3D Printing of High Viscosity UV-Curable Resin for Highly Stretchable and Resilient Elastomer.

Elastomers prepared via vat photopolymerizationus ually exhibit unsatisfied mechanical properties owing to their insufficient growth of molecular weight upon UV exposure. Increasing the weight ratio of oligomer in the resin system is an effective approach to enhance the mechanical properties, yet the viscosity of the UV-curable resin increases dramatically; this hinders its printing. In this study, a linear scan-based vat photopolymerization (LSVP) system which can print high-viscosity resins is implemented to 3D print the oligomer-dominated UV-curable resin via a dual-curing mechanism. A polyurethane methacrylate blocking oligomer is first synthesized and then mixed with a commercialized bifunctional oligomer, photoinitiator, and primary amine as a chain extender to prepare high-viscosity UV-curable resin for the LSVP system. The deblocked isocyanate is further crosslinked with a chain extender via thermal treatment to construct a highly entangled polymer chain network. The optimal thermal treatment parameters are investigated, and the resilience of the 3D-printed elastomer is evaluated through continuous tensile loading and unloading tests. Subsequently, complex structured elastomers are printed, exhibiting favorable mechanical durability without defects. The results obtained from this work will provide a reference for preparing elastomeric devices with excellent physical properties and expand the application scope of vat photopolymerization to new fields.

3D printing of ultra-high viscosity resin by a linear scan-based vat photopolymerization system.

The current printing mechanism of the bottom-up vat photopolymerization 3D printing technique places a high demand on the fluidity of the UV-curable resin. Viscous high-performance acrylate oligomers are compounded with reactive diluents accordingly to prepare 3D printable UV-curable resins (up to 5000 cps of viscosity), yet original mechanical properties of the oligomers are sacrificed. In this work, an elaborated designed linear scan-based vat photopolymerization system is developed, allowing the adoption of printable UV-curable resins with high viscosity (> 600,000 cps). Briefly, this is realized by the employment of four rollers to create an isolated printing area on the resin tank, which enables the simultaneous curing of the resin and the detachment of cured part from the resin tank. To verify the applicability of this strategy, oligomer dominated UV-curable resin with great mechanical properties, but high viscosity is prepared and applied to the developed system. It is inspiring to find that high stress and strain elastomers and toughened materials could be facilely obtained. This developed vat photopolymerization system is expected to unblock the bottleneck of 3D printed material properties, and to build a better platform for researchers to prepare various materials with diversiform properties developed with 3D printing.

Autoimmune hemolytic anemia as an initial presentation in children with systemic lupus erythematosus: two case reports.

We report the cases of two children who presented with autoimmune hemolytic anemia (AIHA) as an initial presentation of systemic lupus erythematosus (SLE). Both patients had a positive Coombs test, anemia, and an increased number of spherocytes in their blood smear. The patient in Case 1 presented with fever, urticarial erythema, facial paresis, AIHA, and leucopenia. Immunological screening revealed low complement protein levels and positive anti-nuclear antibody, anti-double-stranded DNA, and antiphospholipid antibody results. A further laboratory workup revealed a positive lupus anticoagulant (LA) result and low factor II levels. She was diagnosed with lupus anticoagulant hypoprothrombinemia syndrome (LAHPS) in addition to SLE. The patient in Case 2 presented with fever, butterfly rash, thyroid enlargement, leucopenia, and AIHA. She was diagnosed with SLE with thyroiditis. Both patients were started on combined immunosuppressive therapy, and both patients' clinical symptoms finally resolved. A literature review on childhood SLE showed that AIHA is common in patients with SLE. LAHPS is an uncommonly identified cause of bleeding in patients with SLE, and it must be considered when evaluating children with a positive LA result.

MicroRNA-214 promotes alveolarization in neonatal rat models of bronchopulmonary dysplasia via the PlGF-dependent STAT3 pathway.

