The intricacies of Alzheimer’s disease pathogenesis are being increasingly illuminated by the exploration of epigenetic mechanisms,particularly DNA methylation.This review comprehensively surveys recent human-centere...The intricacies of Alzheimer’s disease pathogenesis are being increasingly illuminated by the exploration of epigenetic mechanisms,particularly DNA methylation.This review comprehensively surveys recent human-centered studies that investigate whole genome DNA methylation in Alzheimer’s disease neuropathology.The examination of various brain regions reveals distinctive DNA methylation patterns that associate with the Braak stage and Alzheimer’s disease progression.The entorhinal cortex emerges as a focal point due to its early histological alterations and subsequent impact on downstream regions like the hippocampus.Notably,ANK1 hypermethylation,a protein implicated in neurofibrillary tangle formation,was recurrently identified in the entorhinal cortex.Further,the middle temporal gyrus and prefrontal cortex were shown to exhibit significant hypermethylation of genes like HOXA3,RHBDF2,and MCF2L,potentially influencing neuroinflammatory processes.The complex role of BIN1 in late-onset Alzheimer’s disease is underscored by its association with altered methylation patterns.Despite the disparities across studies,these findings highlight the intricate interplay between epigenetic modifications and Alzheimer’s disease pathology.Future research efforts should address methodological variations,incorporate diverse cohorts,and consider environmental factors to unravel the nuanced epigenetic landscape underlying Alzheimer’s disease progression.展开更多
It is demonstrated by sociolinguistic variation studies that women are more likely than men to use standard speech. This paper reviews the operational methods and analytical means of classic quantitative studies in th...It is demonstrated by sociolinguistic variation studies that women are more likely than men to use standard speech. This paper reviews the operational methods and analytical means of classic quantitative studies in this field, intending to provide guidance and enlightenment for relevant studies and verifications in the context of Chinese culture.展开更多
AIM:To examine how the expression of caudal type homebox transcription factor 2(Cdx2) is regulated in the development of malignancy in Barrett's esophagus.METHODS:Cdx2,mucin(MUC) series(MUC2,MUC5AC and MUC6),p53 a...AIM:To examine how the expression of caudal type homebox transcription factor 2(Cdx2) is regulated in the development of malignancy in Barrett's esophagus.METHODS:Cdx2,mucin(MUC) series(MUC2,MUC5AC and MUC6),p53 and E-cadherin expression in Barrett's esophagus and adenocarcinoma specimens were examined by immunostaining.Isolated clusters of cells from(1) MUC2 and Cdx2-positive intestinal metaplastic mucosa;(2) MUC5AC and MUC6-positive,and MUC2 and Cdx2-negative high-grade dysplasia(HD),or intramucosal adenocarcinoma(IMC);and(3) MUC5AC,MUC6 and Cdx2-positive poorly-differentiated invasive adenocarcinoma(PDA) were analyzed by methylationspecific polymerase chain reaction using sets of primers for detecting methylation status of the Cdx2 gene.RESULTS:Most of the non-neoplastic Barrett's esophageal mucosa showing intestinal-type metaplasia with or without low-grade dysplasia was positive for E-cadherin,MUC series and Cdx2,but negative for p53.A portion of the low-grade to HD was positive for E-cadherin,MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.The definite IMC area was strongly positive for MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.Methylation of the Cdx2 promoter was not observed in intestinal metaplasia,while hypermethylation of part of its promoter was observed in hot dipped and IMC.Hypermethylation of a large fraction of the Cdx2 promoter was observed in PDA.CONCLUSION:Cdx2 expression is restored irrespective of the methylation status of its promoter.Apparent positive immunohistochemical results can be a molecular mark for gene silencing memory.展开更多
Studies examining the inheritance of inflammatory bowel disease (IBD) within different family groups have been the basis for recent molecular advances in the genetics of IBD. The derived heritability in Crohn's dis...Studies examining the inheritance of inflammatory bowel disease (IBD) within different family groups have been the basis for recent molecular advances in the genetics of IBD. The derived heritability in Crohn's disease (CD) is higher than in many other complex diseases. The risk of IBD is highest in first-degree relatives of a CD proband, but first-degree relatives of a proband suffering from ulcerative colitis (UC) and more distant relatives are also at increased risk. Disease concordance rates in IBD have been examined in multiplex families and in three large European twin studies.展开更多
Second language acquisition can not be understood without addressing the interaction between language and cognition. Cognitive theory can extend to describe learning strategies as complex cognitive skills. Theoretical...Second language acquisition can not be understood without addressing the interaction between language and cognition. Cognitive theory can extend to describe learning strategies as complex cognitive skills. Theoretical developments in Anderson’s production systems cover a broader range of behavior than other theories, including comprehension and production of oral and written texts as well as comprehension, problem solving, and verbal learning.Thus Anderson’s cognitive theory can be served as a rationale for learning strategy studies in second language acquisition.展开更多
