Ultra-Compact Low-Pass Spoof Surface Plasmon Polariton Filter Based on Interdigital Structure.

An ultra-compact low-pass spoof surface plasmon polariton (SSPP) filter based on an interdigital structure (IS) is designed. Simulated dispersion curves show that adding the interdigital structure in an SSPP unit effectively reduces its asymptotic frequency compared with traditional and T-shaped SSPP geometries, and the unit dimensions can be conversely reduced. Based on that, three IS-based SSPP units are, respectively, designed with different maximum intrinsic frequencies and similar asymptotic frequencies to constitute the matching and waveguide sections of the proposed filter, and the unit number in the waveguide section is adjusted to improve the out-of-band suppression. Simulation results illustrate the efficient transmission in the 0~5.66 GHz passband, excellent out-of-band suppression (over 24 dB) in the 5.95~12 GHz stopband and ultra-shape roll-off at 5.74 GHz of the proposed filter. Measurement results on a fabricated prototype validate the design, with a measured cut-off frequency of 5.53 GHz and an ultra-compact geometry of 0.5 × 0.16 λ02.

ß-Carotene regulates glucose transport and insulin resistance in gestational diabetes mellitus by increasing the expression of SHBG.

The aim of this work was to study the effect and mechanism of ß-carotene on insulin resistance and glucose transport in gestational diabetes mellitus (GDM). Placental tissue and venous blood of 26 GDM patients and 18 normal women were collected. Mice fed a high-fat diet were established as GDM models and treated with ß-carotene, from which peripheral blood and placenta tissue were collected. HTR-8/SVneo cells were treated with 10-7  mol/L insulin for 48 h and established as insulin resistance cell models. The expression of SHBG, GLUT1, GLUT3, GLUT4, IRS-1, IRS-2, PI3Kp85α, and p-CREB/CREB in placental tissues and HTR-8/SVneo cells was detected. Insulin resistance index was calculated from the values of fasting blood glucose and fasting insulin. The glucose consumption of insulin-resistant cells was calculated by detecting the glucose content of the supernatant. The cyclic adenosine monophosphate (cAMP) kit was applied to measure the concentration of cAMP in cells. SHBG was lowly expressed in GDM. ß-Carotene treatment upregulated SHBG in the placenta of GDM mice and in insulin-resistant HTR-8/SVneo cells. Overexpression of SHBG upregulated GLUT3, GLUT4, and IRS-1 and enhanced glucose consumption in insulin-resistant cells. ß-Carotene treatment promoted the expression of SHBG, GLUT4 and IRS-1 and increased glucose consumption in insulin-resistant cells underexpressing SHBG. Silencing of SHBG decreased the levels of cAMP and pCREB/CREB but ß-carotene treatment increased their expression despite SHBG silencing in insulin-resistant cells. ß-Carotene promotes glucose transport and inhibits insulin resistance in GDM by increasing the expression of SHBG.

Human placenta mesenchymal stem cell-derived exosome shuttling microRNA-130b-3p from gestational diabetes mellitus patients targets ICAM-1 and perturbs human umbilical vein endothelial cell angiogenesis.

OBJECTIVE: The aim of this study was to investigate the roles of miR-130b-3p and ICAM-1 in gestational diabetes mellitus (GDM) and their potential association. METHODS: Human placenta mesenchymal stem cells (PlaMSCs) were isolated from GDM patients, and the effects of the PlaMSCs from GDM patients (GDM-MSCs) and the exosomes secreted by GDM-MSCs on human umbilical vein endothelial cell (HUVEC) proliferation, migration, and angiogenesis were detected. Next, GDM-MSCs were transfected with miR-130b-3p antagomir to modify miR-130b-3p expression in GDM-MSCs-derived exosomes, and the exosomes with modified miR-130b-3p expression were cultured with HUVECs to evaluate exosomal miR-130b-3p on HUVEC function. Furthermore, a target gene of miR-130b-3p was predicted and assessed. The miR-130b-3p-modified exosomes were cultured with HUVECs transfected with ICAM-1 shRNA to determine the effect of miR-130b-3p-ICAM-1 crosstalk on HUVEC function. Additionally, a GDM mouse model was conducted to further study the effect of miR-130b-3p in GDM in vivo. RESULTS: GDM-MSCs inhibited HUVEC proliferation and angiogenesis. The elevated expression of miR-130b-3p was found in GDM-MSCs-derived exosomes. GDM-MSCs-derived exosomes repressed the proliferation and angiogenesis of HUVECs and miR-130b-3p inhibition could restrain the inhibition of the exosomes on HUVEC function. Mechanistically, miR-130b-3p downregulated ICAM-1 expression in a targeted manner, and thereby enhanced HUVEC proliferation, migration, and angiogenesis and increased the expression of angiogenesis-related factors. Moreover, miR-130b-3p inhibition promoted placental angiogenesis in GDM mice and upregulated ICAM-1 expression. CONCLUSION: Conclusively, GDM-MSCs-derived exosomes shuttling miR-130b-3p repressed proliferation, migration, and angiogenesis of HUVECs by regulating ICAM-1 expression.

