Preeclampsia (PE) is a common pregnancy complication with a high mortality rate. Abnormally activated endoplasmic reticulum stress (ERS) is believed to be responsible for the destruction of key placental cells-trophoblasts. Phenylbutyric acid (4-PBA), an ERS inhibitor, is involved in regulating the development of ERS-related diseases. At present, how 4-PBA affects trophoblasts and its mechanisms is still unclear. In this study, PE cell models were established by stimulating HTR-8/SVneo cells with hypoxia. To verify the underlying mechanisms of 4-PBA on PE, CCT020312, an activator of PERK, was also used. The results showed that 4-PBA restored hypoxia-induced trophoblast viability, inhibited HIF-1α protein expression, inflammation, and PERK/ATF-4/CHOP pathway. Hoechst 33342 staining and flow cytometry results confirmed that 4-PBA decreased hypoxia-induced apoptosis in trophoblasts. The results of the JC-1 analysis and apoptosis initiation enzyme activity assay also demonstrated that 4-PBA inhibited apoptosis related to the mitochondrial pathway. Furthermore, by detecting autophagy in trophoblasts, an increased number of autophagic vesicles, damaged mitochondria, enhanced dansylcadaverine fluorescence, enhanced levels of autophagy proteins Beclin-1, LC3II, and decreased p62 were seen in hypoxia-stimulated cells. These changes were reversed by 4-PBA. Furthermore, it was observed that CCT020312 reversed the effects of 4-PBA on the viability, apoptosis, and autophagosome number of hypoxia-induced trophoblasts. In summary, 4-PBA reduces autophagy and apoptosis via the PERK/ATF-4/CHOP pathway and mitochondrial pathway, thereby restoring the viability of hypoxic trophoblasts. These findings provide a solid evidence base for the use of 4-PBA in PE treatment and guide a new direction for improving the outcomes of patients with PE.

Background: Paired-like Homeobox 2B (PHOX2B) is considered the causative gene of Congenital Central Hypoventilation Syndrome (CCHS), a dominant genetic disorder characterized by impaired central respiratory control and subsequent hypoventilation during sleep. Methods: Herein, we present a family with recurrent severe CCHS. The potential causative genetic variant was confirmed through Whole-Exome Sequencing (WES), Sanger sequencing, and droplet digital PCR (ddPCR). Furthermore, prenatal diagnosis was performed on the proband's mother at 20 weeks of her fourth pregnancy upon request. Results: The proband and her brother were both carriers of the PHOX2B polyalanine expansion variant: c.744_758dupCGCGGCAGCGGCGGCGGCGGC. Sanger sequencing revealed that the proband's father had a small variant peak in the gene position, implying potential somatic mosaicism. In addition, ddPCR results showed that the proband's father had germline mosaicism, with a mosaicism proportion of 14.3%. Notably, the detect p. (Ala241[26]) variant was not detected in the fetus. Conclusions: These findings have important implications for improving genetic counseling of CCHS families as they suggest that even parents without CCHS symptoms may have somatic chimerism, necessitating careful genetic counseling and consideration of prenatal testing for subsequent pregnancies.

Background: Preeclampsia (PE) is an idiopathic disorder of pregnancy. The exact cause of PE remains unknown. Emerging evidence indicates that the cause of PE is linked to genetic factors. Therefore, the aim of this study was to identify the susceptibility genes for PE.Methods: Nine families with severe PE were recruited. The whole-exome sequencing (WES) was performed on each family, and Sanger sequencing was used to identify the potential pathogenic genetic variants.Results: After a rigorous bioinformatics analysis, compound heterozygous variants in the NPFFR2 gene, NM_004885.2: c.601A > G, p.Met201Val and c.995C > T, p.Ala332Val were found in the No.4 pedigree. Bio-informatics analysis showed that these sites were highly conserved among several species and were predicted to be pathogenic variants according to multiple online mutational function prediction software packages. Due to the compound heterozygous variants of NPFFR2, more bonds are generated between mutant amino acids and spatial adjacent amino acids, which may lead to more stable active conformation of protein and not easy to be degraded.Conclusions: We demonstrated for the first time that compound heterozygous variants of the NPFFR2 gene might be potentially associated with severe PE, the results of this study provide clinicians and researchers with a better understanding of the molecular mechanisms underlying severe PE in pregnant women.

