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Preeclampsia (PE) is associated with abnormal placental vascular structure. However, the volume density of fetoplacental vessels in PE remains unclear. Additionally, manually annotated CT angiography, which is widely used to analyze placental vessels, has issues regarding inaccuracy. Thus, computer-aided CT angiography for analyzing the volume density of fetoplacental vessels would facilitate the understanding of PE pathogenesis.We performed computer-aided CT angiography to compare differences in placentas among 17 women with PE and 34 normotensive women. The contrast ratio in CT angiography was significantly enhanced using a three-dimensional (3-D) Hessian matrix algorithm. The PE-like mouse model was established by administration of 125 mg/kg/day NG-nitro-l-arginine methyl ester (l-NAME) for 10 days. The presence of endothelial marker CD31 was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). The expression of angiogenic factors (PlGF, VEGFA, and sFlt1) in placentas was detected using qRT-PCR and western blotting.The volume density in fetoplacental vessels and CD31 expression were significantly reduced in women with PE and l-NAME-induced mice. Additionally, the downregulation of angiogenic factors (PlGF/VEGFA) and upregulation of an anti-angiogenic factor (sFlt1) were determined in a mouse model.Contrast-enhanced CT angiography with the aid of a 3-D Hessian matrix algorithm was performed. PE significantly affects the formation of vascular vessels, resulting in a lower volume density of fetoplacental vessels in humans and mice. This may be explained by the abnormal release of angiogenic factors during PE.

Feeder cells provide an optimal microenvironment for the propagation of human embryonic stem cells (hESCs) by supplying currently known or unknown factors. However, the hESCs grown on feeder cells are not suitable for the purpose of clinical application because of the risk of contamination. In recent years, the feeder-free culture method has been developed to eliminate contamination, but some studies show that hESCs exhibit poor growth patterns in a feeder-free culture system. Regarding this phenomenon, we speculate that some genes related to hESC propagation were differently expressed in hESCs grown on feeder cells. To test this hypothesis, 3 hESC lines (NF4, NF5 and P096) were efficiently expanded in a feeder-free culture system or on human foreskin fibroblast (HFF) cells. The different gene expression patterns of hESCs in these 2 conditions were analyzed through microarrays. The results revealed that the hESCs cultured in both conditions maintained the expression of stemness markers and the ability to spontaneously differentiate into the 3 germ layers. The analysis of gene expression profiles revealed that 23 lncRNA and 15 genes were significantly differentially expressed in these two culture conditions. Furthermore, GO analyses showed that these genes were involved in such biological processes as growth factor stimuli, cell growth, and stem cell maintenance. To summarize, our study demonstrated that the hESCs grown on the HFF showed different gene expression patterns compared to those grown in a feeder-free culture system, suggesting that these differently expressed lncRNAs and genes played important roles in maintaining hESC propagation.

Introduction Preeclampsia (PE) is associated with failure of uterovascular transformation due to impaired trophoblast invasion. Previously, TNF-related apoptosis-inducing ligand (TRAIL) has been controversially reported to correlate with PE, but whether it regulates trophoblast invasion yet to be defined. Methods We treated HTR8/SVneo cells with sTRAIL at concentrations of 0.1 ng/mL, 1 ng/mL and 10 ng/mL for a 72-h time course and compared cell proliferation, apoptosis and invasion ability by CCK8 assay, flow cytometry analysis and Matrigel cell invasion assay, respectively. The expressions levels of miR-146a, CXCR4, EGFR and MMP2 were quantified by qRT-PCR and Western blot. Moreover, HTR8/SVneo cells were transfected with miR-146a mimics and miR-146a inhibitor, followed by analyzing invasion ability and gene expressions of CXCR4, EGFR and MMP2. Finally, both serum and placental samples from preeclamptic and gestational week-matched normotensive women were collected and assessed for the expression levels of TRAIL by ELISA assay and immunochemistry staining. Results sTRAIL treatment of HTR8/SVneo cells resulted in no change in proliferation or apoptosis, but dose- and time-dependently enhanced invasion. TRAIL downregulated the expressions of miR-146a and upregulated CXCR4, EGFR and MMP2. Transfection of miR-146a resulted in the inhibition of invasion and downregulation of CXCR4, EGFR and MMP2. Lastly, the expression levels of TRAIL decreased in both serum and placenta of preeclamptic pregnancies and correlated with the disease severity. Discussion TRAIL regulated miR-146a-CXCR/EGFR axis to promote the invasion of trophoblast like cells. Its deceased levels in preeclamptic sera and placenta, suggest that low levels of TRAIL might contribute to the pathogenesis of preeclampsia.