Overexpression of hepatocyte growth factor protects chronic myeloid leukemia cells from apoptosis induced by etoposide.

Resistance to apoptosis induced by chemotherapy is still an obstacle for the treatment of chronic myeloid leukemia (CML). Numerous studies have indicated that upregulation of hepatocyte growth factor (HGF) protein expression reduced apoptosis induced by various factors. However, whether HGF has any effect on apoptosis induced by VP-16 (etoposide) in CML cells and its underlying mechanisms are unclear. HGF was overexpressed in the K562 cell line using transfection. The protein and mRNA expression levels, and the concentration of HGF were measured using western blot analysis, reverse transcription-quantitative (RT-qPCR) and ELISA respectively. Apoptosis in the K562 cell line was determined using flow cytometry and western blot analysis. Changes in cell viability were measured using a MTT assay. RT-qPCR and western blot analysis revealed that HGF was successfully upregulated at both the mRNA and protein expression levels in the K562 cell line, respectively. After VP-16 treatment, the number of apoptotic cells overexpressing HGF was lower compared with that in cells transfected with the empty vector. Mechanistic investigation revealed that overexpression of HGF led to the increase in Bcl-2 protein expression level and inhibition of caspase-3/9 activation. Furthermore, HGF overexpression resulted in activation of the PI3K/Akt signaling pathway. Therefore, the results of the present study revealed that targeting HGF could be used as a strategy to overcome VP-16 resistance in CML.

Colorado potato beetle exploits frass-associated bacteria to suppress defense responses in potato plants.

BACKGROUND: Colorado potato beetle (CPB; Leptinotarsa decemlineata) is a destructive quarantine pest that develops broad physiological adaptations to potato plants. During feeding, CPB deposits a copious amount of wet frass onto the surface of leaves and stems that remains in place for long periods. Insect behaviors such as feeding, crawling and oviposition are able to mediate plant defenses. However, the specific role of CPB defecation-associated cues in manipulating plant defenses remains unclear. RESULTS: CPB larval frass significantly suppressed potato polyphenol oxidase activity and enhanced larval growth on treated potato plants. The incorporation of antibiotics into larval frass triggered higher jasmonic acid (JA)-regulated defense responses in potato plants compared with antibiotic-free frass. Four bacterial symbionts belonging to the genera Acinetobacter, Citrobacter, Enterobacter and Pantoea were isolated from larval frass and suppressed plant defenses. After reinoculation of these bacteria into axenic larvae, Acinetobacter and Citrobacter were found to be highly abundant in the frass, whereas Enterobacter and Pantoea were less abundant probably due to the negative effect of potato steroidal glycoalkaloids (SGA) such as α-solanine. Furthermore, direct application of Acinetobacter and Citrobacter to wounded potato plants significantly inhibited the expression of genes associated with the JA-mediated defense signaling pathway and SGA biosynthesis. CONCLUSION: Our findings demonstrate that CPB exploits frass-associated bacteria as a deceptive strategy of plant defense suppression, adding an interesting dimension to our understanding of how CPB successfully specializes on potato plants. © 2022 Society of Chemical Industry.

Prognostic factors and survival outcome of primary pulmonary acinar cell carcinoma.

