | Letic, Dragica | Bozic, Drago | Markovic, Marija | Ruscuklic, Gordana | Baksa, Dezire | Dunjic, Slobodan | Vesovic, Dusan | Jevdic, Dragan | Jevdic, Aleksandar | Jevdic, Katarina | Djacic, Mihael | Letic, Dragica | Bozic, Drago | Markovic, Marija | Ruscuklic, Gordana | Baksa, Dezire | Dunjic, Slobodan | Vesovic, Dusan | Jevdic, Dragan | Jevdic, Aleksandar | Jevdic, Katarina | Djacic, Mihael | Letic, Dragica | Bozic, Drago | Markovic, Marija | Ruscuklic, Gordana | Baksa, Dezire | Dunjic, Slobodan | Vesovic, Dusan | Jevdic, Dragan | Jevdic, Aleksandar | Jevdic, Katarina | Djacic, Mihael | Letic, Dragica | Bozic, Drago | Markovic, Marija | Vrca, Kenan | Dunjic, Slobodan | Vincent, Ann | Wahner-Roedler, Dietlind | Whipple, Mary | Vogelius, Maria M. | Vollbracht, Claudia | Friesecke, Iris | Gündling, Peter W. | Wahner-Roedler, Dietlind | Mahapatra, Saswati | Hynes, Rebecca | Van Rooy, Kimberly | Looker, Sherry | Ghosh, Aditya | Bauer, Brent | Cutshall, Susanne | Walach, Harald | Flores, Ana Borges | Walach, Harald | Ofner, Michael | Kastner, Andreas | Schwarzl, Gerhard | Schwameder, Hermann | Alexander, Nathalie | Strutzenberger, Gerda | Wang, Jie | Lu, Yan | Gu, Wen | Zhang, Chengcheng | Bu, Xianwei | Zhang, Honghong | Zhang, Jianping | He, Yuxi | Zhang, Xiaoxu | Meng, Fengxian | Wang, Shang | Yu, He | Shi, Jinfeng | Hao, Yu | Liu, Tiegang | Wu, Jun | Qiu, Zeji | Gu, Xiaohong | Wang, Yuh-Hai | Lou, Chi-Jung | Watts, Sam | Wayne, Peter | Osypiuk, Kamila | Vergara-Diaz, Gloria | Bonato, Paolo | Gow, Brian | Hausdorff, Jeffrey | Miranda, Jose | Sudarsky, Lewis | Tarsy, Daniel | Fox, Michael | Macklin, Eric | Wode, Kathrin | Bergqvist, Jenny | Bernhardsson, Britt-Marie | Nordberg, Johanna Hök | Kienle, Gunver | Sharp, Lena | Henriksson, Roger | Woo, Yeonju | Hyun, Min K. | Wu, Hao | Wang, Tian-Fang | Zhao, Yan | Wei, Yu | Tian, Lei | He, Lei | Wang, Xue | Wu, Ruohan | Feng, Shuo | Han, Mei | Caldwell, Patrina H. Y. | Liu, Shigang | Zhang, Jing | Liu, Jianping | Xia, Ruyu | Chai, Qianyun | Fei, Yutong | Guo, Zhongning | Wang, Congcong | Liu, Zhijun | Li, Xun | Zhang, Ying | Liu, Jianping | Yang, I. J. | Lincha, V. Ruberio | Ahn, S. H. | Lee, D. U. | Shin, H. M. | Yang, Lu | Sibbritt, David | Peng, Wenbo | Adams, Jon | Yang, N. | Sung, H. | Shin, S. M. | Go, H. Y. | Jung, H. | Kim, Y. | Park, T. Y. | Yap, Angela | Kwan, Yu H. | Tan, Chuen S. | Ibrahim, Syed | Ang, Seng B. | Yayi, Alfred | Han, Dongwoon | Im, Hyea Bin | Hwang, Jung Hye | Choi, Soo Jeung | Yoo, Jeong E. | Yoo, Ho R. | Jang, Sae B. | Lee, Hye L. | Youssef, Ala’a | Ezzat, Shahira | Motaal, Amira Abdel | El-Askary, Hesham | Yu, Xiaotong | Cui, Yashan | Zhang, Ying | Lian, Fengmei | Yun, Younghee | Ko, Youme | Ahn, Jin-Hyang | Jang, Bo-Hyung | Kim, Kyu-Seok | Ko, Seong-Gyu | Choi, Inhwa | Zerm, Roland | Glinz, Augustina | Pranga, Danilo | Berger, Bettina | ten Brink, Fadime | Reif, Marcus | Büssing, Arnd | Gutenbrunner, Christoph | Kröz, Matthias | Zerm, Roland | Helbrecht, Bert | Pranga, Danilo | Brinkhaus, Benno | Michalsen, Andreas | Kröz, Matthias | Zhang, Honghong | Fang, Tiesheng | Wang, Jie | Zhang, Chengcheng | He, Yuxi | Zhang, Xiaoxu | Zhang, Zhengju | Wang, Dali | Meng, Fengxion | Zhang, Jianping | Zhang, Chengcheng | Bai, Hua | Shen, Zhiming | Ma, Weiguo | Liu, Hui | Bai, Yu | Shang, Xuezheng | Meng, Fengxian | Zhang, Ruixin | Wu, Fan | Li, Ming | Xuan, Xinyun | Shen, Xueyong | Ren, Ke | Berman, Brian | Zhen, Jianhua | Li, Xiaofei | Gu, Xiaohong | Yu, He | Zheng, Zian | Wan, Yuxiang | Wang, Yunhui | Ma, Xueyan | Dong, Fei | Liu, Tiegang | Zhen, Jianhua | Li, Xiaofei | Gu, Xiaohong | Yu, He | Zheng, Zian | Wan, Yuxiang | Wang, Yunhui | Ma, Xueyan | Dong, Fei | Liu, Tiegang | Zick, Suzie | Harris, Richard | Bae, Go E. | Kwon, Jung N. | Lee, Hye Y. | Nam, Jong K. | Lee, Sang D. | Lee, Dong H. | Han, Ji Y. | Yun, Young J. | Lee, Ji H. | Park, Hye L. | Park, Seong H. | Bocci, Chiara | Ivaldi, Giovanni B. | Vietti, Ilaria | Meaglia, Ilaria | Guffi, Marta | Ruggiero, Rubina | Gualea, Marita | Longa, Emanuela | Bonucci, Massimo | Croke, Sarah | Rodriguez, Lourdes Diaz | Caracuel-Martínez, Juan C. | Fajardo-Rodríguez, Manuel F. | Ariza-García, Angélica | la Fuente, Francisca García-De | Arroyo-Morales, Manuel | Estrems, Maria S. | Gómez, Vicente G. | Estrems, Maria S. | Sabater, Mónica Valero | Ferreri, Rosaria | Bernardini, Simonetta | Pulcri, Roberto | Cracolici, Franco | Rinaldi, Massimo | Porciani, Claudio | Firenzuoli, Fabio | Baccetti, Sonia | Di Stefano, Mariella | Monechi, Maria V. | Gallo, Eugenia | Maggini, Valentina | Gori, Luigi | Rossi, Elio | Fisher, Peter | Hughes, John | Mendoza, Ariadna | MacPherson, Hugh | Witt, Claudia | Filshie, Jacqueline | Lewith, George | Di Francesco, Antonia | Bernardini, Alberto | Messe, Monica | Primitivo, Vincenzo | Iasella, Piera A. | Ghelman, Ricardo | Taminato, Monica | Alcantara, Jaqueline Do Carmo | De Oliveira, Katia R. | Rodrigues, Debora C. De Azevedo | Mumme, Juliana R. Campana | Sunakozawa, Olga K. Matsumoto | Filho, Vicente Odone | Seifert, Georg | Goldenberg, Joshua | Day, Andrew | Sasagawa, Masa | Ward, Lesley | Cooley, Kieran | Gunnarsdottir, Thora | Hjaltadottir, Ingibjorg | Hajimonfarednejad, Mahdie
PMCID: PMC5498867
23.  FADS Gene Polymorphisms, Fatty Acid Desaturase Activities, and HDL-C in Type 2 Diabetes 
Polyunsaturated fatty acids (PUFA) correlate with risk of dyslipidemia and cardiovascular diseases. Fatty acid desaturase (FADS) single nucleotide polymorphisms (SNPs) modulate circulating PUFA concentrations. This study examined influence of FADS1 and FADS2 genetic variants on desaturase activities and blood lipid concentrations in type 2 diabetes patients, and further assessed their interrelationships. Selected SNPs (FADS1: rs174547, rs174548, rs174550; FADS2: rs174575, rs174576, rs174583, rs498793 and rs2727270) were genotyped in 820 type 2 diabetes patients and compared with those reported in the HapMap. Patient subgroups (n = 176) without taking lipid-lowering medicine were studied to assess influence of tag SNPs including rs174547, rs174575, rs498793 and rs2727270 on delta-5 desaturase (D5D: 20:4 (n-6)/20:3 (n-6)) and delta-6 desaturase (D6D:18:3 (n-6)/18:2 (n-6)) activities, and blood lipids. FADS1 rs174547 