Background:Very low birth weight infants often require peripherally inserted central catheter (PICC) for long-term venous access. Conventional securement methods are associated with high rates of catheter dislodgement and skin injury, but the clinical effectiveness and cost-effectiveness of modified combination securement methods remain insufficiently validated. This study aimed to investigate the effects of a novel combination securement method on catheter dislodgement and skin injury in very low birth weight infants (VLBWIs) undergoing PICC placement, and to perform a cost-effectiveness analysis to inform evidence-based selection of the optimal securement strategy. Methods:This retrospective, single-center analysis comprised 181 VLBWIs who underwent PICC placement in the neonatal intensive care unit (NICU) between January 2018 and December 2025. Infants were assigned to either a conventional securement group (conventional group) or a modified combination fixation group (modified group), the latter consisting of four steps: pressure relief protection, tension-free fixation, buffer reinforcement, and sealing coverage (termed 'protection-pressure reduction-fixation-sealing'). A 1:1 nearest-neighbor propensity score matching (PSM) approach was used to balance baseline confounders. After matching, clinical outcomes and direct medical costs were compared between groups, and correlations between cost metrics and clinical outcomes were analyzed. Results:Following matching, baseline characteristics were well balanced between groups, with no significant differences (all P>0.05). The modified group showed significantly lower rates of unplanned PICC removal and skin injury than the conventional group (P=0.02 and P<0.001, respectively). Logistic regression identified the modified securement method as an independent protective factor against unplanned PICC removal in VLBWIs [odds ratio (OR) =0.275, P=0.005]. Moreover, total direct medical cost per PICC placement was significantly lower in the modified group (P<0.001). Conclusions:The modified combination securement method significantly improves clinical outcomes associated with PICC placement in VLBWIs, reduces complication rates, and achieves overall cost savings. Offering both clinical and economic benefits, this approach warrants widespread adoption in the NICU.

Background: Neonatal bacterial sepsis represents a major health threat to newborns, leading to high mortality rates globally. However, the correlation between the gut microbiome and bacterial sepsis in neonates remains unclear. Methods: This study utilized publicly available Genome-Wide Association Study data on 473 gut microbiota taxa as exposures. Instrumental variables were rigorously selected, and bidirectional two-sample Mendelian randomization (MR) analyses were performed. The MR and reverse MR analyses results were validated using Bayesian weighted MR (BWMR) analysis. Positive results from MR analysis will be validated through heterogeneity testing, evaluation of horizontal pleiotropy, and univariate sensitivity analysis. Results: The findings revealed a significant genetic causal association between 18 gut microbial species and neonatal bacterial sepsis, including Acetobacterales (odds ratio [OR]: 159.844; p = 0.04), Campylobacter D (OR: 16.225; p = 0.029), and Firmicutes A (OR: 75.643; p = 0.025). Additionally, both MR and inverse MR analyses confirmed the absence of reverse causation (p < 1e-5), supporting the robustness of the findings (p < 0.05) across five statistical methods. Sensitivity analyses indicated high reliability without significant heterogeneity or pleiotropy (p > 0.05). Furthermore, BWMR analysis highlighted the complex roles of probiotic taxa, including Bacteroides A plebeius (OR: 0.526) and pathogenic bacteria, such as Acetobacterales (OR: 192.449), in neonatal sepsis. Conclusions: A causal genetic association exists between gut microbiota and bacterial sepsis in neonates. These results underscore the potential of gut microbiota as biomarkers and therapeutic targets for the prevention and management of neonatal bacterial sepsis.