PURPOSE: The objective of our study was to investigate the epidemiologic characteristics and prognostic factors in patients with pulmonary acinar cell carcinoma (PACC). METHODS: PACC patients diagnosed between 1975 and 2016 were identified from the Surveillance, Epidemiology, and End Results (SEER) database. The trend in PACC incidence was assessed using joinpoint regression software. Overall survival (OS) and disease-specific survival (DSS) were evaluated using the Kaplan-Meier method and log-rank test. Univariate and multivariate Cox regression analysis was performed to identify the independent prognostic factors for OS and DSS. Nomograms to predict survival possibilities were constructed based on the identified independent prognostic factors. RESULTS: A total of 2918 patients were identified with PACC. The mean age was 65.2 ± 8.95 years with a female to male of 1.6:1. The incidence of PACC steadily increased by an annual percentage change (APC) of 3.2% (95% CI 2.1-4.4, p < 0.05). Multivariate Cox regression analysis revealed that age, gender, race, stage, grade, tumor size, number of positive lymph nodes, surgery, and chemotherapy were independent prognostic factors for survival. Nomograms specifically for PACC were constructed to predict 1- and 5-year OS and DSS possibility, respectively. The concordance index (C-index) and calibration plots showed the established nomograms had robust and accurate performance. CONCLUSION: PACC was rare but the incidence has been steadily increasing over the past four decades. Survival has improved in recent years. Surgery or chemotherapy could provide better OS and DSS. The established nomograms specifically for PACC were robust and accurate in predicting 1- and 5-year OS and DSS.

Zc3h12d, a Novel of Hypomethylated and Immune-Related for Prognostic Marker of Lung Adenocarcinoma.

BACKGROUND: Zc3h12d is a negative regulator which plays a crucial role in immune modulation. However, the role of zc3h12d in lung adenocarcinoma (LUAD) remains unclear. We aim to explore the prognostic of zc3h12d and investigate the relationship between zc3h12d expression and immune infiltration in LUAD. METHODS: TIMER site was used to analyze the expression of zc3h12d in LUAD. The zc3h12d protein levels in patient tissue samples were detected by immunohistochemistry staining assays. Meanwhile, based on UALCAN database and samples' data from our cohort, we explored the relationship of clinicopathological features and zc3h12d expression to determine the clinical effect of zc3h12d in LUAD. Several databases including GEPIA, Kaplan-Meier plotter and our samples' data were used to explore the prognostic value of zc3h12d in LUAD. Cox regression analysis was established to further evaluate the prognostic value of zc3h12d in LUAD. In addition, zc3h12d promoter methylation was analyzed by UALCAN database. Genetic alteration analysis was observed in the cBioPortal web. GO and KEGG analyses were conducted to elucidate the underlying mechanisms. Finally, the correlation between zc3h12d and tumor-infiltrating immune cells in LUAD was investigated by TIMER database. The B cells level was investigated by flow cytometry analysis of peripheral blood from our LUAD cohort. RESULTS: Zc3h12d expression was significantly higher in LUAD, compared with adjacent normal tissues. The clinical data from the UALCAN database demonstrated that zc3h12d expression was closely related with cancer stage and nodal metastasis. However, patient sample detection revealed that zc3h12d expression was closely related to pathological N (p = 0.0431) and grade (p = 0.004). Moreover, low zc3h12d expression was associated with poorer overall survival in LUAD. We analyzed the methylation level of zc3h12d in LUAD and found that the methylation levels of zc3h12d promoter in LUAD were significantly reduced. In addition, zc3h12d genetic alterations, including deep deletion, could be found in LUAD. GO and KEGG pathway analysis results indicated that zc3h12d has a certain value in immune infiltration. We investigated the expression of zc3h12d in tumor-immune interactions. It was found that zc3h12d might be associated with the immune infiltration and markers of infiltrating immune cells of LUAD. The results of patient sample detection confirmed that B cells level was significantly lower in the patients with low zc3h12d expression than those in the patients with high zc3h12d expression. CONCLUSION: zc3h12d might be considered as a potential biomarker for determining prognosis and immune-related therapeutic target in LUAD.