BACKGROUND: Recently, the role of several microRNAs (miRNAs or miRs) in pulmonary diseases has been described. The molecular mechanisms by which miR-214 is possibly implicated in bronchopulmonary dysplasia (BPD) have not yet been addressed. Hence, this study aimed to investigate a putative role of miR-214 in alveolarization among preterm neonates with BPD. METHODS: Microarray-based gene expression profiling data from BPD was employed to identify differentially expressed genes. A BPD neonatal rat model was induced by hyperoxia. Pulmonary epithelial cells were isolated from rats and exposed to hyperoxia to establish cell injury models. Gain- and loss-of-function experiments were performed in BPD neonatal rats and hyperoxic pulmonary epithelial cells. MiR-214 and PlGF expression in BPD neonatal rats, and eNOS, Bcl-2, c-myc, Survivin, α-SMA and E-cadherin expression in hyperoxic pulmonary epithelial cells were measured using RT-qPCR and Western blot analysis. The interaction between PlGF and miR-214 was identified using dual luciferase reporter gene and RIP assays. IL-1ß, TNF-a, IL-6, ICAM-1 and Flt-1 expression in the rat models was measured using ELISA. RESULTS: The lung tissues of neonatal rats with BPD showed decreased miR-214 expression with elevated PlGF expression. PlGF was found to be a target of miR-214, whereby miR-214 downregulated PlGF to inactivate the STAT3 pathway. miR-214 overexpression or PlGF silencing decreased the apoptosis of hyperoxic pulmonary epithelial cells in vitro and restored alveolarization in BPD neonatal rats. CONCLUSION: Overall, the results demonstrated that miR-214 could facilitate alveolarization in preterm neonates with BPD by suppressing the PlGF-dependent STAT3 pathway.

Microplastic abundance and distribution in a Central Asian desert.

Microplastic pollution is widespread, affecting even the remotest places on Earth. However, observational data on microplastic deposition in deserts, which comprise 21% of the total land area, are relatively rare. The current study aims to address the knowledge gap in terms of microplastic distribution in Asian deserts. The Badain Jaran Desert in Central Asia is the second largest desert in China. We investigated microplastic distribution and deposition on dunes and lakes of this desert. Microplastics were extracted from surface sediments to determine their characteristics and polymer types by microscopic inspection and µ-FTIR. The abundance of microplastics (detection limit is approximately 40 µm) in the uninhabited area ranged from 0.7 ± 1.5 to 11.7 ± 15.5 items/kg, with an average of 6.0 ± 15.4 items/kg. Fragments and fibers accounted for 77% and 23% of the total microplastics, respectively. Epoxy resin (28%), polyethylene terephthalate (25%), phenoxy resin (25%), and polyamide (9%) were the main polymer components, whose sizes were concentrated at 50-200 µm. Back-trajectory modeling was then performed to explore the possible source direction of the microplastics. The results showed that the microplastics mainly originated from the populated areas southeast of the desert, indicating long-distance atmospheric transport and deposition in deserts. The desert-edge zone with some tourism activity contained more microplastics (8.2 ± 17.9 items/kg) than the non-tourism zone (0.9 ± 1.6 items/kg), indicating a potential contribution from tourism. The abundance in the non-tourism zone (0.9 items/kg) can be used as a reference for microplastic background values in the Central Asian deserts, as this value is critical for simulating and predicting global microplastic yields.

Bedside cardiopulmonary ultrasonography evaluates lung water content in very low-weight preterm neonates with patent ductus arteriosus.