Ewing’s sarcoma is a pediatric tumor that mainly occurs in soft tissues and bones. Malignant characteristics of Ewing’s sarcoma are correlated with expression of EWS oncogene. We achieved knockdown of EWS expression...Ewing’s sarcoma is a pediatric tumor that mainly occurs in soft tissues and bones. Malignant characteristics of Ewing’s sarcoma are correlated with expression of EWS oncogene. We achieved knockdown of EWS expression using a plasmid vector encoding EWS short hairpin RNA (shRNA) to increase anti-tumor mechanisms of taxifolin (TFL), a new flavonoid, in human Ewing’s sarcoma cells in culture and animal models. Immunofluorescence microscopy and flow cytometric analysis showed high expression of EWS in human Ewing’s sarcoma SK-N-MC and RD-ES cell lines. EWS shRNA plus TFL inhibited 80% cell viability and caused the highest decreases in EWS expression at mRNA and protein levels in both cell lines. Knockdown of EWS expression induced morphological features of differentiation. EWS shRNA plus TFL caused more alterations in molecular markers of differentiation than either agent alone. EWS shRNA plus TFL caused the highest decreases in cell migration with inhibition of survival, angiogenic and invasive factors. Knockdown of EWS expression was associated with removal of DNA methylation from p53 promoter, promoting expression of p53, Puma, and Noxa. EWS shRNA plus TFL induced the highest amounts of apoptosis with activation of extrinsic and intrinsic pathways in both cell lines in culture. EWS shRNA plus TFL also inhibited growth of Ewing’s sarcoma tumors in animal models due to inhibition of differentiation inhibitors and angiogenic and invasive factors and also induction of activation of caspase-3 for apoptosis. Collectively, knockdown of EWS expression increased various anti-tumor mechanisms of TFL in human Ewing’s sarcoma in cell culture and animal models.展开更多
In the contemporary digital age,traditional reading habits have been compromised by digital media,a situation that has forced academic libraries to adopt proactive marketing approaches to promote reading among student...In the contemporary digital age,traditional reading habits have been compromised by digital media,a situation that has forced academic libraries to adopt proactive marketing approaches to promote reading among students and faculty.This article investigates the implementation of marketing strategies in promoting reading activities within academic libraries,taking the University of Shanghai for Science and Technology as a case study.The paper explores various marketing strategies employed by academic libraries,including market segmentation,utilization of new media platforms,and the creation of personalized content for readers.Drawing from an extensive literature review and real-world examples,the study establishes a framework for marketing reading promotion activities tailored to academic libraries.These findings underscore how effective marketing strategies can enhance user participation,expand library influence,and optimize resource utilization.展开更多
The ACE (angiotensin converting enzyme) inhibitors are not only drugs widely prescribed drugs in cardiovascular diseases, but also potentially therapeutic agents in dementia. Based on the findings that the ACE inhib...The ACE (angiotensin converting enzyme) inhibitors are not only drugs widely prescribed drugs in cardiovascular diseases, but also potentially therapeutic agents in dementia. Based on the findings that the ACE inhibitors could activate the c-Jun N-terminal kinase signal to increase the ACE gene expression and that the Alu element of the human ACE gene involved in regulating ACE promoter activity, we aimed to investigate whether there are different pharmacogenetic responses of ACE I/D polymorphism to the ACE inhibitors in neurons. The three reporter vectors, pACEpro(0-SEAP, p-I-ACEpro-SEAP, and p-D-ACEpro-SEAP were used to examine the transcriptional activity of the vectors responding to the lisinopril treatment using a transient-transfection method in SH-SY5Y cells. Our results showed that lisinopril increased the promoter activity of an ACE gene by 16.7%. Additionally, we found the lisinopril enhanced the ACE promoter activity of the I-form vector by 17.2%, but adversely reduced that of the D-form vector by 16.8%, as compared with the respective control without the lisinopril treatment. Firstly, our findings had proved that the UD polymorphism of ACE gene contrarily responds to the ACE inhibitors in regulating the ACE expression in neurons, which provide a novel insight suggesting genetic testing to tailor the treatment regimens in AD (Alzheimer's disease) patients.展开更多