Downregulation of DNMT3a expression by RNAi and its effect on NF-κBs expression of thymic epithelial cells.

OBJECTIVE: To understand the characteristics of DNA methyltransferase 3a (DNMT3a) in thymoma associated Myasthenia Gravis reveal its transcriptional regulator network as while as analyze the effect of DNMT3a on Rel/ nuclear factor-kappaB family (RelA/RelB) and its downstream autoimmune regulatory factor (Aire). METHODS: Tissues of 30 patients with thymoma, with or without myasthenia gravis (MG), were collected and the DNMT3a protein expression were evaluated through immunohistochemistry. We performed mRNA expression profiling microarray detection and analysis, and integrated the analysis by constructing protein-protein interaction networks and the integration with other database. We identified molecular difference between low and high DNMT3a in the thymoma by heatmap. We also performed PCR validation in thymoma tissues. The DNMT3a-shRNA plasmid was transfected into TEC cells, and these cells were treated with 5-aza-2-deoxycytidine, a blocker of DNMT3a. After the down-regulation of DNMT3a in TEC cells, the transcript and protein levels of RelA, RelB, Aire, and CHRNA3 were evaluated by western blotting. In addition, changes in gene expression profiles were screened through microarray technology. We performed differential gene analysis in the thymoma cohort by heatmap with R (v.4.3.0) software. RESULTS: In 30 matched tissue specimens, the expression of DNMT3a protein in thymoma with MG was lower than that in thymoma. Through mRNA expression profiling analysis, we constructed a co-expression network of DNMT3a and found direct interaction between IKZF1 and DNMT3a, and this co-expression relationship was overlappted with Cistrome DB database. We found up-regulation of 149 mRNAs and repression of 177 mRNAs in thymoma with MG compared with thymoma. Gene ontology and pathway analysis show the involvement of a multitude of genes in the mis-regulation of MG-related pathways. RNA interference significantly reduced the level of mRNA of DNMT3a, which proved that plasmid DNMT3a was effective. In comparison to the control group, the levels of DNMT3a, Aire, and CHRNA3 mRNA and protein in TEC cells transfected with DNMT3a-shRNA interference plasmid were significantly decreased, while the expression level of RelA and RelA/RelB was significantly increased. CONCLUSIONS: Our study reveals the DNMT3a-NF-κB pathway has a major effect on MG, and can be used as a marker for diagnosis as well as a target for MG treatment.

Mitochondrial copper depletion suppresses triple-negative breast cancer in mice.

Depletion of mitochondrial copper, which shifts metabolism from respiration to glycolysis and reduces energy production, is known to be effective against cancer types that depend on oxidative phosphorylation. However, existing copper chelators are too toxic or ineffective for cancer treatment. Here we develop a safe, mitochondria-targeted, copper-depleting nanoparticle (CDN) and test it against triple-negative breast cancer (TNBC). We show that CDNs decrease oxygen consumption and oxidative phosphorylation, cause a metabolic switch to glycolysis and reduce ATP production in TNBC cells. This energy deficiency, together with compromised mitochondrial membrane potential and elevated oxidative stress, results in apoptosis. CDNs should be less toxic than existing copper chelators because they favorably deprive copper in the mitochondria in cancer cells instead of systemic depletion. Indeed, we demonstrate low toxicity of CDNs in healthy mice. In three mouse models of TNBC, CDN administration inhibits tumor growth and substantially improves survival. The efficacy and safety of CDNs suggest the potential clinical relevance of this approach.

Silicon-mediated multiple interactions: Simultaneous induction of rice defense and inhibition of larval performance and insecticide tolerance of Chilo suppressalis by sodium silicate.