BACKGROUND:Preeclampsia (PE), a pregnancy specific syndrome, is one kind of common gestational hypertension disease, which can cause maternal and perinatal mortality and morbidity. This study was conducted to identify key microRNAs (miRNAs), mRNAs and related signaling pathways in the pathogenesis of PE.METHODS:Whole transcriptome sequencing and small RNA sequencing of the peripheral blood from 3 PE patients and 3 normal pregnant women were performed. Differential expressed (DE) miRNAs were identified using the DEseq2 package. Target genes of the selected upregulated and downregulated DE miRNAs were predicted. Based on the hypergeometric distribution of DE miRNA target genes, we analyzed GO enrichment and KEGG pathway enrichment using R.RESULTS:Total 1291 and 1281 novel RNAs were obtained from the preeclampsia patients and healthy individuals. 70 miRNAs were screened out with significant levels with 51 significantly upregulated and 19 significantly downregulated. 44,306 genes were predicted as the targets of these miRNAs. Besides, KEGG pathway analysis revealed that the upregulated miRNAs were enriched in Glycosaminoglycan biosynthesis-chondroitin sulfate / dermatan sulfate, Base excision repair and the downregulated miRNAs were enriched in Tuberculosis, Phagosome.CONCLUSION:We constructed regulatory networks of miRNAs and target genes, there were 2208 negative miRNA-mRNA interactions in total. The network and pathway information illustrate the potential functions of mRNAs and miRNAs in PE pathogenesis.

目的 对一个生育过脊髓性肌萎缩症患儿的家系进行产前诊断,同时对三种实验室检测技术进行方法学的比较.方法 应用荧光定量PCR、荧光PCR-毛细管电泳法及MLPA对家系外周血样本及绒毛组织、羊水组织进行了检测.同时进行了亲缘鉴定以排除母源污染.结果 第一胎患儿为SMN1基因7、8号外显子纯合缺失合并SMN2基因的3拷贝重复,患儿父亲为SMN1基因第7、8号外显子的杂合缺失携带者合并SMN2基因的3拷贝重复,患儿母亲为SMN1基因第7、8号外显子的杂合缺失携带者,SMN2基因2拷贝.本次妊娠胎儿为SMN1基因第7、8号外显子杂合缺失及SMN2基因3拷贝重复.结论 经检测胎儿仅为SMN1基因杂合缺失的携带者,可继续正常妊娠.同时,荧光PCR-毛细管电泳法和MLPA可同时对SMN1和SMN2基因拷贝数进行检测,检测较为全面,但荧光定量PCR检测操作方便,检测周期短,适合大样本人群的普筛.

Abstract Background: Hirschsprung’s disease (HSCR), a congenital disorder characterized by spasticity and narrowing of the distal colon, as well as abnormalities in peristalsis and defecation, is caused by a deficit of the enteric nervous system of the distal gut. Total colonic aganglionosis (TCA) is a rare type of HSCR. This study aimed to find key microRNAs (miRNAs) and their associated genes from plasma-derived exosomes, as potential biomarkers to study TCA pathogenesis.Results: Plasma-derived exosomal miRNA sequencing of samples from 9 children with HSCR and 10 matched children without HSCR revealed that 62 miRNAs were differentially expressed in plasma-derived exosomes, of which 31 were up-regulated and 31 were down-regulated. The target genes of DEM are predicted from three common databases.There were 652 DEM target gene pairs for the 31 DEMs that were up-regulated and 234 pairs for the 31 DEMs that were down-regulated. Furthermore, 4 DEMs: miR-106b-5p, miR-205-5p, miR-375-3p and miR-34a-5p were differentially expressed between other HSCR types and TCA.Conclusions: Four key miRNAs (miR-106b-5p, miR-205-5p, miR-375-3p, and miR-34a-5p) and their interacting four key genes AF4/FMR2 family member 4 (AFF4), myotubularin-related protein 9 gene (MTMR9), POU domain class 2 transcription factor 1 (POU2F1), and WW-and-C2-domain-containing(WWC2) may be involved in the pathogenesis of TCA.