Objective:To generate recombinant adenovirus that could simultaneously express ornithine decarboxylase(ODC) and S-adenosylmethionine decarboxylase(AdoMetDC) antisenses specifically in prostate cancer cells,and ev...Objective:To generate recombinant adenovirus that could simultaneously express ornithine decarboxylase(ODC) and S-adenosylmethionine decarboxylase(AdoMetDC) antisenses specifically in prostate cancer cells,and evaluate its inhibitory effect on prostate cancer in vivo.Methods:Fragments of ODC and AdoMetDC genes were generated by PCR,cloned into the pPGL-PSES,and then recombined with pAdEasy-1 vectors in AdEasy-1 cells.Ad-PSES-ODC-AdoMetDCas virus was produced in HEK293 cells.Following transfection with Ad-PSES-ODC-AdoMetDCas,the levels of ODC or AdoMetDC were determined by RT-PCR and western blot assays.The effect of Ad-PSES-ODC-AdoMetDCas treatment on tumor formation and growth was evaluated in xenograft models of prostate cancers in vivo.Results:The plasmid pAdEasy-PSES-ODC-AdoMetDCas was successfully constructed and the recombinant Ad-PSES-ODC-AdoMetDCas adenovirus was produced.Transfection with Ad-PSES-ODC-AdoMetDCas adenovirus significantly inhibited the expression of ODC and AdoMetDC genes specifically in prostate DU145 cells,but not H1299,HT29 and HepG2 cancer cells,and disrupted the ability of DU145 cells to form solid prostate cancer in vivo.Intratumoral treatment with Ad-PSES-ODC-AdoMetDCas adenovirus significantly inhibited the growth of engrafted prostate tumors in vivo.Conclusion:The recombinant Ad-PSES-ODC-AdoMetDCas adenovirus specifically reduces the expression of both ODC and AdoMetDC genes in prostate cells and may be used for treatment of prostate cancers at the clinic.展开更多
BACKGROUND; Polymorphisms of urokinase-type plasminogen activator gene (PLAU) have recently been reported to be associated with sporadic Alzheimer' disease (SAD). However, most studies have focused on the exon re...BACKGROUND; Polymorphisms of urokinase-type plasminogen activator gene (PLAU) have recently been reported to be associated with sporadic Alzheimer' disease (SAD). However, most studies have focused on the exon region of this gene, and there is no report on the association between promoter polymorphisms of the PLAU and SAD. OBJECTIVE: To determine whether SAD is associated with promoter polymorphisms of PLAU in Northem Han Chinese. DESIGN, TIME AND SETTING: A case-control study was performed at Neurology Laboratory of Xuanwu Hospital of the Capital Medical University from September 2006 to July 2008. PARTICIPANTS: A total of 397 participants living in Beijing were assigned to SAD [n = 196, including 103 males and 93 females, mean age of (64 ± 7) years] and control [n = 201, including 108 males and 93 females, mean age of (68 ± 6) years] groups. The patients were diagnosed and met the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorder Association criteria for possible Alzheimer's disease. Controls received clinical, mental, and neurological examinations to rule out cognitive deficiencies. All controls had Mini-Mental Status Examination scores 〉 27. METHODS: Genotypes of PLAU and apolipoprotein-E were examined in 196 patients with SAD and 201 age- and sex-matched controls from the same community using polymerase chain reaction-restriction fragment length polymorphism method. SPSS 11.5 software was used for data analysis, distribution of allele and genotypic frequency were calculated, and Hardy-Weinberg was also performed in this study. MAIN OUTCOME MEASURES: The main outcome measures were allele and genotype frequency differences in the promoter region of the PLAU gene between SAD and control subjects. RESULTS: In Chinese Han populations, the two polymorphisms in PLAU promoter were -25 C/T (rs2227579) and 43 G/T (rs2227580). Detection of these promoter polymorphisms revealed significant differences in allele and genotype frequency for -25 CfT and 43 G/T when 196 SAD patients were compared with 201 controls (P〈 0.05). Logistic analyses indicated that, compared with C/T and T/T genotypes, the -25 C/C genotype resulted in a 1.5-fold risk for developing SAD (adjusted odds ratio = 1.510, 95% confidence interval: 0.198 2.281, P= 0.010), while the 43G/G genotype resulted in a 1.3-fold risk for SAD (adjusted odds ratio = 1.300, 95% confidence interval: 0.178 2.051, P= 0.030). CONCLUSION: The present study provided evidence that promoter polymorphisms of PLAU are associated with development of SAD in Northern Han Chinese.展开更多
The promoter region of cauliflower mosaic virus (CaMV) 35s RNA was employed to construct an intermediate expression vector which can be used in Ti plasmid system of Agro-bacterium tumefaciens. The original plasmid, wh...The promoter region of cauliflower mosaic virus (CaMV) 35s RNA was employed to construct an intermediate expression vector which can be used in Ti plasmid system of Agro-bacterium tumefaciens. The original plasmid, which contains a polylinker between CaMV 35s RNA and its 3' termination signal in pUC18 was modified to have another antibiotic resistance marker (kanamycin resistance gene Kmr) to facilitate the selection of recombinant with Ti plasmid. Octopine synthase (ocs) structural gene was inserted into this vector downstream of CaMV 35s RNA promoter. This chimaeric gene was introduced into integrative Ti plasmid vector pGV3850, and then transformed into Nicotiana tobaccum cells. A binary plasmid vector was also used to introduce the chimaeric gene into tobacco cells. In both cases, the expression of ocs gene was demonstrated. The amount of oc-topine was much more than the nopaline synthesized by no-paline synthase (nos) gene transferred at the same time with Ti plasmid vector. This demonstrated that CaMV 35s RNA promoter is stronger in transcriptional function than the promoter of nos in tobacco cells.展开更多
Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumo...Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression, localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 m RNA was assayed.Results Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion; pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in vitro.Conclusion HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.展开更多
Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumo...Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression, localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 m RNA was assayed.Results Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion; pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in vitro.Conclusion HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.展开更多
Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumo...Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of hepatocellular carcinoma(HCC) patients were screened by PCR and direct sequencing.All patients carried HBV with genotype C,except for one B/C heterozygote.The expression,localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro.The expression of endoplasmic reticulum(ER) GRP78 mRNA was assayed.Results Four patterns of pre-S mutations were identified:pre-S 1 in-frame deletion involving the first start codon;pre-S2 in-frame deletion;pre-S2 start codon mutation with or without in-frame deletion;and S promoter in-frame deletion(ASP).The first two types were evenly found in both tumor and non-tumor tissues.They were rarely present as dominant strains.The last two types were frequently found in the dominant strains in tumor tissues.The overall prevalence of HBV carrying ASP was 17.64%(6/34) in tumor tissues,but none were dominant in nontumor tissues.HBV carrying ASP was unable to produce S protein in vitro.Immunocytofluorescence assay showed that the ASP LHBs mutant aggregated in the cytoplasm,accumulating mainly in the ER.Transient transfection and expression of ASP mutant caused GRP78 up-regulation in vitro.Conclusions HBV S promoter deletion was found dominantly in HCC tumor tissue.The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.展开更多
Huntington’s disease(HD)is a currently incurable,late onset,progressive,ultimately fatal neurological disorder(Bates et al.,2015).We have recently published the results of comprehensive genetic interaction tests ...Huntington’s disease(HD)is a currently incurable,late onset,progressive,ultimately fatal neurological disorder(Bates et al.,2015).We have recently published the results of comprehensive genetic interaction tests aimed at identification of histone methyltransferases and demethylases involved in HD pathogenesis in a Drosophila model of the disease(Song et al.,2018).展开更多
Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumo...Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression,localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 mRNA was assayed.Results Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion;pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in vitro.Conclusion HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.展开更多
Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumo...Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression, localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 m RNA was assayed.Results Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion; pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in vitro.Conclusion HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.展开更多
Prospective real-world data from large patient samples, which re- port on the long-term effectiveness of the employed different drug therapies, are rare in Parkinson's disease (PD). The non interven- tional "Trans...Prospective real-world data from large patient samples, which re- port on the long-term effectiveness of the employed different drug therapies, are rare in Parkinson's disease (PD). The non interven- tional "Transdermal Rotigotine User Surveillance Study" (TRUST) trial represents such a real-world study. It investigated long-term treatment with different dopamine substituting treatment regimens in 2195 PD patients (Mfiller et al., 2018). Participation in TRUST meant that the treating neurologists were only asked to document and modify the dopaminergic drug regimen without any prior PD patient selection criteria. Thus this unique trial design reflects the real world of patient maintenance.展开更多
[ Objective ] This study aimed to investigate the major contributors to the measurement uncertainty in quantitative analysis of genetically modified ingreclients and improve the quality of quantitative detection of ge...[ Objective ] This study aimed to investigate the major contributors to the measurement uncertainty in quantitative analysis of genetically modified ingreclients and improve the quality of quantitative detection of genetically modified components. [ Method] The content of CaMV35S promoter (parameter) in GTS40- 3-2 soybean powder samples was measured to estimate the measurement uncertainty preliminarily. [ Result] Type A uncertainty (uA) ' type B uncertainty (uB) and combined standard uncertainty (Uc) were 0.0 004, 0.002 and 0.002, respectively. At a confidence level ofp = 95% and freedom degree of Voff = 3 251, coverage factor k = 1.96, expanded uncertainty U = 0.004. The final measurement result was C = 0.028 ± 0. 004, which was dose to the conventional true value (0.03). Thus, the measurement uncertainty was relatively small, indicating a high quality of measurement. In this study, uncertainty evaluation indicated that the deviation of micro liquid transfer made the greatest contribution to the measurement uncertainty. [ Cludusion ] The deviation of micro liquid transfer should be reduced to im- prove the quality of measurement.展开更多