The rice striped stem borer (SSB, Chilo suppressalis) is one of the most destructive pests of rice plants. Si-mediated rice defense against various pests has been widely reported, and sodium silicate (SS) has been used as an effective source of silicon for application to plants. However, there is quite limited information about the direct effects of Si application on herbivorous insects. SSB larval performance and their insecticide tolerance were examined after they had been reared either on rice plants cultivated in nutrient solution containing 0.5 and 2.0 mM SS or on artificial diets with 0.1% and 0.5% SS. SS amendment in either rice culture medium or artificial diets significantly suppressed the enzymatic activities of acetylcholinesterase, glutathione S-transferases, and levels of cytochrome P450 protein in the midgut of C. suppressalis larvae. Larvae fed on diets containing SS showed lower insecticide tolerance. Additionally, RNA-seq analysis showed that SS-mediated larval insecticide tolerance was closely associated with fatty acid biosynthesis and pyruvate metabolism pathways. Our results suggest that Si not only enhances plant resistance against insect herbivore, but also impairs the insect's capacity to detoxify the insecticides. This should be considered as another important aspect in Si-mediated plant-insect interaction and may provide a novel approach of pest management.

BHLHE40 plays a pathological role in pre-eclampsia through upregulating SNX16 by transcriptional inhibition of miR-196a-5p.

Pre-eclampsia (PE), which results from abnormal placentation, is a primary cause of maternal and neonatal morbidity and mortality. However, the causes of abnormal development of the placenta remain poorly understood. BHLHE40 is a transcriptional repressor in response to hypoxia. Bioinformatics analysis demonstrated that BHLHE40 negatively regulates miR-196a-5p expression, which may decrease miR-196a-5p to target SNX16. Since SNX16 exerts an inhibitory effect on cell migration, it may disrupt trophoblast cell migration in placentation. Therefore, the objective of this study was to explore a possible role of the BHLHE40/miR-196a-5p/SNX16 axis in PE pathogenesis. BHLHE40, miR-196a-5p and SNX16 mRNA and/or protein levels were detected in PE and normal placenta tissues. PE models in vitro and in vivo were constructed by culturing trophoblasts under hypoxia and reducing the uterine perfusion pressure in pregnant C57/BL6N mice, respectively. BHLHE40 and SNX16 were upregulated in PE placenta, while miR-196a-5p was downregulated. Knockdown of BHLHE40 reversed miR-196a-5p expression in trophoblasts under hypoxia, and upregulation of miR-196a-5p inhibited SNX16 expression. As indicated by ChIP assay, BHLHE40 bound to the promoter of the miR-196a-5p gene; luciferase reporter analysis showed that miR-196a-5p could bind to the 3'-untranslated region of SNX16 mRNA. Knockdown of either BHLHE40 or SNX16, or an increase in miR-196a-5p, restored cell viability, migration, invasion and matrix metalloprotein (MMP)-2 and MMP-9 expression under hypoxia. BHLHE40 knockdown also alleviated PE symptoms in pregnant C57/BL6N mice. This study supports involvement of the BHLHE40/miR-196a-5p/SNX16 axis in PE pathogenesis; Proper adjustment of the BHLHE40/miR-196a-5p/SNX16 axis is able to attenuate PE symptoms.

Association between risk of preeclampsia and maternal plasma trimethylamine-N-oxide in second trimester and at the time of delivery.

BACKGROUND: The data on the association between the microbiota-dependent metabolite trimethylamine-N-oxide (TMAO) during pregnancy and risk of preeclampsia (PE) is limited. METHODS: We, therefore, conducted a prospective nested case control study during Sep 2017 to Dec 2018 to examine the association between plasma TMAO measured during pregnancy and the risk of PE. Total of 17 patients diagnosed with early onset PE (EOPE), 49 with late onset PE (LOPE) and 198 healthy controls were enrolled. Blood samples were collected at 15-23 weeks gestation and time at delivery. The Logistic regression model was used to assess the odds ratio (OR) and 95% confidence interval (CI) for TMAO and risk of PE, EOPE, LOPE, mild PE, and severe PE. RESULTS: We found that the mean TMAO levels of overall subjects in the second trimester (T2) and at the time of delivery (TD) were 90.39 µg/m3 (standard deviation (SD) =45.91) and 175.01 µg/m3 (SD = 160.97), respectively. No significant spearman correlation was found between the TMAO in those two periods (p > 0.05). T2 TMAO was not significantly associated with risk of PE or risk of any PE subtypes (p > 0.05). However, TD TMAO was significant associated with risk of PE, EOPE and severe PE (adjusted OR and 95%CI were 1.24(1.09, 1.40), 1.62(1.29, 2.03), and 1.41(1.17, 1.70)) per 50 µg/m3 increment, respectively). CONCLUSION: Our study found that plasma TMAO level would alter over the course of pregnancy. The major role of TMAO in PE development might be in the accelerating process not in the initiation.