Neurogenesis, a highly orchestrated process, entails the transition from a pluripotent to neural state and involves neural progenitor cells (NPCs) and neuronal/glial subtypes. However, the precise epigenetic mechanisms underlying fate decision remain poorly understood. Here, we delete KDM6s (JMJD3 and/or UTX), the H3K27me3 demethylases, in human embryonic stem cells (hESCs) and show that their deletion does not impede NPC generation from hESCs. However, KDM6-deficient NPCs exhibit poor proliferation and a failure to differentiate into neurons and glia. Mechanistically, both JMJD3 and UTX are found to be enriched in gene loci essential for neural development in hNPCs, and KDM6 impairment leads to H3K27me3 accumulation and blockade of DNA accessibility at these genes. Interestingly, forced expression of neuron-specific chromatin remodelling BAF (nBAF) rescues the neuron/glia defect in KDM6-deficient NPCs despite H3K27me3 accumulation. Our findings uncover the differential requirement of KDM6s in specifying NPCs and neurons/glia and highlight the contribution of individual epigenetic regulators in fate decisions in a human development model., Neurogenesis is an ordered transition from pluriptotent cells to neural precursor cells (NPCs) to neurons. Here the authors show that loss of the lysine demethylases JMJD3 and UTX leads reduced DNA accessibility at neurogenesis loci in human NPCs, and that the chromatin remodeller BAF can rescue differentiation defects.

Polycomb repressive complexes (PRCs) are essential in mouse gastrulation and specify neural ectoderm in human embryonic stem cells (hESCs), but the underlying molecular basis remains unclear. Here in this study, by employing an array of different approaches, such as gene knock-out, RNA-seq, ChIP-seq, et al., we uncover that EZH2, an important PRC factor, specifies the normal neural fate decision through repressing the competing meso/endoderm program. EZH2−/− hESCs show an aberrant re-activation of meso/endoderm genes during neural induction. At the molecular level, EZH2 represses meso/endoderm genes while SOX2 activates the neural genes to coordinately specify the normal neural fate. Moreover, EZH2 also supports the proliferation of human neural progenitor cells (NPCs) through repressing the aberrant expression of meso/endoderm program during culture. Together, our findings uncover the coordination of epigenetic regulators such as EZH2 and lineage factors like SOX2 in normal neural fate decision. Supplementary Information The online version contains supplementary material available at 10.1186/s13619-021-00092-6.

A simple and efficient strategy to generate human trophoblast stem cells is reported to aid investigations of early placentation., Human trophoblast stem cells (hTSCs) provide a valuable model to study placental development and function. While primary hTSCs have been derived from embryos/early placenta, and transdifferentiated hTSCs from naïve human pluripotent stem cells (hPSCs), the generation of hTSCs from primed PSCs is problematic. We report the successful generation of TSCs from primed hPSCs and show that BMP4 substantially enhances this process. TSCs derived from primed hPSCs are similar to blastocyst-derived hTSCs in terms of morphology, proliferation, differentiation potential, and gene expression. We define the chromatin accessibility dynamics and histone modifications (H3K4me3/H3K27me3) that specify hPSC-derived TSCs. Consistent with low density of H3K27me3 in primed hPSC-derived hTSCs, we show that knockout of H3K27 methyltransferases (EZH1/2) increases the efficiency of hTSC derivation from primed hPSCs. Efficient derivation of hTSCs from primed hPSCs provides a simple and powerful model to understand human trophoblast development, including the pathogenesis of trophoblast-related disorders, by generating disease-specific hTSCs.