China Society for Human Rights Studies, I would like to extend my warm greetings to the launch of your Human Rights magazine. Enjoying human rights fully is a lofty goal long pursued after by human race. Over the year...China Society for Human Rights Studies, I would like to extend my warm greetings to the launch of your Human Rights magazine. Enjoying human rights fully is a lofty goal long pursued after by human race. Over the years when they carried out revolution, construction and reforms, the Chinese people have struggled indomitably and strived incessantly to achieve this goal. Progress made in this regard has caught worldwide attention. When struggling for, safeguarding, promoting and developing human rights, the Chinese people have always combined the universality prin-展开更多
文摘The intricacies of Alzheimer’s disease pathogenesis are being increasingly illuminated by the exploration of epigenetic mechanisms,particularly DNA methylation.This review comprehensively surveys recent human-centered studies that investigate whole genome DNA methylation in Alzheimer’s disease neuropathology.The examination of various brain regions reveals distinctive DNA methylation patterns that associate with the Braak stage and Alzheimer’s disease progression.The entorhinal cortex emerges as a focal point due to its early histological alterations and subsequent impact on downstream regions like the hippocampus.Notably,ANK1 hypermethylation,a protein implicated in neurofibrillary tangle formation,was recurrently identified in the entorhinal cortex.Further,the middle temporal gyrus and prefrontal cortex were shown to exhibit significant hypermethylation of genes like HOXA3,RHBDF2,and MCF2L,potentially influencing neuroinflammatory processes.The complex role of BIN1 in late-onset Alzheimer’s disease is underscored by its association with altered methylation patterns.Despite the disparities across studies,these findings highlight the intricate interplay between epigenetic modifications and Alzheimer’s disease pathology.Future research efforts should address methodological variations,incorporate diverse cohorts,and consider environmental factors to unravel the nuanced epigenetic landscape underlying Alzheimer’s disease progression.
文摘It is demonstrated by sociolinguistic variation studies that women are more likely than men to use standard speech. This paper reviews the operational methods and analytical means of classic quantitative studies in this field, intending to provide guidance and enlightenment for relevant studies and verifications in the context of Chinese culture.
基金Supported by Grant-in Aid from Ministry of Education,Sports and Culture (GP Program for Basic Science),Japan
文摘AIM:To examine how the expression of caudal type homebox transcription factor 2(Cdx2) is regulated in the development of malignancy in Barrett's esophagus.METHODS:Cdx2,mucin(MUC) series(MUC2,MUC5AC and MUC6),p53 and E-cadherin expression in Barrett's esophagus and adenocarcinoma specimens were examined by immunostaining.Isolated clusters of cells from(1) MUC2 and Cdx2-positive intestinal metaplastic mucosa;(2) MUC5AC and MUC6-positive,and MUC2 and Cdx2-negative high-grade dysplasia(HD),or intramucosal adenocarcinoma(IMC);and(3) MUC5AC,MUC6 and Cdx2-positive poorly-differentiated invasive adenocarcinoma(PDA) were analyzed by methylationspecific polymerase chain reaction using sets of primers for detecting methylation status of the Cdx2 gene.RESULTS:Most of the non-neoplastic Barrett's esophageal mucosa showing intestinal-type metaplasia with or without low-grade dysplasia was positive for E-cadherin,MUC series and Cdx2,but negative for p53.A portion of the low-grade to HD was positive for E-cadherin,MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.The definite IMC area was strongly positive for MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.Methylation of the Cdx2 promoter was not observed in intestinal metaplasia,while hypermethylation of part of its promoter was observed in hot dipped and IMC.Hypermethylation of a large fraction of the Cdx2 promoter was observed in PDA.CONCLUSION:Cdx2 expression is restored irrespective of the methylation status of its promoter.Apparent positive immunohistochemical results can be a molecular mark for gene silencing memory.
文摘Studies examining the inheritance of inflammatory bowel disease (IBD) within different family groups have been the basis for recent molecular advances in the genetics of IBD. The derived heritability in Crohn's disease (CD) is higher than in many other complex diseases. The risk of IBD is highest in first-degree relatives of a CD proband, but first-degree relatives of a proband suffering from ulcerative colitis (UC) and more distant relatives are also at increased risk. Disease concordance rates in IBD have been examined in multiplex families and in three large European twin studies.
文摘Second language acquisition can not be understood without addressing the interaction between language and cognition. Cognitive theory can extend to describe learning strategies as complex cognitive skills. Theoretical developments in Anderson’s production systems cover a broader range of behavior than other theories, including comprehension and production of oral and written texts as well as comprehension, problem solving, and verbal learning.Thus Anderson’s cognitive theory can be served as a rationale for learning strategy studies in second language acquisition.