BACKGROUND: Patent ductus arteriosus (PDA) is a common congenital heart abnormality in preterm neonates with a high incidence in neonates with very low birth weights. When PDA persists, interstitial lung water content increases, which could lead to abnormal circulation hemodynamics and pulmonary edema. It is important to perform early and reliable assessment of lung water content in very low-weight preterm neonates with persistent PDA. AIM: To evaluate the role of bedside cardiopulmonary ultrasonography in the lung water content assessment in very low-weight preterm neonates with persistent PDA. METHODS: From January 2018 to March 2020, 69 very low-weight preterm neonates with echocardiography-confirmed PDA were selected as the PDA group. At the same time, 89 very low-weight preterm neonates without PDA were randomly selected as the control group. All neonates underwent echocardiography and 6-segment lung ultrasonography on the fourth day after birth. The clinical characteristics and main ultrasonography results were compared between the two groups. Pearson's analysis was used to analyze the correlation between lung ultrasonography score (LUS) and other related clinical and ultrasonography results in all neonates. In the PDA group, PDA diameters were recorded, and the correlation with LUS and left atrium to aortic (LA/AO) dimension ratio were also analyzed. LA/AO ratio is one of the ultrasonic diagnostic criteria for hemodynamically significant PDA. When the ratio is ≥ 1.5, it suggests the possibility of hemodynamic changes in persistent PDA. A receiver operating characteristic curve was established using the sensitivity of LUS to predict the hemodynamic changes in neonates with PDA as the ordinate and 1-specificity as the abscissa. RESULTS: A total of 158 neonates were enrolled in this study, including 69 in the PDA group and 89 in the control group. There were no statistical differences in sex, gestational age, birth weight, ventilator dependence, hospitalization length and left ventricular ejection fraction between the two groups (P > 0.05). The LUS and LA/AO ratio in the PDA group were higher than those in the control group (P < 0.05), but there was no difference of LUS in neonates with or without use of the ventilator (t = 0.58, P = 0.16). In all cases, LUS was negatively correlated with gestational age (r = -0.28, P < 0.01) and birth weight (r = -0.36, P < 0.01), while positively correlated with the LA/AO ratio (r = 0.27, P < 0.01). In the PDA group, PDA diameter was positively correlated with the LA/AO ratio (r = 0.39, P < 0.01) and LUS (r = 0.31, P < 0.01). Receiver operating characteristic results showed that LUS had the moderate accuracy for predicting hemodynamic changes in PDA (area under the curve = 0.741; sensitivity = 93.75%; specificity = 50.94%). CONCLUSION: Bedside cardiopulmonary ultrasonography can evaluate lung content in neonates with PDA and predict the possibility of hemodynamic changes in persistent PDA.

Lung Ultrasound Score Predicts the Extravascular Lung Water Content in Low-Birth-Weight Neonates with Patent Ductus Arteriosus.

BACKGROUND Patent ductus arteriosus (PDA) is a common congenital cardiac abnormality in premature infants. In low-birth-weight infants weighing less than 2500 g, if the PDA continues to open, abnormal circulation hemodynamics and pulmonary edema may occur. This study aimed to investigate the role of lung ultrasound score in the assessment of pulmonary edema in low-weight neonates with PDA. MATERIAL AND METHODS Two hundred and twenty-one neonates with low birth weight were selected as the subjects, children with PDA as the observation group, and children with closed ductus arteriosus as the control group. On the fourth postnatal day, lung ultrasound examination and 6-segment lung ultrasound scoring were performed. RESULTS All 221 infants (94 in the observation group, 127 controls) underwent ultrasound examinations of the lungs. Intergroup differences in gestational age, birth weight, length of hospital stay, and left ventricular ejection fraction were not statistically significant. There was a significant difference in lung ultrasound score (t=0.005, P=0.000) and aortic root ratio to left atrial (t=0.085, P=0.000), which was negatively correlated with gestational age (r=-0.235, P=0.000) and positively correlated with PDA diameter (r=0.261, P=0.011). CONCLUSIONS Low-birth-weight children often have PDA. Its continued opening changes the circulation hemodynamics in children. Lung ultrasound score can semi-quantitatively evaluate the extravascular lung water content, identifying the need to intervene and follow up the hemodynamic significance of PDA over time.

Anti-placental growth factor antibody ameliorates hyperoxia-mediated impairment of lung development in neonatal rats.