COVID-19 is associated with increased incidence of preterm birth (PTB). We assessed pathways by which SARS-CoV-2 could access the placenta. Placentae, from PTB with or without chorioamnionitis (ChA), or from term pregnancies (n = 12/13/group) were collected. Peripheral blood was collected from healthy pregnant women (n = 6). Second trimester placental explants (16–20 weeks, n = 5/group) were treated with lipopolysaccharide (LPS, to mimic bacterial infection) and ACE2, CCL2, IL-6/8 and TNFα mRNA was assessed. ChA-placentae exhibited increased ACE2 and CCL2 mRNA expression (p &lt, 0.05). LPS increased cytokine and ACE2 mRNA in placental explants. Placental ACE2 protein localized to syncytiotrophoblast, fetal endothelium, extravillous trophoblast and in immune cells-subsets (M1/M2 macrophage and neutrophils) within the villous stroma. Significantly increased numbers of M1 macrophage and neutrophils were present in the ChA-placenta (p &lt, 0.001). Subsets of peripheral immune cells from pregnant women express the ACE2 mRNA and protein. A greater fraction of granulocytes was positive for ACE2 protein expression compared to lymphocytes or monocytes. These data suggest that in pregnancies complicated by ChA, ACE2 positive immune cells in the maternal circulation have the potential to traffic SARS-CoV-2 virus to the placenta and increase the risk of vertical transmission to the placenta/fetus.

BACKGROUND Dinoprostone is the recommended primary option for induction of labor (IOL) in late-term pregnancies (LTPs). However, oxytocin is used in developing and rural areas, and studies have supported similar effectiveness for oxytocin and dinoprostone in reducing the rate of cesarean delivery of LTPs with a Bishop's score of between 4-6. This study aimed to compare dinoprostone and oxytocin for IOL in LTPs and the rate of cesarean section in ten centers in South China. MATERIAL AND METHODS A retrospective study included 1,408 women with LTP, with subgroups including a Bishop's score of 0-3 and 4-6. Rates of cesarean delivery were compared between women given vaginal dinoprostone and intravenous oxytocin for IOL. Secondary outcomes included the duration of labor, and maternal and fetal complications. RESULTS Comparison between women who received oxytocin (N=365) and dinoprostone (N=1,043) showed significantly lower rates of cesarean delivery with dinoprostone, but no significant difference between the subgroups with Bishop's scores of 0-3 and 4-6. The interval between induction to labor and duration of the active phase of labor were significantly reduced in the dinoprostone group with a Bishop's score of between 4-6. CONCLUSIONS For LTPs with a Bishop's score of 0-3, dinoprostone was superior to oxytocin for IOL with a lower rate of cesarean delivery, but both agents had a similar outcome for women with a Bishop's score of 4-6. These findings may have implications for the choice of agent used in IOL when dinoprostone is unavailable.

ANP32A is a member of acidic leucine-rich nuclear phosphoprotein 32 family, which is involved in diverse biochemical processes, including chromatin modification and remodeling. Here, we established the CRISPR/Cas9-mediated ANP32A homozygous knockout human embryonic stem cell (ESC) line to investigate the roles of ANP32A in pluripotency maintenance and differentiation process of human ESCs. This cell line shows the normal karyotype and typical stem cell morphology, in accordance with high expression of pluripotent genes and the differentiation potential in vitro. Consequently, the ANP32A knockout cell line provides a promising approach for investigating the roles of ANP32A in human ESC cell fate decisions.

Objective Intracellular protein fibroblast growth factor 13 (FGF13) is highly expressed in human placenta, although its biological function remains unexplored. The aims of this study were to investigate the expression of FGF13 in placentae with early-onset preeclampsia (PE) and the associated mechanisms in the pathophysiology of PE. Methods The expression levels of FGF13 in placentae obtained from patients with early-onset PE and normal pregnancies were assessed using immunofluorescent staining, Western blot assays and quantitative PCR. We knocked down FGF13 in trophoblast cell lines BeWo and HTR8/SVneo, and analyzed cell permeability. Clinical trophoblast cell-cell junctions were identified by cytokeratin 7 (CK7) immunofluorescent staining of human placental sections. The expressions of FGF13 were manipulated in BeWo and HTR8/SVneo cell lines, and the expressions of E-cadherin were quantified by reverse transcription followed by quantitative PCR, Western blot assays and immunofluorescent staining. The expressions of FGF13 and E-cadherin were further confirmed in the isolated human primary trophoblasts. Results Downregulation of FGF13 along with trophoblast disarrangement were found in human placentae with early-onset PE. In trophoblast cell lines decreased FGF13 expression resulted in increased cell permeability and decreased E-cadherin expression. The FGF13 insufficiency-mediated loss of E-cadherin was further confirmed in the human villous trophoblasts isolated from PE patients. Conclusion FGF13 was downregulated in human placentae with early-onset PE. FGF13 played an important role in maintaining placental trophoblast permeability via the modulation of E-cadherin.