文摘Ewing’s sarcoma is a pediatric tumor that mainly occurs in soft tissues and bones. Malignant characteristics of Ewing’s sarcoma are correlated with expression of EWS oncogene. We achieved knockdown of EWS expression using a plasmid vector encoding EWS short hairpin RNA (shRNA) to increase anti-tumor mechanisms of taxifolin (TFL), a new flavonoid, in human Ewing’s sarcoma cells in culture and animal models. Immunofluorescence microscopy and flow cytometric analysis showed high expression of EWS in human Ewing’s sarcoma SK-N-MC and RD-ES cell lines. EWS shRNA plus TFL inhibited 80% cell viability and caused the highest decreases in EWS expression at mRNA and protein levels in both cell lines. Knockdown of EWS expression induced morphological features of differentiation. EWS shRNA plus TFL caused more alterations in molecular markers of differentiation than either agent alone. EWS shRNA plus TFL caused the highest decreases in cell migration with inhibition of survival, angiogenic and invasive factors. Knockdown of EWS expression was associated with removal of DNA methylation from p53 promoter, promoting expression of p53, Puma, and Noxa. EWS shRNA plus TFL induced the highest amounts of apoptosis with activation of extrinsic and intrinsic pathways in both cell lines in culture. EWS shRNA plus TFL also inhibited growth of Ewing’s sarcoma tumors in animal models due to inhibition of differentiation inhibitors and angiogenic and invasive factors and also induction of activation of caspase-3 for apoptosis. Collectively, knockdown of EWS expression increased various anti-tumor mechanisms of TFL in human Ewing’s sarcoma in cell culture and animal models.
文摘In the contemporary digital age,traditional reading habits have been compromised by digital media,a situation that has forced academic libraries to adopt proactive marketing approaches to promote reading among students and faculty.This article investigates the implementation of marketing strategies in promoting reading activities within academic libraries,taking the University of Shanghai for Science and Technology as a case study.The paper explores various marketing strategies employed by academic libraries,including market segmentation,utilization of new media platforms,and the creation of personalized content for readers.Drawing from an extensive literature review and real-world examples,the study establishes a framework for marketing reading promotion activities tailored to academic libraries.These findings underscore how effective marketing strategies can enhance user participation,expand library influence,and optimize resource utilization.
文摘The ACE (angiotensin converting enzyme) inhibitors are not only drugs widely prescribed drugs in cardiovascular diseases, but also potentially therapeutic agents in dementia. Based on the findings that the ACE inhibitors could activate the c-Jun N-terminal kinase signal to increase the ACE gene expression and that the Alu element of the human ACE gene involved in regulating ACE promoter activity, we aimed to investigate whether there are different pharmacogenetic responses of ACE I/D polymorphism to the ACE inhibitors in neurons. The three reporter vectors, pACEpro(0-SEAP, p-I-ACEpro-SEAP, and p-D-ACEpro-SEAP were used to examine the transcriptional activity of the vectors responding to the lisinopril treatment using a transient-transfection method in SH-SY5Y cells. Our results showed that lisinopril increased the promoter activity of an ACE gene by 16.7%. Additionally, we found the lisinopril enhanced the ACE promoter activity of the I-form vector by 17.2%, but adversely reduced that of the D-form vector by 16.8%, as compared with the respective control without the lisinopril treatment. Firstly, our findings had proved that the UD polymorphism of ACE gene contrarily responds to the ACE inhibitors in regulating the ACE expression in neurons, which provide a novel insight suggesting genetic testing to tailor the treatment regimens in AD (Alzheimer's disease) patients.
基金supported by the National Natural Science Foundation of China(No.30900730)the grants from the Natural Science Foundation of Shangdong Province(No.Q2007D01)
文摘Objective:To generate recombinant adenovirus that could simultaneously express ornithine decarboxylase(ODC) and S-adenosylmethionine decarboxylase(AdoMetDC) antisenses specifically in prostate cancer cells,and evaluate its inhibitory effect on prostate cancer in vivo.Methods:Fragments of ODC and AdoMetDC genes were generated by PCR,cloned into the pPGL-PSES,and then recombined with pAdEasy-1 vectors in AdEasy-1 cells.Ad-PSES-ODC-AdoMetDCas virus was produced in HEK293 cells.Following transfection with Ad-PSES-ODC-AdoMetDCas,the levels of ODC or AdoMetDC were determined by RT-PCR and western blot assays.The effect of Ad-PSES-ODC-AdoMetDCas treatment on tumor formation and growth was evaluated in xenograft models of prostate cancers in vivo.Results:The plasmid pAdEasy-PSES-ODC-AdoMetDCas was successfully constructed and the recombinant Ad-PSES-ODC-AdoMetDCas adenovirus was produced.Transfection with Ad-PSES-ODC-AdoMetDCas adenovirus significantly inhibited the expression of ODC and AdoMetDC genes specifically in prostate DU145 cells,but not H1299,HT29 and HepG2 cancer cells,and disrupted the ability of DU145 cells to form solid prostate cancer in vivo.Intratumoral treatment with Ad-PSES-ODC-AdoMetDCas adenovirus significantly inhibited the growth of engrafted prostate tumors in vivo.Conclusion:The recombinant Ad-PSES-ODC-AdoMetDCas adenovirus specifically reduces the expression of both ODC and AdoMetDC genes in prostate cells and may be used for treatment of prostate cancers at the clinic.