This study investigates the effect of the overexpression of the placental growth factor (PGF) and hyperoxia on lung development and determines whether anti-PGF antibody ameliorates hyperoxia-mediated impairment of lung development in newborn rats. After exposure to normoxic conditions for seven days, newborn rats subjected to normoxia were intraperitoneally or intratracheally injected with physiological saline, adenovirus-negative control (Ad-NC), or adenovirus-PGF (Ad-PGF) to create the Normoxia, Normoxia+Ad-NC, and Normoxia+Ad-PGF groups, respectively. Newborn rats subjected to hyperoxia were intraperitoneally injected with physiological saline or anti-PGF antibodies to create the Hyperoxia and Hyperoxia+anti-PGF groups, respectively. Our results revealed significant augmentation in the levels of PGF and its receptor Flt-1 in the lung tissues of newborn rats belonging to the Normoxia+Ad-PGF or Hyperoxia groups. PGF overexpression in these groups caused lung injury in newborn rats, while anti-PGF antibody treatment significantly cured the hyperoxia-induced lung injury. Moreover, PGF overexpression significantly increased TNF-α and Il-6 levels in the bronchoalveolar lavage (BAL) fluid of the Normoxia+Ad-PGF and Hyperoxia groups. However, their levels were significantly reduced in the BAL fluid of the Hyperoxia+anti-PGF group. Immunohistochemical analysis revealed that PGF overexpression and hyperoxia treatment significantly increased the expression of the angiogenesis marker, CD34. However, its expression was significantly decreased upon administration of anti-PGF antibodies (compared to the control group under hyperoxia). In conclusion, PGF overexpression impairs lung development in newborn rats while its inhibition using an anti-PGF antibody ameliorates the same. These results provided new insights for the clinical management of bronchopulmonary dysplasia in premature infants.

Anti-placental growth factor antibody ameliorates hyperoxia-mediated impairment of lung development in neonatal rats

This study investigates the effect of the overexpression of the placental growth factor (PGF) and hyperoxia on lung development and determines whether anti-PGF antibody ameliorates hyperoxia-mediated impairment of lung development in newborn rats. After exposure to normoxic conditions for seven days, newborn rats subjected to normoxia were intraperitoneally or intratracheally injected with physiological saline, adenovirus-negative control (Ad-NC), or adenovirus-PGF (Ad-PGF) to create the Normoxia, Normoxia+Ad-NC, and Normoxia+Ad-PGF groups, respectively. Newborn rats subjected to hyperoxia were intraperitoneally injected with physiological saline or anti-PGF antibodies to create the Hyperoxia and Hyperoxia+anti-PGF groups, respectively. Our results revealed significant augmentation in the levels of PGF and its receptor Flt-1 in the lung tissues of newborn rats belonging to the Normoxia+Ad-PGF or Hyperoxia groups. PGF overexpression in these groups caused lung injury in newborn rats, while anti-PGF antibody treatment significantly cured the hyperoxia-induced lung injury. Moreover, PGF overexpression significantly increased TNF-α and Il-6 levels in the bronchoalveolar lavage (BAL) fluid of the Normoxia+Ad-PGF and Hyperoxia groups. However, their levels were significantly reduced in the BAL fluid of the Hyperoxia+anti-PGF group. Immunohistochemical analysis revealed that PGF overexpression and hyperoxia treatment significantly increased the expression of the angiogenesis marker, CD34. However, its expression was significantly decreased upon administration of anti-PGF antibodies (compared to the control group under hyperoxia). In conclusion, PGF overexpression impairs lung development in newborn rats while its inhibition using an anti-PGF antibody ameliorates the same. These results provided new insights for the clinical management of bronchopulmonary dysplasia in premature infants.

Noninvasive high-frequency oscillatory ventilation as respiratory support in preterm infants: a meta-analysis of randomized controlled trials.

BACKGROUND: Noninvasive high-frequency oscillatory ventilation (nHFOV), a relatively new modality, is gaining popularity despite scarce evidence. This meta-analysis was designed to evaluate the efficacy and safety of nHFOV as respiratory support in premature infants. METHODS: We searched MEDLINE, EMBASE, CINAHL, and Cochrane CENTRAL from inception of the database to January 2019. All published randomized controlled trials (RCTs) evaluating the effect of nHFOV therapy with nasal continuous positive airway pressure (nCPAP) or biphasic nCPAP (BP-CPAP) in newborns for respiratory support were included. All meta-analyses were performed using Review Manager 5.3. RESULTS: A total of 8 RCTs involving 463 patients were included. The meta-analysis estimated a lower risk of intubation (relative risk = 0.50, 95% confidence interval of 0.36 to 0.70) and more effective clearance of carbon dioxide (weighted mean difference = - 4.61, 95% confidence interval of - 7.94 to - 1.28) in the nHFOV group than in the nCPAP/BP-CPAP group. CONCLUSIONS: Our meta-analysis of RCTs suggests that nHFOV, as respiratory support in preterm infants, significantly remove carbon dioxide and reduce the risk of intubation compared with nCPAP/BP-CPAP. The appropriate parameter settings for different types of noninvasive high-frequency ventilators, the effect of nHFOV in extremely preterm infants, and the long-term safety of nHFOV need to be assessed in large trials.