Mesenchymal stem cells (MSCs) have demonstrated promising therapeutic potential in the treatment of type 1 diabetes mellitus (T1DM); however, the underlying mechanism remains unclear. The primary pathological mechanism of T1DM involves activated T cells infiltrating the pancreas, leading to islet inflammation and the destruction of β-cells. However, the question of whether exosomes derived from MSCs can suppress the migration of T cells to the pancreas in the context of T1DM remains unresolved. In this study, we observed that miR-25 was highly expressed in MSCs exosomes and associated with signaling pathways related to cell migration. In vitro assay, we synthesized a miR-25 mimic and transiently transfected it into activated T cells, which revealed that miR-25 can effectively reduce the expression of CXCR3. Additionally, according to the in vivo T1DM mouse model, we found that there was a significant increase in miR-25 levels in T1DM mice treated with MSCs and the number of T cells decreased. Overall, our findings suggest that MSCs exosomes containing miR-25 can impede the infiltration of activated T cells into the pancreas in T1DM by repressing CXCR3 expression in these cells.

Ferroptosis, an iron-dependent form of programmed cell death, arises from the accumulation of lipid peroxides at toxic levels. Sorafenib, a first-line treatment for advanced hepatocellular carcinoma, shows limited clinical efficacy due to drug resistance. However, the mechanisms underlying Sorafenib resistance, especially related to ferroptosis, remain poorly understood. In this study, we identify activating transcription factor 7-interacting protein (ATF7IP) as a key inhibitor of ferroptosis. ATF7IP depletion promotes Sorafenib-induced ferroptosis, resulting in decreased cell viability, reduced cellular glutathione (GSH) levels, increased lipid peroxidation, and altered mitochondrial crista structure. Notably, ATF7IP knockdown shows cooperative effects with Sorafenib in inhibiting hepatocellular carcinoma growth in mice. Mechanistically, ATF7IP interacts with SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) to epigenetically silence the transcription of cytochrome b5 reductase 2 (CYB5R2), thereby reducing cellular Fe2+ levels. Meanwhile, ATF7IP stabilizes the antioxidant sensor Parkinsonism-associated deglycase (PARK7) protein which preserves the transsulfuration pathway to produce GSH, also leading to the inhibition of Sorafenib-induced ferroptosis. In conclusion, our findings identify ATF7IP as a critical ferroptosis inhibitor and represent ATF7IP as a novel therapeutic target for Sorafenib-based combination therapies of hepatocellular carcinoma.

Few studies focused on the roles of high glucose combined with high lipid in placental development or fetal growth. This study was designed to investigate the roles of high glucose combined with high lipid in mitochondrial dysfunction of JEG-3 cells. We determined the cellular proliferation and apoptosis, superoxide dismutase (SOD) activity, concentration of malondialdehyde (MDA), and lactic acid dehydrogenase in control group, high glucose group, high lipid group, and high glucose and high lipid group, together with the mitochondrial dysfunction, Nrf2, HO-1, SMAC, and cytochrome C (Cyt-C) expression. Significant decrease of SOD and significant elevation of MDA was seen in high glucose and high lipid group compared with the other three groups. There was significant decrease in mitochondrial SMAC and Cyt-C in high glucose group, high lipid group, and high glucose and high lipid group compared with those of control group. Nrf2 and HO-1 protein expression in high glucose combined with high lipid group showed significant decrease compared with that of high lipid group or high glucose group. We speculated that combination of high glucose and high lipid induced oxidative stress in JEG-3 cells, and Nrf2/ARE pathway may be related to this process.

Abstract Polycomb group proteins are often dysregulated in cancer, leading to disruption of epigenetic landscapes and acquisition of cancer hallmarks. Chromobox 8 (CBX8) is a core component of canonical polycomb repressive complex 1; however, its role in transcriptional regulation and in ovarian carcinoma progression has not been extensively investigated. In this study, we find that CBX8 is upregulated in ovarian cancer. Overexpression and knockdown approaches show that CBX8 facilitates the growth and migration of CAOV3, A2780, and SKOV3 cells in vitro. Consistently, depletion of CBX8 suppresses the growth and metastasis of ovarian carcinoma in vivo. Mechanistically, RNA-sequencing assays together with functional rescue experiments identify a tumor suppressor, SUSD2, as the functional target of CBX8 in ovarian carcinoma cells. Significantly, FLAG affinity coupled with mass spectrometry discovers that CBX8 interacts with a subunit of inhibitor of acetyltransferases (INHAT), SET, which also promotes the growth and migration of A2780 cells. CBX8 and SET cobind to the promoter of SUSD2 to establish H2AK119ub1 and prevent the acetylation of histone H3, resulting in transcriptional suppression of SUSD2. Implications: Our study uncovers a novel mechanism CBX8 explores to execute gene repression, and provides new therapeutic targets for ovarian carcinoma.