基金the National Key Technology R&D Program in the Eleventh Five-year Plan Period,No.2006BAI02B01the National Basic Research 973 Program,No.2006CB500700+1 种基金the Beijing Natural Science Foundation,No.7071004Funding Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality
文摘BACKGROUND; Polymorphisms of urokinase-type plasminogen activator gene (PLAU) have recently been reported to be associated with sporadic Alzheimer' disease (SAD). However, most studies have focused on the exon region of this gene, and there is no report on the association between promoter polymorphisms of the PLAU and SAD. OBJECTIVE: To determine whether SAD is associated with promoter polymorphisms of PLAU in Northem Han Chinese. DESIGN, TIME AND SETTING: A case-control study was performed at Neurology Laboratory of Xuanwu Hospital of the Capital Medical University from September 2006 to July 2008. PARTICIPANTS: A total of 397 participants living in Beijing were assigned to SAD [n = 196, including 103 males and 93 females, mean age of (64 ± 7) years] and control [n = 201, including 108 males and 93 females, mean age of (68 ± 6) years] groups. The patients were diagnosed and met the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorder Association criteria for possible Alzheimer's disease. Controls received clinical, mental, and neurological examinations to rule out cognitive deficiencies. All controls had Mini-Mental Status Examination scores 〉 27. METHODS: Genotypes of PLAU and apolipoprotein-E were examined in 196 patients with SAD and 201 age- and sex-matched controls from the same community using polymerase chain reaction-restriction fragment length polymorphism method. SPSS 11.5 software was used for data analysis, distribution of allele and genotypic frequency were calculated, and Hardy-Weinberg was also performed in this study. MAIN OUTCOME MEASURES: The main outcome measures were allele and genotype frequency differences in the promoter region of the PLAU gene between SAD and control subjects. RESULTS: In Chinese Han populations, the two polymorphisms in PLAU promoter were -25 C/T (rs2227579) and 43 G/T (rs2227580). Detection of these promoter polymorphisms revealed significant differences in allele and genotype frequency for -25 CfT and 43 G/T when 196 SAD patients were compared with 201 controls (P〈 0.05). Logistic analyses indicated that, compared with C/T and T/T genotypes, the -25 C/C genotype resulted in a 1.5-fold risk for developing SAD (adjusted odds ratio = 1.510, 95% confidence interval: 0.198 2.281, P= 0.010), while the 43G/G genotype resulted in a 1.3-fold risk for SAD (adjusted odds ratio = 1.300, 95% confidence interval: 0.178 2.051, P= 0.030). CONCLUSION: The present study provided evidence that promoter polymorphisms of PLAU are associated with development of SAD in Northern Han Chinese.
文摘The promoter region of cauliflower mosaic virus (CaMV) 35s RNA was employed to construct an intermediate expression vector which can be used in Ti plasmid system of Agro-bacterium tumefaciens. The original plasmid, which contains a polylinker between CaMV 35s RNA and its 3' termination signal in pUC18 was modified to have another antibiotic resistance marker (kanamycin resistance gene Kmr) to facilitate the selection of recombinant with Ti plasmid. Octopine synthase (ocs) structural gene was inserted into this vector downstream of CaMV 35s RNA promoter. This chimaeric gene was introduced into integrative Ti plasmid vector pGV3850, and then transformed into Nicotiana tobaccum cells. A binary plasmid vector was also used to introduce the chimaeric gene into tobacco cells. In both cases, the expression of ocs gene was demonstrated. The amount of oc-topine was much more than the nopaline synthesized by no-paline synthase (nos) gene transferred at the same time with Ti plasmid vector. This demonstrated that CaMV 35s RNA promoter is stronger in transcriptional function than the promoter of nos in tobacco cells.
基金supported by grants from the National Projects on Major Infectious Diseases,Ministry of Science and Technolog of China(No.2009ZX10004-903)the Doctoral Fund of Ministry of Education of China(No.20100001110055)
文摘Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression, localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 m RNA was assayed.Results Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion; pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in vitro.Conclusion HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.
基金supported by grants from the National Projects on Major Infectious Diseases,Ministry of Science and Technolog of China(No.2009ZX10004-903)the Doctoral Fund of Ministry of Education of China(No.20100001110055)
文摘Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression, localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 m RNA was assayed.Results Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion; pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in vitro.Conclusion HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.