Quantitative analysis for modified Schall's classification by stimulation test with dynamic scintigraphy in Sjögren's syndrome.

OBJECTIVES: To update Schall's classification for Sjögren's syndrome (SS) by the new quantitative stimulation test with dynamic salivary glands scintigraphy (qsDSGS) and to standardize quantitative salivary gland scintigraphy. METHODS: The histopathology, oral, ocular, serological examination and qsDSGS of 268 consecutive patients with suggestive SS were evaluated in this retrospective cohort study. The serological examination included 15 autoantibodies, antinuclear antibodies (ANA) and so on. The diagnostic thresholds of the functional parameters were set by the quantitative method, and the modified Schall's classification is well established and verified. RESULTS: Based on the quantitative analysis of qsDSGS, the peak uptake level (PUL) and stimulation excretion fraction (sEF) of each parotid gland were determined as the key imaging features, which had good diagnostic performance for SS. By the modified Schall's classification, all patients were classified into: Class 1 (normal; n = 44), Class 2 (mild to moderate involvement; n = 130), Class 3 (severe involvement; n = 56) and Class 4 (very severe involvement, non-function; n = 38). Using the threshold PUL ≤ 10 counts per sec/pixel as positivity, the modified Schall's classification could provide better diagnostic performance with 88.4% specificity, 71.3% sensitivity, 96.14% positive predictive value and 43.20% negative predictive value for SS (likelihood ratio 6.15). The trends of serologically positive frequencies against SSA/Ro, anti-SSB/La and ANA were significantly increased with the new classification. CONCLUSION: The modified Schall's classification by the new stimulation test with dynamic scintigraphy is eligible to standardize quantitative salivary gland scintigraphy for SS, and may be more convenient and suitable in daily practice for clinical research and management of SS.

Effect of Wendantang-containing Serum on Apoptosis and Expressions of PI3K，Akt and GSK3β in Astrocytes Under Glutamate Environment / 中国实验方剂学杂志

Objective:To investigate the protective effect of Wendantang-containing serum on astrocytes in glutamate environment and its effect on phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt)/glycogen synthetase kinase 3β (GSK3β) signal pathway. Method:Totally 60 rats were randomly divided into 5 groups, normal group (n=20), clozapine group, and high, medium and low-dose Wendantang groups, with 10 rats in each group. Normal group was given 20 mL·kg-1 normal saline, clozapine group was given 20 mg·kg-1 clozapine, Wendantang groups were given 40, 20, 10 g·kg-1 Wendantang, once a day. Eight days later, the rats were killed, their blood was taken, serum was centrifuged, inactivated, filtrated, sterilized and filled in separate centrifugal tubes. The astrocytes were divided into normal group, model group, clozapine group, and high, medium and low-dose Wendantang groups. The normal group and the model group were cultured with normal serum, and the rest groups were cultured with corresponding drug containing serum. The other groups were treated with 10 mmol·L-1 glutamic acid for 24 hours, and then the apoptosis of astrocytes was detected by flow cytometry. Western blot and Real-time fluorescent quantitative polymerase chain reaction (Real-time PCR) were used to determine protein, and mRNA expressions of PI3K, Akt, GSK3β in astrocytes. Result:Compared with the normal group, apoptosis in model group increased significantly (P<0.01). Compared with the model group, apoptosis in Wendantang groups decreased significantly (P<0.01). Compared with the normal group, protein and phosphorylation expressions of PI3K, Akt, GSK3β in model groups decreased significantly (P<0.05, P<0.01). Compared with the model group, protein and phosphorylation expressions of PI3K, Akt, GSK3β in Wendantang groups increased (P<0.05, P<0.01). Compared with the normal group, expressions of PI3K, Akt and GSK3β mRNA decreased in model group(P<0.01). Compared with the model group, expressions of PI3K, Akt and GSK3β mRNA increased significantly in Wendantang groups group (P<0.05，P<0.01). Conclusion:Wendantang-containing serum can effectively increase expressions of PI3K, Akt and GSK3β, so as to regulate PI3K/Akt/GSK3β signal pathway and protect nerve cells.