Objective To assess a novel three-dimensional (3D) magnetic resonance imaging (MRI) model for determining position of uterine incision during cesarean delivery among patients with placenta previa. Methods A prospective study was conducted among women with singleton pregnancies complicated by placenta previa who delivered by cesarean at a hospital in China between January 1, 2014, and January 1, 2016. Patients chose whether to undergo 3D MRI modeling to guide uterine incision (study group) or the standard intervention (control group). Medical records were reviewed to collect data on maternal, neonatal, and operative characteristics. Results Among 134 women enrolled, 45 were in the study group and 89 in the control group. When compared with the control group, patients in the study group experienced less intraoperative blood loss (678.65 ± 649.54 vs 933.96 ± 695.25 mL; P=0.042) and shorter operative times (65.13 ± 27.38 vs 86.88 ± 54.43 minutes; P=0.013). Fewer patients in the study group received transfusions (11 [24%] vs 38 [43%]; P=0.038). No between-group differences were found for hysterectomy rate, hospitalization days and cost, or neonatal outcomes. Conclusion Uterine incision guided by a 3D MRI model could improve maternal outcomes during cesarean delivery, including reductions in intraoperative blood loss, transfusion frequency, and operative time. This article is protected by copyright. All rights reserved.

To describe a modified "Triple-P" procedure and evaluate its outcome in women with morbidly adherent placenta (MAP) after previous caesarean section (CS).A retrospective cohort study of 96 women with MAP after CS was recruited with 45 women receiving the modified "Triple-P" procedure as study group and the other 51 cases receiving the conventional managements as the control. The maternal outcomes were compared.The modified "Triple-P" procedure was described in step by step. Women in study group demonstrated reduction of blood loss, transfusion blood volume and operation time, as well as less hospital days and lower hospitalization cost (P 0.05). In addition, there was no difference in uterine healing rate, hysterectomy rate, and ICU transferring rate (P 0.05).Our modified "Triple-P" procedure for MAP after previous CS maintained the advantages of Chandraharan's "Triple-P" procedure in preservation of uterus for further fertility, less intraoperative blood loss, shorter hospital stays, and lower hospitalization cost but also advanced in feasibility and convenience during introducing into routine clinical practice.

Forkhead box D3 (FOXD3) is a key transcription factor maintaining pluripotency in mouse embryonic stem cells (ESCs). Yet to date studies on its role in human ESCs are quite limited. In this study, we report that deletion of FOXD3 in human ESCs results in loss of pluripotency and spontaneous differentiation toward meso-endoderm. Ectopic overexpression of FOXD3 in hESCs leads to two different phenotypes: Human ESCs expressing high levels of FOXD3 undergo spontaneous meso-endoderm differentiation, whereas those with lower levels of FOXD3 maintain pluripotency. Next we deleted endogenous FOXD3 in the low ectopic expression model and find that addition of exogenous FOXD3 at a low level could rescue FOXD3-deficiency phenotype in hESCs. In summary, our findings suggest that FOXD3 dose-dependently regulates the balance of human ESCs between pluripotency and meso-endoderm fates, which adds to our understanding of the role of FOXD3 in humans.

Small extracellular vesicles (sEVs) are important mediators of cell-to-cell communication involved in the successful establishment of a pregnancy. Human decidual stromal cells play a key role in regulating trophoblast invasion. Nevertheless, the regulatory functions of decidual stromal cells-derived sEVs in human trophoblast cells are still unclear. In this study, primary human decidual stromal cells were isolated, and immortalized human endometrial stromal cell line (HESCs) were decidualized into human decidual stromal cells (HDSCs) using hormonal cocktail containing medroxy progesterone 17-acetate (MPA), estrogen and cAMP analog. HDSC-sEVs were isolated from both primary human decidual stromal cells and immortal HDSCs, respectively, and identified by transmission electron microscopy and western blotting. EV uptake assay indicated that HDSC-sEVs could be uptaken by trophoblast cells. HDSC-sEVs could increase the invasiveness and the expression level of N-cadherin of trophoblast cells with elevated phosphorylation of SMAD2 and SMAD3 in the cells. Silencing of N-cadherin could block cell invasion induced by HDSC-sEVs, while knockdown of SMAD2 and SMAD3 could inhibit the upregulation of N-cadherin in trophoblast cells. Taken together, our results suggested a regulatory effect of HDSC-sEVs in the invasion of trophoblast cells, and HDSC-sEVs may be important mediators of trophoblasts during embryo implantation and placentation.