Two case reports of neonatal autoantibody-associated congenital heart block.

RATIONALE: Neonatal lupus erythematosus (NLE) is an infrequent disease caused by transplacental maternal autoantibodies. The most common effects of NLE include cutaneous involvement and congenital heart block (CHB), although it might involve multiple organs, such as the liver, lungs, blood, and nervous or digestive systems. Izmirly PM1 and Tonello et al recently reported cutaneous manifestations of neonatal lupus and risk of subsequent CHB. The most serious complication of NLE is complete atrioventricular (AV) block. PATIENT CONCERNS: We experienced 2 cases of NLE that were diagnosed in the past year in our Neonatal Intensive Care Unit. These cases showed 2 different clinical spectrums (CHB, multisystemic effects). One case was a 32-week pregnant woman with combined liver damage and fever, and her fetus was premature due to bradycardia and pericardial effusion. The second case was a young pregnant woman who had systemic lupus erythematosus for 2 years and had been taking methylprednisolone and hydroxychloroquine for a long time since her illness. When prenatal testing at 28 weeks of pregnancy showed that the fetus had CHB, the mother began taking dexamethasone. DIAGNOSIS: The first case was diagnosed as NLE with CHB after birth, while the second was diagnosed as NLE with CHB, ductus arteriosus, and atrial septal defect when she was born at 34 weeks. INTERVENTIONS: Both of 2 cases were treated with steroids, intravenous immunoglobulin, and a diuretic. But the second case was treated with isoprenaline in addition to the above. OUTCOMES: Both of the infants was followed up and found to be clinically normal. During the clinic follow-up of the first case, the 8-month-old infant was still asymptomatic with normal growth and development. Her heart rate fluctuated from 40 to 90 beats/minute. LESSONS: Autoimmune CHB is a severe, potentially life-threatening disorder associated with passive transfer of maternal anti-Sjogren's syndrome A/Ro and anti-Sjogren's syndrome B/La autoantibodies. Mothers who are positive for these autoantibodies are recommended to have serial echocardiography and obstetric ultrasonography from the early second trimester. Newborns should be delivered at an early stage of gestation if there is evidence of pericardial effusion, ascites, increasing ventricular ectopy, reduced ventricular shortening fraction, or AV valve regurgitation. Aggressive medical management after birth should be coupled with pacemaker implantation in infants who do not respond to medical therapies alone.

Upregulation of CASC2 sensitized glioma to temozolomide cytotoxicity through autophagy inhibition by sponging miR-193a-5p and regulating mTOR expression.

OBJECTIVE: Numerous studies suggested autophagy was involved in temozolomide (TMZ) resistance in glioma. Long non-coding RNA (lncRNA) CASC2 was shown to be downregulated in glioma tissues and cell lines, and was related to the TMZ resistance. However, whether CASC2 affects TMZ resistance through regulating autophagy is unknown. The aim of this study was to assess the role and mechanism of CASC2 in TMZ-induced drug resistance in glioma cells. METHODS: Glioma and the adjacent non-cancerous tissues from 32 patients were collected. The expressions of CASC2 and miR-193a-5p were determined by PCR, and their correlation was analyzed. The correlation between CASC2 expression and the clinical characteristics of patients was also studied. Glioma cells were treated with TMZ to acquire the TMZ-resistant cell lines in which the expressions of CASC2, miR-193a-5p, and mTOR were measured. The regulatory roles of CASC2, miR-193a-5p, and mTOR were defined through the loss of function and luciferase reporter assays. Autophagy was inhibited by autophagy inhibitor 3-MA, CASC2 and mTOR overexpression, or miR-193a-5p inhibitor, and the effect of which on cell viability, apoptosis, and migration of TMZ-resistant glioma cells was evaluated. RESULTS: CASC2 downregulation and miR-193a-5p upregulation was found to be associated with advanced clinical stage and TMZ response in patients with glioma. CASC2 negatively regulates miR-193a-5p expression by direct interaction in glioma cells. Overexpression of CASC2 or inhibition of miR-193a-5p reduced TMZ-induced autophagy via mTOR upregulation, which makes the glioma cells become sensitive to TMZ cytotoxicity. CONCLUSION: CASC2 is downregulated in gliomas, resulting in increased miR-193a-5p level and a decrease in mTOR expression, which further induces protective autophagy, leading to TMZ resistance. Inhibition of autophagy helps to increase the efficacy of TMZ.