OBJECTIVE:Fetal growth restriction (FGR) refers to impaired and insufficient intrauterine growth potential caused by a variety of adverse factors and is a serious perinatal complication that leads to fetal or neonatal mortality and morbidity. FGR has numerous causes, and its pathogenesis has not been fully understood. Recently, increasing numbers of researchers have begun to focus on the placenta, the only link between the fetus and the mother. The placenta is a vital organ that plays key roles in fetal development. PLAC1 is a trophoblast-specific gene located on the X chromosome and is important for placental development. However, the biological role of PLAC1 in fetal growth restriction is not well understood. In this study, we investigated the changes in the expression of placental-specific protein 1(PLAC1) in the placentas of pregnant women with FGR and in the placentas of normal pregnancies. We also explored the regulation of PLAC1 in the growth of trophoblast cells.METHODS:Western blotting was used to detect the expression of PLAC1 in FGR and in normal placenta tissues. Cell counting kit 8 (CCK-8), wound healing, and transwell assays were used to detect the effects of PLAC1 knockdown on trophoblast cell proliferation, migration, and invasion. Western blotting was used to detect the expression of PLAC1 under hypoxic conditions, and the cell viability and apoptosis of trophoblast cells in a low oxygen concentration after overexpression of PLAC1 were detected by CCK-8 and flow cytometry assay.RESULTS:Compared with the placentas in the control group of normal pregnancies, the expression of PLAC1 in the placentas of the FGR group was significantly down-regulated (p<0.05). Knocking down PLAC1 by siRNA significantly inhibited the proliferation, migration, and invasion of trophoblast cells. After treatment with alow oxygen concentration, the expression of PLAC1 protein was significantly reduced (p<0.05). The overexpression of PLAC1 can reverse the cell viability of trophoblast cells (p<0.05) and inhibit apoptosis of trophoblast cells (p<0.05) in low oxygen concentration.CONCLUSION:The expression of PLAC1 was reduced in fetal growth restriction and did not protect trophoblast cells from hypoxic damage, suggesting that PLAC1 may be an important regulator in the occurrence of fetal growth restriction.

Background Molecular genetic testing for the 11p15-associated imprinting disorder Beckwith-Wiedemann syndrome (BWS) is challenging because of the molecular heterogeneity and complexity of the affected imprinted regions. An integrated molecular approach to analyze the epigenetic-genetic alterations is required for accurate diagnosis of BWS. Case presentation : We reported a Chinese case with BWS detected by SNP array analysis and methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA). The genetic analysis showed a de novo duplication of 24 Mb at 11p15.5p14.3 is much longer than ever reported. MS-MLPA showed copy number changes with a peak height ratio value of 1.5 (three copies) at 11p15. The duplication of paternal origin with increase of methylation index of 0.68 at H19 and decreased methylation index of 0.37 at KCNQ1OT1 . Conclusion Combined chromosome microarray analysis and methylation profiling provided reliable diagnosis for this paternally derived duplication of BWS. The phenotype associated with 11p15 duplications depends on the size, genetic content, parental inheritance and imprinting status. Identification of these rare duplications is crucial for genetic counselling.

目的 探讨孕妇血清尿酸水平与其妊娠期高血压疾病(HDP)严重程度之间的相关性.方法 选取2016年12月-2019年10月该院待产的200例孕妇为研究对象,妊娠≥34周且伴有妊娠期的血压升高,分为HDP、子痫前期及子痫3组,比较其血清尿酸水平并分析其与疾病严重程度的关联、对分娩方式及妊娠结局的影响.结果 200例研究对象中,63例(31.5％)为HDP组,131例(65.5％)为子痫前期组,6例(3.0％)为子痫组.子痫前期孕妇中81例(61.8％)为轻度,50例(38.2％)为重度;3组患者的血清尿酸平均值分别为(314.16±84.49) μmol/L、(405.79±126.14) μmol/L及(526.58±163.03) μmol/L.HDP患者组62例、子痫前期组115例及子痫组2例在产后即刻保持稳定状态;1例HDP、15例严重子痫前期及2例子痫患者产后即刻需要进行重症监护,但不需要机械通气;另外由于病情十分严重子痫前期组1例和2例子痫组患者在产后需要进行机械通气和高度依赖的重症监护.病情平稳者尿酸水平均显著低于病情危重者(均P＜0.05),且随患者病情加重尿酸水平呈显著升高的趋势,尤其是至ICU治疗的危重组患者(P=0.032);子痫前期组轻度与重度患者的血清尿酸水平比较差异有统计学意义[(406.52±100.26) μmol/L vs.(518.96±114.85) μmol/L,P=0.015].结论 孕妇血清尿酸水平与HDP病情严重程度及分娩预后之间存在显著相关性,具有潜在的价值作为生物标志物之一应用于临床实践当中.