A potential regulatory network among WDR86-AS1, miR-10b-3p, and LITAF is possibly involved in preeclampsia pathogenesis.

Preeclampsia (PE), a pregnancy-specific disorder, is a leading cause of perinatal maternal and fetal mortality and morbidity. Impaired migration and invasion of trophoblastic cells and an imbalanced systemic maternal inflammatory response have been proposed as possible causes of pathogenesis of PE. Comparative analysis of PE-affected placentas and healthy placentas has uncovered differentially expressed long noncoding RNAs, microRNAs, and mRNAs. This study was conducted to investigate the effect of a regulatory network among these RNAs on PE pathogenesis. Long noncoding RNA WDR86-AS1, microRNA miR-10b-3p, and mRNA of protein LITAF were identified by screening of genes in existing databases with aberrant expression in PE-affected placentas and potential mutual interactions as revealed by TargetScan, miRanda, and PicTar analyses. This study identified their expression in PE-affected and healthy placentas by RT-PCR. An in vitro experiment was performed on human trophoblast HTR-8/SVneo cells cultured under normoxic or hypoxic conditions. MiR-10b-3p targets were identified in luciferase reporter assays and RNA pull-down assays. The mouse model of PE was set up using a soluble form of FLT-1 for in vivo testing. Lower levels of miR-10b-3p but higher expression of WDR86-AS1 and LITAF were observed in PE-affected placentas and trophoblast cells under hypoxia. WDR86-AS1 and LITAF mRNA were confirmed as targets of miR-10b-3p. WDR86-AS1 downregulated miR-10b-3p but promoted LITAF expression. Microarray analyses revealed that LITAF controlled the inflammatory responses and migration and proliferation of HTR-8/SVneo cells under hypoxia. Indeed, knockdown of WDR86-AS1 and LITAF or overexpression of miR-10b-3p attenuated the hypoxia-induced inhibition of cellular viability, migration, and invasion. Moreover, miR-10b-3p overexpression attenuated the pathological symptoms caused by soluble FLT-1 in vivo. In summary, the WDR86-AS1/miR-10b-3p/LITAF network is probably involved in PE pathogenesis.

Effect of enhancer of zeste homolog 2 on the expression of glial cell line-derived neurotrophic factor family receptor α-1 in the colon tissue of children with Hirschsprung's disease / 中国当代儿科杂志

OBJECTIVE@#To study the expression levels of glial cell line-derived neurotrophic factor family receptor α-1 (GFRα1) and enhancer of zeste homolog 2 (EZH2) in the intestinal tissue of children with Hirschsprung's disease (HSCR), as well as the role of EZH2 in the regulation of GFRα1 gene expression and the pathogenesis of HSCR.@*METHODS@#The samples of colon tissue with spasm from 24 children with HSCR after radical treatment of HSCR were selected as the experimental group, and the samples of necrotized colon tissue from 18 children with neonatal necrotizing enterocolitis after surgical resection were selected as the control group. Real-time PCR and Western blot were used to measure the expression levels of GFRα1 and EZH2 in colon tissue in both groups. Human neuroblastoma SH-SY5Y cells were divided into an EZH2 over-expression group and a negative control group. The cells in the EZH2 over-expression group were transfected with pCMV6-EZH2 plasmid, and those in the negative control group were transfected with pCMV6 plasmid. The expression levels of EZH2 and GFRα1 were measured after transfection.@*RESULTS@#Compared with the control group, the experimental group had significant reductions in the mRNA and protein expression levels of GFRα1 and EZH2 in colon tissue (P<0.05), and the protein expression of EZH2 was positively correlated with that of GFRα1 (r=0.606, P=0.002). Compared with the negative control group, the EZH2 over-expression group had significant increases in the expression levels of EZH2 and GFRα1 after SH-SY5Y cells were transfected with EZH2 over-expression plasmid (P<0.05).@*CONCLUSIONS@#Low expression of EZH2 in the colon tissue of children with HSCR may be one of the causes of inadequate expression of GFRα1 and onset of HSCR.