Airway administration of corticosteroids for prevention of bronchopulmonary dysplasia in premature infants: a meta-analysis with trial sequential analysis.

BACKGROUND: Uncertainly prevails with regard to the use of inhalation or instillation steroids to prevent bronchopulmonary dysplasia in preterm infants. The meta-analysis with sequential analysis was designed to evaluate the efficacy and safety of airway administration (inhalation or instillation) of corticosteroids for preventing bronchopulmonary dysplasia (BPD) in premature infants. METHODS: We searched MEDLINE, EMBASE, CINAHL, and Cochrane CENTRAL from their inceptions to February 2017. All published randomized controlled trials (RCTs) evaluating the effect of airway administration of corticosteroids (AACs) vs placebo or systemic corticosteroid in prematurity were included. All meta-analyses were performed using Review Manager 5.3. RESULTS: Twenty five RCTs retrieved (n = 3249) were eligible for further analysis. Meta-analysis and trial sequential analysis corrected the 95% confidence intervals estimated a lower risk of the primary outcome of BPD (relative risk 0.71, adjusted 95% confidence interval 0.57-0.87) and death or BPD (relative risk 0.81, adjusted 95% confidence interval 0.71-0.97) in AACs group than placebo and it is equivalent for preventing BPD than systemic corticosteroids. Moreover, AACs fail to increasing risk of death compared with placebo (relative risk 0.90, adjusted 95% confidence interval 0.40-2.03) or systemic corticosteroids (relative risk 0.81, 95% confidence interval 0.62-1.06). CONCLUSIONS: Our findings suggests that AACs (especially instillation of budesonide using surfactant as a vehicle) are an effective and safe option for preventing BPD in preterm infants. Furthermore, the appropriate dose and duration, inhalation or instillation with surfactant as a vehicle and the long-term safety of airway administration of corticosteroids needs to be assessed in large trials.

MicroRNA-564 is downregulated in glioblastoma and inhibited proliferation and invasion of glioblastoma cells by targeting TGF-ß1.

Increasing evidence has indicated that aberrant expression of miRNAs has been shown to be strongly implicated in the initiation and progression of glioblastoma. Here, we identified a novel tumor suppressive miRNA, miR-564, and investigated its role and therapeutic effect for glioblastoma. We showed that miR-564 was down-regulated in human glioblastoma tissues and cell lines. Introduction of miR-564 dramatically inhibited cell growth and invasion in glioblastoma cells. Subsequent experiments revealed that Transforming growth factor-ß1 (TGF-ß1) was a direct and functional target of miR-564 in glioblastoma cells. Furthermore, overexpression of miR-564 decreased p-SMAD and SMAD4 expression, which are the downstream signaling molecules of TGF-ß. Meanwhile, ectopic of miR-564 reduced the messenger RNA (mRNA) and protein expression of epidermal growth factor receptor (EGFR) and MMP9. Furthermore, the upregulation of miR-564 suppressed TGF-ß-mediated U87 proliferation and migration. The expression of EGFR and MMP9 was upregulated in glioblastoma tissues compared to their normal tissues. The EGFR and MMP9 expression levels were inverse correlated with the expression of miR-564. miR-564 suppressed the growth of U87-engrafted tumors. These findings reveal that miR-564/TGF-ß1 signaling that may be required for glioblastoma development and may consequently serve as a new therapeutic target for the treatment of glioblastoma.