Background Preeclampsia (PE) is a pregnancy-specific syndrome, belongs to the gestational hypertension diseases category and is considered among the causes of maternal and perinatal mortality and morbidity. However, the pathogenesis of PE is still vague. Methods In the present study, the circular RNA (circRNA) expression patterns of normal pregnant women and PE patients were investigated using whole RNA sequencing. Results A total of 151 differential expressed circRNAs were identified including 121 upregulated and 30 downregulated ones. Functional and pathway enrichment analysis was conducted on the differentially expressed circRNAs using Gene Ontology and KEGG databases. The results of this analysis indicated that several crucial biological processes and pathways were enriched in PE patients. circRNA–microRNA (miRNA) interaction analysis indicated that the reported differentially expresse circRNAs may be associated with some regulatory functions through miRNAs in PE patients. Two ceRNAs networks were constructed according to the targeting relationship between circRNAs/miRNAs and miRNAs/mRNAs. One sub-network contained one upregulated circRNA, four downregulated miRNAs and five upregulated mRNAs, and another sub-network contained 10 downregulated circRNAs, 21 upregulated miRNAs and 15 downregulated mRNAs. Conclusion CircRNA expression patterns have been investigated and this analysis revealed their potential regulatory mechanisms in PE patients. We constructed the ceRNAs (competing endogenous RNA) to reveal the potential molecular roles of dysregulated circRNAs in the PE patients using RNA sequencing data. circRNA_13301 was the only one upregulated circRNA in ceRNA being targeted by four miRNAs.

Background .Preeclampsia (PE) is a pregnancy-specific syndrome, belongs to the gestational hypertension diseases category and is considered among the causes of maternal and perinatal mortality and morbidity.However, the pathogenesis of PE is still vague. Methods.In the present study, the circular RNA (circRNA) expression patterns of normal pregnant women and PE patients were investigated using whole RNA sequencing.Results.151 differential expressed circRNAs were identified including 121 upregulated and 30 downregulated ones.Functional and pathway enrichment analysis was conducted on the differentially expressed circRNAs using Gene Ontology and KEGG databases.The results of this analysis indicated that several crucial biological processes and pathways were enriched in PE patients.circRNA-microRNA (miRNA) interaction analysis indicated that the reported differentially expresse circRNAs may be associated with some regulatory functions through miRNAs in PE patients.Two ceRNAs networks were constructed according to the targeting relationship between circRNAs/miRNAs and miRNAs/mRNAs.One sub-network contained one upregulated circRNA, four downregulated miRNAs and five upregulated mRNAs, and another sub-network contained 10 downregulated circRNAs, 21 upregulated miRNAs and 15 downregulated mRNAs. Conclusion .CircRNA expression patterns have been investigated and this analysis revealed their potential regulatory mechanisms in PE patients.We constructed the ceRNAs (competing endogenous RNA) to reveal the potential molecular roles of dysregulated circRNAs in the PE patients using RNA sequencing data.circRNA_13301 was the only one upregulated circRNA in ceRNA being targeted by four miRNAs.

Background .Preeclampsia (PE) is a pregnancy-specific syndrome, belongs to the gestational hypertension diseases category and is considered among the causes of maternal and perinatal mortality and morbidity.However, the pathogenesis of PE is still vague. Methods.In the present study, the circular RNA (circRNA) expression patterns of normal pregnant women and PE patients were investigated using whole RNA sequencing.Results.151 differential expressed circRNAs were identified including 121 upregulated and 30 downregulated ones.Functional and pathway enrichment analysis was conducted on the differentially expressed circRNAs using Gene Ontology and KEGG databases.The results of this analysis indicated that several crucial biological processes and pathways were enriched in PE patients.circRNA-microRNA (miRNA) interaction analysis indicated that the reported differentially expresse circRNAs may be associated with some regulatory functions through miRNAs in PE patients.Two ceRNAs networks were constructed according to the targeting relationship between circRNAs/miRNAs and miRNAs/mRNAs.One sub-network contained one upregulated circRNA, four downregulated miRNAs and five upregulated mRNAs, and another sub-network contained 10 downregulated circRNAs, 21 upregulated miRNAs and 15 downregulated mRNAs. Conclusion .CircRNA expression patterns have been investigated and this analysis revealed their potential regulatory mechanisms in PE patients.We constructed the ceRNAs (competing endogenous RNA) to reveal the potential molecular roles of dysregulated circRNAs in the PE patients using RNA sequencing data.circRNA_13301 was the only one upregulated circRNA in ceRNA being targeted by four miRNAs.