The disruption of epigenetic regulation is common in tumors; the abnormal expression of epigenetic factors leads to cancer occurrence and development. In this study, to investigate the potential function of histone methylation regulators in lung adenocarcinoma (LUAD), we performed differential expression analysis using RNA-seq data downloaded from The Cancer Genome Atlas (TCGA) database, and identified CBX2 and EZH2 as obviously upregulated histone methylation regulators. CBX2 knockdown significantly inhibited LUAD cell growth and metastasis in vitro and in vivo. The combined high expression of CBX2 and EZH2 was an indicator of poor prognosis in LUAD. The inhibition of both CBX2 and EZH2 exerted cooperative suppressive effects on the growth and metastasis of LUAD cells. Mechanistically, we revealed that CBX2 and EZH2 downregulated several PPAR signaling pathway genes and tumor suppressor genes through binding to their promoter cooperatively or separately. Furthermore, knockdown of CBX2 improved the therapeutic efficiency of EZH2 inhibitor on A549 cells. Our study reveals the cooperative oncogenic role of CBX2 and EZH2 in promoting LUAD progression, thereby providing potential targets for LUAD diagnosis and therapy.

OBJECTIVE:To identify risk factors for minimally invasive surfactant administration (MISA) failure in the treatment of preterm infants with respiratory distress syndrome (RDS) and the influence of MISA failure on neonatal outcome.METHODS:A retrospective analysis was performed for the clinical data of 148 preterm infants with a gestational age of ≤32 weeks and a clinical diagnosis of RDS, who were admitted to the neonatal intensive care unit of eight tertiary hospitals in Beijing, Tianjin and Hebei Province from July 1, 2017 to December 31, 2018 and were treated with MISA (bovine pulmonary surfactant, PS). According to whether MISA failure (defined as the need for mechanical ventilation within 72 hours after MISA) was observed, the infants were divided into two groups: MISA failure group (n=16) and MISA success (n=132). A logistic regression analysis was used to investigate the risk factors for MISA failure and its influence on neonatal outcome.RESULTS:The MISA failure rate was 10.8% (16/148). The logistic regression analysis showed that a high incidence rate of grade >II RDS before PS administration, low mean arterial pressure and high pulse pressure before administration, a low dose of initial PS administration, and long injection time and operation time were the risk factors for MISA failure (OR=5.983, 1.210, 1.183, 1.055, 1.036, and 1.058 respectively, P<0.05). After the control for the above risk factors, the logistic regression analysis showed that the MISA failure group had a significantly higher incidence rate of bronchopulmonary dysplasia (BPD) (OR=8.537, P<0.05).CONCLUSIONS:A high grade of RDS, a low mean arterial pressure, and a high pulse pressure before administration are independent risk factors for MISA failure, and a low dose of initial PS administration, a long injection time, and a long operation time may increase the risk of MISA failure. MISA failure may increase the incidence rate of BPD in preterm infants.