TT/TC/CC and FADS2 rs2727270 CC/CT/TT were significantly (p for trend < 0.05) associated with reduced HDL-C, D5D and D6D activities. Upon adjustment for confounders, D5D (p = 0.006) correlated significantly and D6D marginally (p = 0.07) correlated with increased HDL-C levels, whereas rs174547 and rs2727270 polymorphisms were not associated. D6D andD5D activities may play a role in modulating HDL-C levels in type 2 diabetes. Future studies with larger sample sizes are needed to investigate how FADS genetic variations interact with desaturase activities or PUFAs in the metabolism of lipoproteins in diabetic patients.
PMCID: PMC5486258  PMID: 28555039
diabetes; FADS1; FADS2; HDL; genetic polymorphisms; polyunsaturated fatty acids
24.  Molecular mechanism of G1 arrest and cellular senescence induced by LEE011, a novel CDK4/CDK6 inhibitor, in leukemia cells 
Overexpression of cyclin D1 dependent kinases 4 and 6 (CDK4/6) is a common feature of many human cancers including leukemia. LEE011 is a novel inhibitor of both CDK4 and 6. To date, the molecular function of LEE011 in leukemia remains unclear.
Leukemia cell growth and apoptosis following LEE011 treatment was assessed through CCK-8 and annexin V/propidium iodide staining assays. Cell senescence was assessed by β-galactosidase staining and p16INK4a expression analysis. Gene expression profiles of LEE011 treated HL-60 cells were investigated using an Arraystar Human LncRNA array. Gene ontology and KEGG pathway analysis were then used to analyze the differentially expressed genes from the cluster analysis.
Our studies demonstrated that LEE011 inhibited proliferation of leukemia cells and could induce apoptosis. Hoechst 33,342 staining analysis showed DNA fragmentation and distortion of nuclear structures following LEE011 treatment. Cell cycle analysis showed LEE011 significantly induced cell cycle G1 arrest in seven of eight acute leukemia cells lines, the exception being THP-1 cells. β-Galactosidase staining analysis and p16INK4a expression analysis showed that LEE011 treatment can induce cell senescence of leukemia cells. LncRNA microarray analysis showed 2083 differentially expressed mRNAs and 3224 differentially expressed lncRNAs in LEE011-treated HL-60 cells compared with controls. Molecular function analysis showed that LEE011 induced senescence in leukemia cells partially through downregulation of the transcriptional expression of MYBL2.
We demonstrate for the first time that LEE011 treatment results in inhibition of cell proliferation and induction of G1 arrest and cellular senescence in leukemia cells. LncRNA microarray analysis showed differentially expressed mRNAs and lncRNAs in LEE011-treated HL-60 cells and we demonstrated that LEE011 induces cellular senescence partially through downregulation of the expression of MYBL2. These results may open new lines of investigation regarding the molecular mechanism of LEE011 induced cellular senescence.
Electronic supplementary material
The online version of this article (doi:10.1186/s12935-017-0405-y) contains supplementary material, which is available to authorized users.