目的 探讨胎盘特异性蛋白-1(PLAC-1)在胎儿生长受限中的表达,以及PLAC-1表达下调后对人胎盘滋养层JEG-3细胞生物学行为的影响,明确PLAC-1在胎儿生长受限中的生物学作用.方法 收集20例胎儿生长受限和20例正常对照胎盘组织,免疫印迹法检测PLAC-1在对照组和胎儿生长受限组间表达差异;针对PLAC-1的靶序列合成3条反向互补的寡聚核苷酸序列,采用瞬时转染的方法转染人胎盘滋养层JEG-3细胞,48h后收取细胞,提取总蛋白,免疫印迹法验证siRNA干扰效果.选择敲低效果最佳的siRNA进行细胞表型实验,采用CCK-8、Transwell和细胞划痕等实验方法分别检测细胞增殖、迁移和侵袭情况.结果 (1)与对照组胎盘相比,胎儿生长受限组胎盘中PLAC-1蛋白的表达水平明显下调,两组比较,差异有统计学意义(P<0.01).(2)siRNA的敲低效果:3条siRNA均具有PLAC-1的敲低效果,其中siPLAC1-1敲低效果最佳达到90％以上,选择siPLAC1-1进行后续的细胞表型实验.(3)CCK-8检测细胞增殖能力:分别在24、48、72h检测siCtrl和siPLAC-1两组细胞活性,在24h两者差异显著(P<0.05),48h和72h两者间差异极显著(P<0.01).(4)Transwell检测细胞迁移和侵袭能力:在迁移实验中,siPLAC-1组的穿膜细胞数为(67±3)个,明显少于siCtrl组(157±4)个(P<0.01);侵袭实验中,siPLAC-1组的穿膜细胞数为(25±5)个,明显少于siCtrl组(84±6)个(P<0.01).(5)细胞划痕实验检测细胞迁移:在72h时,siPLAC-1敲低组细胞迁移率为(18.1±2.4)％,对照组为(26.1±3.7)％,细胞迁移差异明显(P<0.05).结论 PLAC- 1在胎儿生长受限胎盘组织明显下调,通过RNAi在JEG- 3细胞中干扰PLAC- 1表达后,抑制细胞增殖、迁移和侵袭能力,进而影响胎盘发育异常导致胎儿生长受限的发生.

目的 针对嘉兴地区15 574名新生儿群体进行中国人群常见耳聋基因突变的分子筛查,分析嘉兴地区人群耳聋基因突变携带情况.方法 新生儿分娩时,采集新生儿脐带血2-3ml,采用PCR与导流杂交法相结合技术,检测中国人群中最常见的4个耳聋致病基因上的9个突变位点.并对复合杂合突变及双杂合突变和纯合突变的样本进行了随访.结果 15 574例受检新生儿中共有696例(4.47％)携带至少1个耳聋基因突变.其中GJB2基因杂合突变363例,占2.33％;GJB3基因杂合突变的36例,占0.23％;SLC26A4基因杂合突变233例,占1.50％;线粒体12SrRNA基因47例,占0.30％;携带有两个耳聋基因位点突变的有13例.目前听力语言发育正常.另外,存在GJB2基因c.235delC、c.176-191de116复合杂合突变1例(0.64‰),GJB2基因c.235delC纯合突变2例(1.28‰).SLC26A4基因c.919-2A＞G纯合突变1例(0.64‰).出生时、三个月时的听力筛查双耳均未通过,目前仍在继续随访.结论 本研究对嘉兴地区人群遗传性耳聋热点突变筛查进行大样本的探索,丰富了非综合征耳聋基因突变谱,为耳聋基因突变筛查、耳聋基因诊断及遗传咨询提供了重要数据资料.从而进行早发现、早干预、早治疗,提高聋儿的生存质量,并对耳聋基因突变携带者进行婚育指导,降低本地区出生缺陷.