TNF-α induces vascular endothelial cells apoptosis through overexpressing pregnancy induced noncoding RNA in Kawasaki disease model.

Kawasaki disease (KD) is an autoimmune disease in which the medium-sized blood vessels throughout the body become inflamed. The increased evidences showed that TNF-α was association with vascular inflammation in KD patients. However the detailed mechanism was still unclear. Recent studies indicated abnormal expressed long non-coding RNAs (LncRNAs) involved in many diseases. Thus the purpose of this study is to explore the role of lncRNAs in KD and find out the new target for KD treatment. In this study, firstly we verified the overexpressed TNF-α in KD patients, and found TNF-α was able to induce HUVECs apoptosis and inhibit HUVECs proliferation. After this we screened out pregnancy induced noncoding RNA (PINC) was significantly overexpression in TNF-α treated HUVECs. We also found PINC overexpressed in KD patients. For further study, we designed two siRNA of PINC. After silenced the expression of PINC in HUVECs, we found the Knockdown of PINC enhanced the viability of HUVECs treated with TNF-α, and increased the expression of anti-apoptotic and reduced the expression of apoptotic gene. These results suggest PINC involves in the process of TNF-α induces vascular endothelial cell apoptosis, it may become a new target for KD treatment.

DNA repair gene ERCC1 polymorphisms and glioma susceptibility among Chinese population: a meta-analysis.

BACKGROUND: Excision repair cross complementation group 1 (ERCC1) has been shown to be involved in the progression of glioma susceptibility. However, the results remain conflict. The aim of this study was to systematically review and evaluate the role of ERCC1 C118T and C8092A polymorphisms in glioma risk among Chinese population. METHODS: Related case-control studies were searched in online electronic databases. Odds ratio (OR) with its 95% confidence interval (CI) were employed to calculate the extracted data. RESULTS: Total seven articles were retrieved, including 4426 subjects (1926 were glioma patients and 2500 were matched controls). No significant heterogeneity was found between studies (I(2)=0%, P>0.01). Our results demonstrated that A allele and AA genotype of ERCC1 C8092A polymorphism have a positive association with increasing the risk of glioma in the fixed-effect model (A vs. C: OR=1.13, 95% CI=1.02-1.25, P=0.02; AA vs. CC: OR=1.29, 95% CI=1.04-1.61, P=0.02; AA vs. CA+CC: OR=1.25, 95% CI=1.01-1.55, P=0.04). However, no significant relationship was found between C118T variant and glioma susceptibility. CONCLUSIONS: Our results indicated that ERCC1 C8092A, not C118T polymorphism might be a biomarker for patients with glioma among Chinese population. Future studies with more ethnicities are needed to explore the precise association.

Effects of Vascular Endothelial Growth Factor in Recovery Phase of Acute Lung Injury in Mice.

AIM: To test the hypothesis that exogenous administration of vascular endothelial growth factor (VEGF) promotes lung repair in acute lung injury (ALI). METHODS: ALI was induced by intranasal lipopolysaccharide (LPS) administration in mice, followed by different treatment protocols for 7 days in 3 groups (n = 6, each) including the LPS, the VEGF and the anti-VEGF group. At day 7, peripheral blood and lungs were collected. Lung wet-to-dry (W/D) ratio and lung injury score were measured. Immunohistochemistry assay was employed to detect the number of pulmonary vessels. Circulating endothelial progenitor cells (EPCs) was detected using flow cytometric analysis, and the apoptosis of lung cells was determined by TUNEL staining. RESULTS: VEGF treatment reduced W/D ratio and pulmonary neutrophil infiltration in the VEGF group compared with the LPS group. The treatment of VEGF increased the number of pulmonary vessels, and significantly increased the number of circulating EPC cells. Moreover, administration of VEGF decreased the percentage of apoptotic cells in the VEGF group. CONCLUSIONS: Our results suggest that VEGF may contribute to vascular endothelial repair and function as a protective factor against ALI.