The placenta is an essential organ for the fetus, but its regulatory mechanism for formation of functional trophoblast lineage remains elusive in humans. Although widely known in mice, TEAD4 and its downstream targets CDX2 and GATA3 have not been determined in human models. In this work, we used a human model of trophoblast transition from BAP (BMP4, A83-01 and PD173074)-treated human embryonic stem cells (hESCs) and performed multiple gain- and loss-of-function tests of TEAD4, CDX2 or GATA3 to study their roles during this process. Although hESCs with TEAD4 deletion maintain pluripotency, their trophoblast transition potentials are attenuated. This impaired trophoblast transition could be rescued by separately overexpressing TEAD4, CDX2 or GATA3. Furthermore, trophoblast transition from hESCs is also attenuated by knockout of CDX2 but remains unaffected with deletion of GATA3. However, CDX2-overexpressed hESCs maintain pluripotency, whereas overexpression of GATA3 in hESCs leads to spontaneous differentiation including trophoblast lineage. In brief, our findings using a human model of trophoblast transition from BAP-treated hESCs reveal transcription roles of TEAD4, CDX2 and GATA in humans that are different from those in mice. We hope that this evidence can aid in understanding the distinct transcriptional network regulating trophoblast development in humans.

Human RNF2 (RING1B) gene is a critical epigenetic modification factor for embryonic development, pluripotency and differentiation of embryonic stem cells (ESCs). To further gain insights into the role of RNF2 in cell fate decisions of human ESCs, here we generated two RNF2 homozygous knockout human ESC lines by CRISPR/Cas9 genome editing technology. These cell lines maintained a normal karyotype and typical undifferentiated state in terms of morphology, pluripotent gene expression, and had differentiation potential in vivo. These cell lines provide good cell resources to explore the role of RNF2 gene in embryonic development and lineage differentiation in vitro.

Despite the high incidence of trophoblast-related diseases, the molecular mechanism of inadequate early trophoblast development is still unclear due to the lack of an appropriate cellular model in vitro. In the present study, we reprogrammed the amniotic cells to be induced pluripotent stem cells (iPSCs) via a non-virus and non-integrated method and subsequently differentiated them into trophoblast-like cells by a modified BMP4 strategy in E6 medium. Compared with the previously studied trophoblast-like cells from ESCs, the iPSCs derived trophoblast-like cells behave similarly in terms of gene expression profiles and biofunctions. Also we confirmed the differentiating tendency from iPSCs to be syncytiotrophoblasts-like cells might be caused by inappropriate differentiating oxygen condition. Additionally, we preliminarily indicated in vitro “artificial” differentiation of iPSCs also undergoing a possible trophoblastic stem cell stage, as witnessed in vivo. In conclusion, we provided an in vitro cellular model to study early trophoblast development for specific individual, by using the feasible amnion.

Transient receptor potential vanilloid 6 (TRPV6) has been shown to promote caner proliferation in several solid tumors, leading to unfavorable clinical outcomes. Our study aimed to elucidate the clinical significance of TRPV6 in patients with early-stage cervical squamous cell carcinoma (CSCC). The mRNA expression of TRPV6 was measured in 12 paired early-stage CSCC specimens and six cervical carcinoma cell lines using quantitative real-time PCR (qRT-PCR). Western blotting and immunohistochemistry (IHC) were employed to examine the protein expression level of TRPV6 in four paired specimens, 175 paraffin-embedded early-stage CSCC specimens, and 50 normal cervical tissues (NCTs), respectively. Statistical analyses were performed to evaluate the clinical significance of TRPV6 expression. The expressions of TRPV6 mRNA and protein were both significantly downregulated in early-stage CSCC tissues and cervical cancer cell lines. IHC analyses revealed that TRPV6 was downregulated in 136 (77.7 %) of 175 early-stage CSCC specimens. Moreover, TRPV6 expression in early-stage CSCC was significantly correlated with the tumor stage (P