PMCID: PMC5340031
LEE011; Leukemia; CDK4/6; Cellular senescence; Arraystar Human LncRNA array
25.  Abstracts from the 8th International Congress of the Asia Pacific Society of Infection Control (APSIC) 
Sutthiruk, Nantanit | Botti, Mari | Considine, Julie | Driscoll, Andrea | Hutchinson, Ana | Malathum, Kumthorn | Cucunawangsih, Cucunawangsih | Wiwing, Veronica | Puspitasari, Vivien | Shanmugakani, Rathina Kumar | Akeda, Yukihiro | Kodera, Takuya | Santanirand, Pitak | Tomono, Kazunori | Yamanaka, Takayuki | Moriuchi, Hiroyuki | Kitajima, Hiroyuki | Horikoshi, Yuho | Lavrinenko, Alyona | Azizov, Ilya | Tabriz, Nurlan | Kozhamuratov, Margulan | Serbo, Yekatherine | Yang, Dahae | Lee, Woonhyoung | Bae, Il Kwon | Lee, Jae Hyun | Lee, Hyukmin | Kim, Jung Ok | Jeong, Seok Hoon | Lee, Kyungwon | Peremalo, Thiba | Madhavan, Priya | Hamzah, Sharina | Than, Leslie | Wong, Eng Hwa | Desa, Mohd Nasir Mohd | Ng, Kee Peng | Geronimo, Marionne | Tayzon, Maria Fe | Maño, Maria Jesusa | Chow, Angela | Hon, Pei-Yun | Win, Mar-Kyaw | Ang, Brenda | Leo, Yee-Sin | Chow, Angela | Hon, Pei-Yun | See, Tina | Ang, Brenda | Marin, Rocio Alvarez | de Sousa, Marta Aires | Kieffer, Nicolas | Nordmann, Patrice | Poirel, Laurent | Laochareonsuk, Wison | Petyu, Sireekul | Wanasitchaiwat, Pawin | Thana, Sutasinee | Bunyaphongphan, Chollathip | Boonsomsuk, Woranan | Maneepongpermpoon, Pakpoom | Jamulitrat, Silom | Sureshkumar, Dorairajan | Supraja, Kalyanaraman | Sharmila, Soundararajan | Cucunawangsih, Cucunawangsih | Setiawan, Benny | Lumbuun, Nicolaski | Nakayama, Haruo | Ota, Toshiko | Shirane, Naoko | Matuoka, Chikako | Kodama, Kentaro | Ohtsuka, Masanobu | Bacolcol, Silverose Ann Andales | Velmonte, Melecia | Alde, Allan | Chavez, Keithleen | Esteban, Arlene Joy | Lee, Aisa Jensen | Hsieh, Tai-Chin | Shio-ShinJean | Huang, Huey-Jen | Huang, Shu-Ju | Huang, Yu-Huan | Cheng, Pei-Chen | Yu, Su-Fang | Tsao, Shih-Ming | Lee, Yuan-Ti | Li, Chien-Feng | Lu, Min-Chi | Pruetpongpun, Nattapol | Khawcharoenporn, Thana | Damronglerd, Pansachee | Suwantarat, Nuntra | Apisarnthanarak, Anucha | Rutjanawech, Sasinuch | Cushinotto, Lisa | McBride, Patty | Williams, Harding | Liu, Hans | Hang, Phan Thi | Anh, Dinh Pham Phuong | Le, Ngai | Khu, Dung | Nguyen, Lam | Castillo, Roel Beltran | Sureshkumar, Dorairajan | Gopalakrishnan, Ram | Ramasubramanian, Venkatasubramanian | Sreevidya, Subramanian | Jayapradha, Ranganathan | Umetsu, Atsushi | Noda, Tetsuhiro | Hashimoto, Kenyuu | Hayashi, Akihiro | Kabashima, Mikie | Jadczak, Ursula | Elvelund, Knut | Johnsen, Marit | Borgen, Bente | Lingaas, Egil | Mao, Chia-Hua | Chang, Fu-Chieh | Liu, Chang-Pan | Chao, Ru-Hui | Chang, Fu-chieh | Liu, Chang-pan | Pawapotako, Junpen | Prasertpan, Chadanan | Malaihuan, Wantanee | Uirungroj, Phisit | Prasertpan, Chadanan | Saenjum, Chalermpong | Ouirungrog, Teerapat | Uirungroj, Phisit | Borrell, Sue | Bass, Pauline | Worth, Leon | Xian-li, Zhao | Xiao-long, Li | Xue-hua, Yao | Wei, Ren | Zeng, Zhang Xia | Kong, Man Ying | Lai, Christopher Koon Chi | Lee, Suet Yi | Tsang, Ngai Chong | O’Donoghue, M. 