目的 为临产妇和产科医生提供一种无创、方便、客观、准确的宫口开大测量装置.方法 通过两个柔性测量指环和位于两个测量指环间的测量尺完成宫口测量,测量方法符合临床常规宫口测量习惯且不受测量时手掌形变及阴道特定生理弯曲角度影响,准确测量宫口开大距离.结果 在产前宫颈变化与产道关系模型中使用宫口测量器测量比徒手测量准确度高,测量结果客观可靠.结论 可计量宫口测量器可较准确测量临产妇宫口开大距离,为临床提供了一种简便、客观、无创的宫口测量方法.

本文提供了一种简单的透射电镜生物样品批量制备装置及方法,该装置及方法可同时制备近百至几百例样品,既适用于组织块样品也适用于分散的细胞样品,具有高通量、高平行性和低成本的特点.操作方法简单易行,为实验人员节省了大量时间,为临床诊断和科学研究提供了高效的电镜样品制备工具和方法.

目的 研究产钳助产术对产后出血量的影响及其原因分析.方法 回顾性分析我院2016年167例行产钳助产术产妇的产后出血量,分别与175例自然分娩产妇和51例经阴道分娩过程中行会阴侧切术产妇的产后出血量进行比较.同时针对行产钳助产术的三病因(6例胎位不正,118例胎儿宫内窘迫以及43例第二产程延长)分别与自然分娩产妇的出血量相比较.结果 产钳助产组的平均产后出血量为(294.97±84.28)ml,较自然分娩组的平均产后出血量(242.17±56.96)ml多,两组之间具有显著性差异(P＜0.05).同时,产钳助产组出血量较会阴侧切组(245±46.41mL)多,具有统计学差异(P＜0.05).另外,产钳助产组三病因的平均出血量(胎位不正组(316.67±68.31)mL,胎儿宫内窘迫组(285.59±60.63) ml,第二产程延长组(317.67±128.21) mL均较自然分娩组多,存在统计学差异.结论 产钳助产对产后出血量的增加提示产钳助产本身或产钳运用的病因可能会增加产后出血,但产钳助产对困难分娩依然有着其独特的优势.

Rapid and efficient methods for the determination of cured tuberculosis (TB) are lacking. A total of 85 differentially expressed serum proteins were identified by iTRAQ labeling coupled with two-dimensional liquid chromatography-tandem mass spectrometry (2D LC-MS/MS) analysis (fold change >1.50 or <0.60, P < 0.05). We validated albumin (ALB), Rho GDP-dissociation inhibitor 2 (ARHGDIB), complement 3 (C3), ficolin-2 (FCN2), and apolipoprotein (a) (LPA) using the enzyme-linked immunosorbent assay (ELISA) method. Significantly increased ALB and LPA levels (P = 0.036 and P = 0.012, respectively) and significantly reduced ARHGDIB, C3, and FCN2 levels (P < 0.001, P = 0.035, and P = 0.018, respectively) were observed in cured TB patients compared with untreated TB patients. In addition, changes in ALB and FCN2 levels occurred after 2 months of treatment (P < 0.001 and P = 0.030, respectively). We established a cured TB model with 87.10% sensitivity, 79.49% specificity, and an area under the curve (AUC) of 0.876. The results indicated that ALB, ARHGDIB, C3, FCN2, and LPA levels might serve as potential biomarkers for cured TB. Our study provides experimental data for establishing objective indicators of cured TB and also proposes potential markers for evaluating the efficacy of anti-TB drugs.

阴虚"上火"属于中医阴虚证候,口腔炎性反应反复发作是其标志性临床体征.探究阴虚"上火"本质特征对于治疗具有十分重要意义.有研究表明,三碘甲腺原氨酸(triiodo-thyronine;T3)处理大鼠,能模拟甲亢多汗、怕热、急躁、神经过敏、震颤、心输出量增加和心率加快等类似于阴虚症状,形成大鼠阴虚模型.本实验通过腹腔注射T3处理SD大鼠建立阴虚模型,并在此基础上叠加口腔牙龈炎模型,建立阴虚"上火"大鼠模型,以iTRAQ-2DLC- MS/MS蛋白组筛选鉴定技术与生物学信息手段从血清蛋白层面探究阴虚"上火"的本质特征,为阴虚"上火"研究与治疗提供生物学依据.