A Study on the Correlation Between PetCO2 and PaCO2 in Children Cardiopulmonary Bypass Perioperative Period / 昆明医科大学学报

Objective To investigate the clinical significance and correlation of end-tidalcarbon dioxide partial pressure (PetCO2) and arterial blood carbon dioxide pressure (PaCO2) of children with different types of congenital heart disease in perioperative period of cardiopulmonary bypass.Methods 60 children undergoing selective cardiopulmonary bypass surgery for congenital heart disease were chosen (aged 1-14 years old, ASA class II or III).According to echocardiographic results, the children were divided into two groups. Group A:Left-to-right shunt in children, involving 15 cases of atrial septal defect and 15 cases of ventricular septal defect;Group B: Right-to-left shunt in children, involving 30 cases of Fallot tetrad. All 60 children underwent intravenous general anesthesia and rapid induction of orotracheal intubation. All patients underwent ventilator-assisted ventilation in the surgical intensive care unit for 8 hours after surgery. The brachial artery blood was collected for arterial blood gas analysis to measure PaCO2 at the beginning of surgery (T1), 15 min after anesthesia (T2), before CPB (T3), 15 min after CPB (T4), end of surgery (T5), time to transfer to SICU (T6), 2 h after monitored in ICU (T7), 4 h after monitored in SICU (T8), 6 h after monitored in SICU (T9), 8 h after monitored in SICU (T10).The PaCO2 and PetCO2 were recorded at each time point. According to the result of PetCO2 and PaCO2, we studied the correlation of the two indexes at each time point.Results In group A, there was a positive correlation between PetCO2 and PaCO2 at each time point (the correlation was 0.55 to 0.87, P＜0.001). The correlation between PETCO2 and PaCO2 decreased gradually during T2-6, and the correlation gradually increased during T7-10. There was no significant correlation between PetCO2 and PaCO2 (the correlation was0.21 to 0.38, P＞ 0.05) before operation in group B until 15 minutes after CPB. From the end of surgery to 8 hours after SICU monitoring, PetCO2 was positively correlated with PaCO2 (the correlation was0.54 to 0.83, P ＜ 0.05).The correlation between the two indexes increased gradually during T5-10. Conclusions During the perioperative period of cardiopulmonary bypass, PetCO2 can be used as an evaluation indicator for clinical monitoring in the children with Left-to-right shunt of congenital heart disease.There was no significant correlation between PetCO2 and PaCO2 in the children with congenital heart disease of right-to-left shunting before the end of surgery. PetCO2 could not replace PaCO2.With the improvement of postoperative conditions, It is significant to dynamically observe changes in PetCO2 to guide the analysis of PaCO2.

Balloon dilation of epidermolysis bullosa-related esophageal strictures: A report of two cases

Epidermolysis bullosa (EB) is a very rare inherited disease featured with skin blistering resulting from minor trauma. Sometimes the esophageal mucosa could also be involved, which leads to esophageal strictures. Here we report two cases of EB-related esophageal strictures who were successfully treated with esophageal balloon dilations. The two cases with EB had severe dysphagia. Clinical examination showed signs of malnutrition, skin blisters and loss of toenails due to EB. They underwent careful fluoroscopic balloon dilation with 10- and 16-mm-sized balloon catheters, respectively. They could ingest soft and some solid foods after the procedure and maintained during the 20 months and 16 months follow-up periods.

Novel Ag-doped glass frits for high-efficiency crystalline silicon solar cells.

Glass frits play an important role in the front contact electrodes of crystalline silicon (c-Si) solar cells. In this work, we developed a novel glass frit by doping Ag into a glass frit in the process of high-temperature synthesis. When the Ag paste including this novel glass frit was used as the front contact electrode of silicon solar cells, the conversion efficiency of poly-crystalline silicon (pc-Si) solar cells was improved by 1.9% compared to the glass frit without Ag. Through SEM characterisation and calculation of series resistance, we further found that the interface between Ag and Si was improved and the contact resistance of Ag and Si was greatly reduced, which were believed to be responsible for the improvement of solar cell performance. This work shows great guidance significance to develop novel and highly efficient commercial glass frits applied in solar cells in the future.