背景 新生儿败血症是导致早产儿死亡的主要原因之一,尤其是早发型败血症(EOS),因此早诊断、及时治疗尤为重要.血培养是诊断败血症的金标准,但新生儿外周血采血量有限,而脐血作为新生儿出生后最早的血液标本,血量充分,且收集方便.目的 探讨EOS早产儿脐血培养的临床应用价值,同时观察脐血培养阳性患儿炎性指标变化,以期为EOS的临床治疗提供依据.方法 选取天津医科大学第二医院2018年6月—2019年6月疑似或确诊宫内感染的产妇及其早产儿(胎龄≤37周)共150对,其中102例早产儿诊断为EOS,48例早产儿未诊断为EOS.于早产儿出生后即刻留取脐血,出生后24 h内留取外周静脉血,行血培养.分别于EOS患儿出生后0～<24、24～<48、48～72 h检测炎性指标〔超敏C反应蛋白(hs-CRP)、降钙素原(PCT)、白细胞计数(WBC)、血小板计数(PLT)〕,比较脐血培养阳性与脐血培养阴性EOS患儿不同时间炎性指标.EOS患儿脐血、外周血培养报警阳性后,进行脐血、外周血细菌鉴定.结果 EOS患儿脐血培养阳性率〔19.6％(20/102)〕与外周血培养阳性率〔16.7％(17/102)〕比较,差异无统计学意义(P>0.05).非EOS患儿脐血、外周血培养阳性率均为0.脐血培养阳性EOS患儿出生后0～<24、24～<48、48～72 h hs-CRP、PCT高于脐血培养阴性EOS患儿(P<0.05);脐血培养阳性EOS患儿出生后0～<24 h WBC低于脐血培养阴性EOS患儿(P<0.05);脐血培养阳性EOS患儿出生后48～72 h PLT低于脐血培养阴性EOS患儿(P<0.05).EOS患儿脐血培养共鉴定出20株致病菌,其中革兰阳性菌15株(包括葡萄球菌10株、单核细胞增生李斯特菌3株、无乳链球菌2株),革兰阴性菌5株(包括大肠埃希菌3株、肺炎克雷伯菌肺炎亚种1株、鲍曼不动杆菌1株).EOS患儿外周血培养共鉴定出17株致病菌,其中15例患儿外周血培养鉴定结果 与脐血培养鉴定结果 一致.结论 EOS患儿脐血培养阳性率与外周血培养阳性率相似,但脐血取血方便,留血量充分,有利于进行EOS的诊断.新生儿出生后若hs-CRP、PCT升高,WBC、PLT降低,提示可能存在EOS,可酌情调整抗生素用药,并依据细菌培养结果 及时确定抗感染疗程及进一步诊治方案.

Background/Aims: Nasal continuous positive airway pressure (nCPAP) was recommended as the initial respiratory support for spontaneous breathing in infants with very low birth weight and neonatal respiratory distress syndrome (NRDS). Less invasive surfactant administration (LISA) and minimally invasive surfactant therapy (MIST) have been reported to reduce the incidence of bronchopulmonary dysplasia (BPD). This study aimed to explore the applicability of minimally invasive surfactant administration (MISA) in China. Materials and Methods: MISA was a randomized controlled study conducted at eight level III neonatal intensive care units (NICUs) in China. Spontaneously breathing infants born at 25+0 to 31+6 weeks' gestation who progressively developed respiratory distress during the first 6 h after birth were randomly assigned to receive MISA or endotracheal intubation surfactant administration (EISA). The primary outcome was the difference in the morbidity of BPD between two groups of infants with MISA and EISA at 36 weeks corrected gestational age. Results: Demographic and clinical characteristics of the 151 infants in the MISA group were similar to the 147 infants in the EISA group. The comparison showed no clear benefits in the MISA group in the incidence of BPD, while infants from the EISA group had higher rates of patent ductus arteriosus (PDA) (60.5 vs. 41.1%, p = 0.001). The duration of surfactant infusion and the total time of surfactant administration in the MISA group were significantly longer than in the EISA group. A slightly increased heart rate was noted 1 h post surfactant administration in the EISA group. In subgroup analysis, the comparison of 51 smaller (<30 weeks) preterm infants, named MISAs (n = 31) and EISAs (n = 20), showed a significant reduction of BPD (29.0 vs. 70.0%, p = 0.004) and PDA (29.0 vs. 65.0%, p = 0.011). In the subgroup analysis of blood gas, arterial oxygen saturation (SaO2) value at 1 and 12 h and partial pressure of arterial oxygen (PaO2) at 12 h were all higher in the EISA group compared to the MISA group. Conclusion: MISA had no clear benefit on the incidence of BPD, but it was related to a reduction in PDA. It is an appropriate therapy for spontaneous breathing in infants with extremely low birth weight and NRDS.