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Jay | Vergara, Justine | Añonuevo, Nicolo Andrei | Kwek, Marion | Acuin, Jose | Sanchez, Anna Josea | Bathan, Avel | Jantan, Jamilah Binte | Guek, Chua Chor | Kian, Eu Chiow | Pirido, Pampe Anak | Aron, Nur Fadilah Binte Mohd | Estacio, Leah May | Palana, Francis Alvarez | Gracia, Michelle | Shamsuddin, Nur Syafiqah Binte | Castro, Kersten Timbad | Baloria, Madonna | Adam, Faezah Binte | Wei, Zhang | Fong, Poh Bee | Kalisvar, Marimuthu | Chow, Angela | Ang, Brenda | Chuang, I-Ju | Yi-ChunCho | Chiu, Yu-Fen | Chen, Lung-Chih | Lin, Yi-Chun | Dong, Shao-Xing | Lee, Yi-Chieh | Kuan, Hui-Chen | Lin, Hsin-Hua | Chi, Chia-Chun | Lu, Chin-Te | Chang, Fu-chieh | Liu, Chang-pan | Ya-Fen, Tang | Li-Hsiang, Su | Jien-Wei, Liu | Chao, Hsuehlan | ChangChien, PinRu | Chen, WeiFang | Lai, ChungHsu | Ara, Lutfe | Mowla, Syed Mohammad Niaz | Vashkar, Shaikh Mahmud Kamal | Chan, Wai Fong | ChunYau, Mabel Yin | LingChong, Karen Kam | OnLi, Tze | Kaur, Rajwinder | Yan, Ng Po | Chiu, Gloria Chor Shan | Cheung, Christina W. 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James | Kwek, Marion | Flor, Jose Paulo | Bautista, Marko | Vergara, Justine | De Roxas, V James | AndreiAñonuevo, Nicolo | Kwek, Marion | Ho, Yeng May | Kum, Jia Qi | Poh, Bee Fong | Marimuthu, Kalisvar | Ang, Brenda | Liu, Tzu-Yin | Chu, Sin-Man | Chen, Hui-Zhu | Chen, Tun-chieh | Chen, Yichun | Tsao, Ya-Ching | Skuntaniyom, Sumawadee | Malathum, Kumthorn | Tipluy, Pirawadee | Paengta, Sangwan | wongsaen, Ratchanee | thanomphan, Sutthiphun | Tariyo, Samettanet | Thongchuea, Buachan | Khamfu, Pattama | Thanomphan, Sutthiphan | Songtaweesin, Wipaporn Natalie | Anugulruengkit, Suvaporn | Samransamruajkit, Rujipat | Sosothikul, Darintr | Tansrijitdee, Ornanong | Nakphunsung, Anry | Srimuan, Patchareeyawan | Sophonphan, Jirachaya | ThanyaweePuthanakit | Payuk, Kunyanut | Picheansathian, Wilawan | Viseskul, Nongkran | DeNardo, Elizabeth | Leslie, Rachel | Cartner, Todd | Barbosa, Luciana | Werner, Heinz-Peter | Brill, Florian H. 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N. | Ng, Lady S. H. | Wong, Lindy M. T. | Poon, Lenina S. L. | Lai, Mary K. L. | Cheng, Holly H. S. | Fong, S. K. | Leung, Cindy F. Y. | Hasegawa, Jumpei | Shirakawa, Hiroki | Wakai, Sachiko | Mieno, Makiko | Hatakeyama, Shuji | Tateishi, Mariko | Mihashi, Mutsuko | Sato, Yuka | Saenjum, Chalermpong | Deeudom, Manu | Tharavichitkul, Prasit | Ouirungrog, Teerapat | Ouirungroj, Phisit | Chinniah, Terrence | Tan, Jackson | Prabu, Kavitha | Alam, Sartaj | Wynn, Aung Kyaw | Ahmad, Rashidah | Sidek, Amalina | Samsuddin, Dg Azizah | Ajis, Noraini | Ahmad, Aliyah | Magon, Susylawathi | Chu, Boon | Kuang, Jiqiu | Gao, Yan | Wang, Shoujun | Hao, Yunxiao | Liu, Rong | Li, Dongmei | Wang, Hui | Yan, Ng Po | Nishio, Hisanori | Mori, Hitomi | Morokuma, Yoshiko | Yamada, Takaaki | Kiyosuke, Makiko | Yasunaga, Sachie | Toyoda, Kazuhiro | Shimono, Nobuyuki | Babenko, Dmitriy | Turmuhambetova, Anar | Cheşcă, Antonella | Toleman, Mark A. | Babenko, Dmitriy | Turmuhambetova, Anar | Cheşcă, Antonella | Toleman, Mark A. | Babenko, Dmitriy | Turmuhambetova, Anar | Azizov, Ilya | Cheşcă, Antonella | Toleman, Mark A. | Akhmaltdinova, Lyudmila L. | Turmuhambetova, Anar | Cheşcă, Antonella | Babenko, Dmitriy | Magsakay, Mark Albert | Macatibag, Angelo | Tayzon, Maria Fe | Lerios, Jeannica Kriselle | Azizov, Ilya | Lavrineko, Alyona | Babenko, Dmitry | Sheck, Eugene | Edelstein, Mikhail | Liu, Tzu-Yin | Li, Lih-Yue | Chan, Chiung-Wen | Pan, Hui-Chuan | Chen, Tun-chieh | Vanishakije, Wipa | Jaikampun, Warisra | Cheng, Pei-Chen | Huang, Huey-Jen | Huang, Shu-Ju | Huang, Yu-Huan | Li, Su-Yin | Yu, Su-Fang | Li, Jian-Feng | Wu, Yu-Ping | Lee, Yuan-Ti | Lin, Chiao-Hui | Chang, Ping-Chin | Tariyo, Samatanet | Paengta, Sangwan | Wongsaen, Ratchanee | Thanompan, Suttsiphan | Skuntaniyom, Sumawadee | Malathum, Kumthorn | Sukkra, Suchada | Zaman, Khalequ | Zaman, Sheikh Farzana | Zaman, Farzana | Aziz, Asma | Faisal, Sayeed-Bin | Traskine, Magali | Ruiz-Guiñazú, Javier | Borys, Dorota | Zaman, Khalequ | Zaman, Sheikh Farzana | Zaman, Farzana | Aziz, Asma | Faisal, Sayeed-Bin | Traskine, Magali | Ruiz-Guiñazú, Javier | Borys, Dorota | Lam, Wendy Wai Yee | Chow, May | Choy, Lucy | Kam, Joseph | Salleh, Sharifah Azura | Yacob, Razila | Yusof, Siti Rokiah | Jalil, Nordiah Awang | Flor, Jose Paulo | Añonuevo, Nicolo Andrei | Bautista, Marko | De Roxas, V. Jay | Vergara, Justine | Millan, Maria Lourdes | Kwek, Marion | Acuin, Jose Lito | Lee, Aisa Jensen | Velmonte, Melecia A. | Bacolcol, Silverose Ann A. | Alde, Allan | Chavez, Keitleen | Esteban, Arlene Joy | Ting, Ching-I | Dissayasriroj, Sunisa | Chinniah, Terrence Rohan | Prabu, Kavitha | Ahmad, Rashidah | Magon, Susylawathi | DiniSuhaimi, Jauharatud | Mirasin, Aizzuddin | Morni, Nurul | Chu, Boon | Samsuddin, Azizah | Ahmad, Aliyah | Sidek, Amalina | Ajis, Noraini | AbuBakar, Amalina | Shafiee, Amanie | Safar, Julaini | Yan, Ng Po | Annie, Leung | Ling, Fung Yuk | Edna, Lau | Kristine, Luk | Shinomiya, Satoshi | Yamamoto, Kumiko | Kjiwara, Kayoko | Yamaguchi, Mitsuhiro | Chow, Angela | Tin, Grace | Zhang, Wei | Hon, Pei-Yun | Poh, Bee-Fong | Marimuthu, Kalisvar | Ang, Brenda | Chan, Ming-Chin | Wang, Chih-Chien | Huang, Shu-Ju | Huang, Huey-Jen | Yu, Su-Fang | Huang, Huan-Yu | Cheng, Pei-Chen | Li, Jian-Feng | Lee, Yuan-Ti | Lai, Chiung-Ling | Lu, Min-Chi | Kosol, Sajeerat | Sakolwirat, Wantana | Paepong, Patchanee | Jansanga, Sawalee | Jaisamoot, Pattarin | Thongnuanual, Nuttha | Srithong, Chittima | Somsakul, Somporn | Malathum, Kumthorn | Plongpunth, Sutima | Punpop, Mukkapon | Malathum, Porntip | Malathum, Kumthorn | Thanomphan, Sutthiphan | Wongsaen, Ratchanee | Peautiwat, Kulada | boon kirdram, Nattawipa | Picheansathian, Wilawan | Klunklin, Pimpaporn | Samethadka, Geetha | Suzuki, Naoko | Asada, Hitomi | Katayama, Masao | Komano, Atsushi | Sato, Akihiro | Nakamura, Itaru | Watanabe, Hidehiro | Matsumoto, Tetsuya | Seo, Hye Kyung | Hwang, Joo-Hee | Shin, Myoung Jin | Kim, Su Young | Kim, Eu Suk | Song, Kyoung-Ho | Kim, Hong Bin | Un, Lai-Si | Vong, Choi-Ian | Flor, Jose Paulo | Añonuevo, Nicolo Andrei | Bautista, Marko | De Roxas, V. James | Vergara, Justine | Kwek, Marion | Koh, Jocelyn | Agustinus, Sherly | Hassan, Rozita Bte Abu | Thinn, Yin Phyu | Ng, Benjamin | Tun, Soe Pyae | Ha, Su Mon Thi | Xiaoting, Xue | Li, Lin | Chuang, Leyland | Niroshika, Attanayaka Mudiyanselage Chulani | Perera, Kaluarachchige Anoma Kaluarachchi | Fernando, Dimingo Kankanamalage Diana Grace | Hemamala, Bodhipakshage Rohini | Yeh, Chiu-yin | Chao, Huwi-chun | Yang, Hui-Chun | Chiu, Hsiang-Ju | Shih, Ya-Ling | Chien, Yu-Shan | Lin, Wan-Yi | Pan, Chia-Yun | Chang, Ying-Yun | Yea, Chiu-Yuch | Chu, Ming-Hsien | Lee, Li-Chu | Chiu, Hsiang-Ju | Shih, Ya-Ling | Yang, Hui-Chun | Yu-Hsiu, Lin | Siao-Pei, Guo | Pak-On, Leung | Mei-Fe, Sie | Jyh-Jou, Chen | Yu-Hsiu, Lin | Yong-Yuan, Chang | Kuo, Shu-Yuan | Lin, Yu-Hsiu | Zhang, Ji-Sheng | Leung, Pak-On | Sie, Mei-Fe | Chen, Jyh-Jou | Chen, Yan-Ru | Lin, Yu-Hsiu | Chen, Ying-Ling | Taou, Chi-Fen | Chen, Hsiao-Shan | Tang, Hung-Jen | Chen, Shin Yu | Chen, Yin Yin | Der Wang, Fu | Shih, Tzu-Ping | Chen, Chin-Yu | Chen, Su-Jung | Wu, Mei-chi | Yang, Wan-ju | Chou, Mei-ling | Yu, Man-Ling | Li, Li-Chu | Chu, Cheng-Wei | Tsou, Wen-Hao | Wu, Wen-Chih | Cheng, Wen-Chi | Sun, Cho-Ching | Shih, Tzu-Ping | Chen, Chin-Yu | Lu, Shu-Hua | Chen, Su-Jung | Yang, Hsin-Ling | Lu, Cheng-Yu | Yu, Man-Ling | Li, Li-Chu | Chu, Cheng-Wei | Tsou, Wen-Hao | Wu, Wen-Chih | Cheng, Wen-Chi | Sun, Cho-Ching | Hirunprapakorn, Nitchawan | Malathum, Kumthorn | Apivanich, Sirilux | Pornmee, Ttipakorn | Beowsomboon, Chonnikarnt | Rajborirug, Songyos | Pruekrattananapa, Yada | Sangsuwan, Tharntip | Jamulitrat, Silom | Kumkoom, Itthaporn | Kasatpibal, Nongyao | Chitreecheur, Jittaporn | Kasatpibal, Nongyao | Whitney, JoAnne D. | Saokaew, Surasak | Kengkla, Kirati | Heitkemper, Margaret M. | Apisarnthanarak, Anucha | Muntajit, Thanomvong | Apivanich, Siriluk | Malathum, Kumthorn | Somsakul, Somporn | Phan, Hang Thi | Dinh, Anh Pham Phuong | Nguyen, Tuyet Thi Kim
PMCID: PMC5333188

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