基金supported by grants from the National Projects on Major Infectious Diseases, Ministry of Science and Technolog of China(No. 2009ZX10004-903)the Doctoral Fund of Ministry of Education of China(No.20100001110055)
文摘Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of hepatocellular carcinoma(HCC) patients were screened by PCR and direct sequencing.All patients carried HBV with genotype C,except for one B/C heterozygote.The expression,localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro.The expression of endoplasmic reticulum(ER) GRP78 mRNA was assayed.Results Four patterns of pre-S mutations were identified:pre-S 1 in-frame deletion involving the first start codon;pre-S2 in-frame deletion;pre-S2 start codon mutation with or without in-frame deletion;and S promoter in-frame deletion(ASP).The first two types were evenly found in both tumor and non-tumor tissues.They were rarely present as dominant strains.The last two types were frequently found in the dominant strains in tumor tissues.The overall prevalence of HBV carrying ASP was 17.64%(6/34) in tumor tissues,but none were dominant in nontumor tissues.HBV carrying ASP was unable to produce S protein in vitro.Immunocytofluorescence assay showed that the ASP LHBs mutant aggregated in the cytoplasm,accumulating mainly in the ER.Transient transfection and expression of ASP mutant caused GRP78 up-regulation in vitro.Conclusions HBV S promoter deletion was found dominantly in HCC tumor tissue.The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.
基金supported by Hungarian National Research,Development and Innovation Office(NKFIH) grants K-112294GINOP-2.3.2-15-2016-00032 and GINOP-2.3.2-15-2016-00034 to LB
文摘Huntington’s disease(HD)is a currently incurable,late onset,progressive,ultimately fatal neurological disorder(Bates et al.,2015).We have recently published the results of comprehensive genetic interaction tests aimed at identification of histone methyltransferases and demethylases involved in HD pathogenesis in a Drosophila model of the disease(Song et al.,2018).
基金supported by grants from the National Projects on Major Infectious Diseases,Ministry of Science and Technolog of China(No.2009ZX10004-903)and the Doctoral Fund of Ministry of Education of China(No.20100001110055)
文摘Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression,localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 mRNA was assayed.Results Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion;pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in vitro.Conclusion HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.
基金supported by grants from the National Projects on Major Infectious Diseases,Ministry of Science and Technolog of China(No.2009ZX10004-903)the Doctoral Fund of Ministry of Education of China(No.20100001110055)
文摘Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue specific.Methods HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression, localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 m RNA was assayed.Results Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion; pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in vitro.Conclusion HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.
文摘Prospective real-world data from large patient samples, which re- port on the long-term effectiveness of the employed different drug therapies, are rare in Parkinson's disease (PD). The non interven- tional "Transdermal Rotigotine User Surveillance Study" (TRUST) trial represents such a real-world study. It investigated long-term treatment with different dopamine substituting treatment regimens in 2195 PD patients (Mfiller et al., 2018). Participation in TRUST meant that the treating neurologists were only asked to document and modify the dopaminergic drug regimen without any prior PD patient selection criteria. Thus this unique trial design reflects the real world of patient maintenance.
基金Supported by Project of Standardized Technology System of Sichuan Bureau of Quality and Technical Supervision(ZYBZ2013-39)
文摘[ Objective ] This study aimed to investigate the major contributors to the measurement uncertainty in quantitative analysis of genetically modified ingreclients and improve the quality of quantitative detection of genetically modified components. [ Method] The content of CaMV35S promoter (parameter) in GTS40- 3-2 soybean powder samples was measured to estimate the measurement uncertainty preliminarily. [ Result] Type A uncertainty (uA) ' type B uncertainty (uB) and combined standard uncertainty (Uc) were 0.0 004, 0.002 and 0.002, respectively. At a confidence level ofp = 95% and freedom degree of Voff = 3 251, coverage factor k = 1.96, expanded uncertainty U = 0.004. The final measurement result was C = 0.028 ± 0. 004, which was dose to the conventional true value (0.03). Thus, the measurement uncertainty was relatively small, indicating a high quality of measurement. In this study, uncertainty evaluation indicated that the deviation of micro liquid transfer made the greatest contribution to the measurement uncertainty. [ Cludusion ] The deviation of micro liquid transfer should be reduced to im- prove the quality of measurement.
文摘China Society for Human Rights Studies, I would like to extend my warm greetings to the launch of your Human Rights magazine. Enjoying human rights fully is a lofty goal long pursued after by human race. Over the years when they carried out revolution, construction and reforms, the Chinese people have struggled indomitably and strived incessantly to achieve this goal. Progress made in this regard has caught worldwide attention. When struggling for, safeguarding, promoting and developing human rights, the Chinese people have always combined the universality prin-