Epigenetics refers to how chromatin-associated factors and reversible chromatin modifications maintain DNA-based programs by regulating the chromatin structure （Strahl and Allis,2000）.In recent years,genome sequencing studies of cancer have shown that genes encoding epigenetic factors are commonly mutated in cancer（Garraway and Lander,2013）.Dys regulated,or mutant,epigenetic factors influence tumorigenesis progression (Dawson and Kouzarides,

Metabolic disorders usually increase the level of reactive oxygen species (ROS) and damage mitochondrial function. The placenta supplies nutrients and hormonal signals to the fetus for regulating fetal metabolism, and is also prone to injury by oxidants. The aim of this study was to determine the effect of pre-existing maternal type 2 diabetes mellitus (DM) combined with obesity on placental mitochondrial function and metabolism disorders of offspring. The study included 96 pregnant women. The women were put into the following groups: healthy women (control, n=24), women with DM (DM, n=24), women with obesity (OB, n=24) and women with both DM and obesity (DM+OB, n=24). The ROS level, mitochondrial content, and the mitochondrial respiratory complex activities of the placenta were measured in the four groups. The expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was detected by immunofluorescence staining and western blotting. In addition, serum levels of insulin, glucose, leptin, nonesterified fatty acid (NEFA), adiponectin and triglycerides of their offspring were also measured. Maternal DM combined with obesity markedly increased ROS level, reduced mitochondrial DNA (mtDNA) content and mitochondrial respiratory complex I, II–III activities in placenta compared to the placenta from the control group and the DM group. Maternal DM combined with obesity significantly decreased Nrf2 and HO-1 expression. Furthermore, maternal DM combined with obesity influenced the glucose and lipid metabolism in their offspring. In conclusion, women with both DM and obesity detrimentally alter placenta function in oxidative stress regulation, and the Nrf2/ARE (antioxidant responsive element) pathway is involved. This may increase metabolic disturbance susceptibility in their offspring.

Whether transcriptional regulators are functionally involved in mitosis is a fundamental question in cell biology. Here we report that the RNF20/40 complex, a major ubiquitin ligase catalysing histone H2B monoubiquitination, interacts with the motor protein Eg5 during mitosis and participates in spindle assembly. We show that the RNF20/40 complex monoubiquitinates and stabilizes Eg5. Loss of RNF20/40 results in spindle assembly defects, cell cycle arrest and apoptosis. Consistently, depletion of either RNF20/40 or Eg5 suppresses breast cancer in vivo . Significantly, RNF20/40 and Eg5 are concurrently upregulated in human breast carcinomas and high Eg5 expression is associated with poorer overall survival of patients with luminal A, or B, breast cancer. Our study uncovers an important spindle assembly role of the RNF20/40 complex, and implicates the RNF20/40-Eg5 axis in breast carcinogenesis, supporting the pursuit of these proteins as potential targets for breast cancer therapeutic interventions.