The expression of nearly all smooth muscle genes are controlled by serum response factor binding sites in their promoter regions. However, SRF alone is not sufficient for regulating smooth muscle cell development. It associates with other cardiovascular specific cofactors to regulate smooth muscle gene expression. Previously, we showed that the transcription co-factor CRP2 was a regulator of smooth muscle gene expression. Here, we report that CSRP2BP, a coactivator for CRP2, is a histone acetyltransferase and a driver of smooth muscle gene expression. CSRP2BP directly interacted with SRF, CRP2 and myocardin. CSRP2BP synergistically activated smooth muscle gene promoters in an SRF-dependent manner. A combination of SRF, GATA6 and CRP2 required CSRP2BP for robust smooth muscle gene promoter activity. Knock-down of Csrp2bp in smooth muscle cells resulted in reduced smooth muscle gene expression. We conclude that the CSRP2BP histone acetyltransferase is a coactivator for CRP2 that works synergistically with SRF and myocardin to regulate smooth muscle gene expression.

Acylglycerol kinase (AGK) had been shown to contribute to cancer progression and unfavorable clinical outcomes of patients. Our study aimed to investigate the expression pattern and clinical significance of AGK in patients with early-stage cervical squamous cell cancer (CSCC). The protein and messenger RNA (mRNA) expression of AGK was analyzed in six cervical cancer cell lines and four paired early-stage CSCC specimens and normal cervical tissues (NCT), using Western blotting and real-time PCR (RT-PCR). And we investigated the AGK protein expression in paraffin-embedded specimens from 140 patients with early-stage CSCC and 30 cases of NCT by immunohistochemistry (IHC). Statistical analyses were performed to evaluate the clinicopathological significance of AGK expression. The expressions of AGK protein and mRNA were significantly up-regulated in cervical cancer cell lines and cancer tissues. IHC analyses revealed that AGK was highly expressed in 93 (66.4 %) of 140 early-stage CSCC specimens, but in none of the NCT. Moreover, AGK expression in early-stage CSCC was significantly correlated with tumor stage (P

RNA sequencing and short-read assembly were utilized to produce a transcriptome of livers from loaches (Misgurnus anguillicaudatus) fed with three different diets respectively containing fresh fish oil (FO group), medium oxidized fish oil (MO group) and high oxidized fish oil (HO group). A total of 60,663 unigenes were obtained in this study, with mean length 848.74 bp. 50,814, 49,584 and 49,814 unigenes were respectively obtained from FO, MO and HO groups. There were 2,343 differentially expressed genes between FO and MO, with 855 down- and 1,488 up-regulated genes in the MO group. 2,813 genes were differentially expressed between FO and HO, including 1,256 down- and 1,552 up-regulated genes in the HO group. 2,075 differentially expressed genes were found in the comparison of MO and HO, including 1,074 up- and 1,001 down-regulated genes in the MO group. Some differentially expressed genes, such as fatty acid transport protein (fatp), fatty acid binding protein (fabp), apolipoprotein (apo), peroxisome proliferator activated receptor-gamma (ppar-γ), acetyl-CoA synthetase (acs) and arachidonate 5-lipoxygenase (alox5), were involved in lipid metabolism, suggesting these genes in the loach were responsive to dietary oxidized fish oil. Results of transcriptome profilings here were validated using quantitative real time PCR in fourteen randomly selected unigenes. The present study provides insights into hepatic transcriptome profile of the loach, which is a valuable resource for studies of loach genomics. More importantly, this study identifies some important genes responsible for dietary oxidized fish oil, which will benefit researches of lipid metabolism in fish.

The paper deals with working principle and design methods about gas flow standard facilities by master meter method. A wind tunnel was designed to work as the flow velocity measurement and calibration platform. The distribution of the facility uncertainty was calculated. And finally the test results of the facility performance were given including the effect of the wind tunnel on the airflow, the impact of the humidity on the air density in the pipe and the flow-meter coefficient and the calibration of orifice flow-meter.

In this paper, the evaluation methods of flow standard facility in every regulations were compared and analyzed. Analysis of the two performance parameters of the flow stability within cumulative time and the flow stability between cumulative time. From the two angles of the structure of turbine flow meter itself and the calculation formula of the stability parameter, the selection principle of the stability parameter is determined. The flow stability between cumulative time is selected as the main parameter, and the flow stability within cumulative time as reference. And the results of flow stability test between the method of turbine flow meter and the weighing method were compared. The results show that the method of turbine flow meter can also be an accurate method for testing the flow stability of flow standard facility.