Histone methyltransferase DOT1L is implicated in various biological processes including cell proliferation, differentiation and embryogenesis. Gene ablation of Dot1l results in embryonic lethality and cardiovascular defects including decreased vasculature. However, how DOT1L might contribute to the development of vasculature is not clear. Here, we report that DOT1L is required for angiogenesis. We demonstrated that silencing of DOT1L in human umbilical vein endothelial cells (HUVECs) leads to decreased cell viability, migration, tube formation, and capillary sprout formation in vitro, as well as reduced formation of functional vascular networks in matrigel plugs in vivo. Genome-wide analysis of DOT1L targets via H3K79me2 ChIP-seq annotation in HUVECs identified a number of genes including VEGFR2 that are critically involved in angiogenesis. We showed that DOT1L cooperates with transcription factor ETS-1 to stimulate the expression of VEGFR2, thereby activating ERK1/2 and AKT signaling pathways and promoting angiogenesis. Our study revealed a mechanistic role for DOT1L in the promotion of angiogenesis, adding to the understanding of the biological function of this histone methyltransferase.

目的 探讨低分子肝素(LMH)联合肺泡表面活性物质(PS)对幼年大鼠急性肺栓塞的治疗作用.方法 将雄性4周龄SD大鼠45只随机分为5组,对照组、肺栓塞组、LMH组、PS组、LMH-PS组,每组9只.除对照组外,其余各组均采用明胶海绵颗粒溶液经颈静脉注射制作急性肺栓塞模型;LMH组在术后给予LMH 0.01 ml/kg,2次/d皮下注射,PS组术后气管内灌注PS 120 mg/kg,1次/d.LMH-PS组则联合应用上述两种干预方式.对照组采用等量生理盐水颈静脉注射.各组均在术后1、4、7d检测动脉血气、肺动脉压力(mPAP)及右心室压力(RVP)、肺组织内皮素-1(ET-1)和基质金属蛋白酶9 (MMP-9)基因及蛋白表达水平和肺组织切片苏木精-伊红(HE)染色.结果 各组大鼠血气分析PaO2在l、4、7d时的差异均具有统计学意义(P均＜0.05).ld和4d时,LMH-PS组大鼠PaO2分别为(85.4±6.8)和(87.8±4.7) mmHg,显著高于栓塞组、LMH组和PS组,但低于对照组,差异均有统计学意义(P＜0.05).LMH-PS组的mPAP在术后ld时与对照组差异具有统计学意义(18.3±1.9 vs 16.3±1.5,P＜0.05),而在4d和7d时,两组差异已无统计学意义(P＞0.05),但LMH-PS组大鼠肺动脉压(mPAP)仍显著低于其余三组,差异有统计学意义(P＜0.05).各组ET-1 mRNA及蛋白表达水平在4d、7d时差异均具有统计学意义(P＜0.05),LMH-PS组ET-1 mRNA及蛋白水平在术后4d时迅速下降,低于其余3组,差异均有统计学意义(P均＜0.05),但与对照组的差异无统计学意义(P＞0.05).各组MMP-1 mRNA及蛋白水平在4d和7d时的差异也均具有统计学意义(P＜0.05).结论 LMH联合PS能够有效治疗幼年大鼠的急性肺栓塞.

Objectives To investigate the effect of different dosages of low molecular weight heparin on acute pulmonary embolism and inhibition of pulmonary intimal hyperplasia in immature rats. Methods 90 male immature SD rats were randomly divided into ifve groups: sham group, pulmonary embolism group, low-low molecular heparin group (L-LMH), medium-low molecular heparin group (M-LMH) and high-low molecular heparin group (H-LMH). The model of acute pulmonary embolism was established through jugular vein injection with gel-foam solution. The rates in the L-LMH, M-LMH, H-LMH groups were treated with low molecular weight heparin by subcutaneous injection after surgery with a dosage of 0 . 005 ml/kg, 0 . 01 ml/kg, 0 . 02 ml/kg, twice a day. Animals in the control group were given saline injection. Arterial blood gas, pulmonary artery pressure (mPAP), right ventricular pressure (RVP), wall area/tube area, wall thickness/tube diameter, and the expression of PDGF-B and MCP-1 at gene and protein levels in lung tissue were detected on the 7 th ( 7 d), 14 th ( 14 d) and 28 th ( 28 d) after opration. Results There were signiifcant differences of PaO 2 among 5 groups on 7 d, 14 d and 28 d. PaO 2 in group M-LMH ( 105 . 1 ± 4 . 6 mm Hg) were signiifcantly higher than that of embolization group, L-LMH, but not H-LMH group at 28 d. mPAP of M-LMH group was lower than that in the other three intervention groups, but showed no signiifcant difference compared with sham group (P?>0 . 05 ). There were signiifcant differences of RVP on 7 d and 14 d. PDGF-B, MCP-1 of M-LMH group were signiifcantly lower compared with the other three intervention groups (P?<?0 . 05 ), but showed no signiifcant difference compared with sham group (P?>0 . 05 ). Wall area/tube area, wall thickness/tube diameter scores of M-LMH group had no signiifcance differences compared with sham group on 28 d (P?>?0 . 05 ). Conclusion Medium dose of low molecular weight heparin could ameliorate the acute pulmonary embolism and inhibit the proliferation of pulmonary arteries in rats.

The prevalence of maternal obesity has risen dramatically in recent years. Maternal obesity increases the risk of adverse pregnancy outcomes, and can lead to chronic inflammation, oxidative stress, the change of cell factor homeostasis. The metabolic status of maternal obesity in the pre-pregnancy and pregnancy can alter the level of DNA methylation in the placenta, change the fetal programming, influence the pregnancy outcomes, and increase the risk of obesity related metabolic syndrome and other chronic diseases of offspring. Actively preventing and intervening in the maternal obesity can reduce the adverse pregnancy outcomes and increase the survival quality of the offspring.

Although clinically associated with severe developmental defects, the biological function of FOXK2 remains poorly explored. Here we report that FOXK2 interacts with transcription corepressor complexes NCoR/SMRT, SIN3A, NuRD, and REST/CoREST to repress a cohort of genes including HIF1β and EZH2 and to regulate several signaling pathways including the hypoxic response. We show that FOXK2 inhibits the proliferation and invasion of breast cancer cells and suppresses the growth and metastasis of breast cancer. Interestingly, FOXK2 is transactivated by ERα and transrepressed via reciprocal successive feedback by HIF1β/EZH2. Significantly, the expression of FOXK2 is progressively lost during breast cancer progression, and low FOXK2 expression is strongly correlated with higher histologic grades, positive lymph nodes, and ERα−/PR−/HER2- status, all indicators of poor prognosis.

BACKGROUND:It is of high incidence of brain injuries in premature infants, so it is necessary to diagnose and treat the brain injury early for neonatal clinical practice. We are aimed to investigate the relationship between early postnatal cranial ultrasonography and psychomotor and mental development in prematrue infants at the age of 12 months.METHODS:Two-hundred and eight premature infants were selected and underwent follow-up from January, 2007 to November, 2012. Cranial ultrasonography was performed on them. The developmental outcomes of these premature infants at the age of 12 months were assessed by the psychomotor developmental index (PDI) scale and mental development index (MDI). The relationship between ultrasonic gray-scale value and PDI and MDI was analyzed.RESULTS:The worse prognosis for psychomotor and mental development was associated with the gestational age, Apgar score(1 min), gender, chorioamnionitis, duration of mechanical ventilation and duration of mechanic ventilation. The differences between the prognosis of psychomotor and mental development, and peri-intraventricular hemorrhage (PIVH) and periventricular white matter damage (PWMD), were statistically significant (P<0.05). There were also significant differences between the early postnatal ultrasonic gray-scale value and prognoses of both psychomotor development and mental development (P<0.05). There were negative correlations between ultrasonic gray-scale and both PDI and MDI (r=-0.753, P<0.05; r=-0.764, P<0.05).CONCLUSIONS:The early postnatal cranial ultrasonography can assist to predict the prognosis of psychomotor and mental development for premature infants. The higher grade of PIVH and PWMD was associated with the worse prognosis of psychomotor and mental development.