Rutin suppresses the malignant biological behavior of gastric cancer cells through the Wnt/ß-catenin pathway.

Rutin is a natural flavonoid compound that is widely found in a variety of plants and has a variety of biological effects, including anti-inflammatory, antioxidant, and anti-tumor effects. Rutin has been shown to have anti-tumor effects in a variety of cancers, but its effects on gastric cancer need to be further explored. The aim of this study was to explore the effects of Rutin on gastric cancer cells and the potential molecular regulatory mechanisms. Gastric cancer cells (AGS and MGC803) were treated with different concentrations of Rutin. Cell proliferation, apoptosis, migration, and invasion were determined by MTT, flow cytometry, scratch assay, and Transwell analysis, respectively. Cell epithelial mesenchymal transition (EMT) markers and Wnt/ß-catenin pathway were analyzed by RT-qPCR and western blot assay. The results showed that Rutin significantly inhibited the proliferation, migration and invasion ability of gastric cancer cells, induced apoptosis, and suppressed the EMT process. Further experiments revealed that Rutin achieved the effect of inhibiting the biological behavior of gastric cancer cells by suppressing the activation of the Wnt/ß-catenin pathway. Therefore, Rutin may become a potential therapeutic candidate for gastric cancer.

Gut microbiota characteristics of colorectal cancer patients in Hubei, China, and differences with cohorts from other Chinese regions.

The research on the correlation or causality between gut microbiota and the occurrence, development, and treatment of colorectal cancer (CRC) is receiving increasing emphasis. At the same time, the incidence and mortality of colorectal cancer vary among individuals and regions, as does the gut microbiota. In order to gain a better understanding of the characteristics of the gut microbiota in CRC patients and the differences between different regions, we initially compared the gut microbiota of 25 CRC patients and 26 healthy controls in the central region of China (Hubei Province) using 16S rRNA high-throughput sequencing technology. The results showed that Corynebacterium, Enterococcus, Lactobacillus, and Escherichia-Shigella were significantly enriched in CRC patients. In addition, we also compared the potential differences in functional pathways between the CRC group and the healthy control group using PICRUSt's functional prediction analysis. We then analyzed and compared it with five cohort studies from various regions of China, including Central, East, and Northeast China. We found that geographical factors may affect the composition of intestinal microbiota in CRC patients. The composition of intestinal microbiota is crucial information that influences colorectal cancer screening, early detection, and the prediction of CRC treatment outcomes. This emphasizes the importance of conducting research on CRC-related gut microbiota in various regions of China.

Establishment of a transgene-free iPS cell line (SDCHi007-A) from a young patient bearing a ATP1A2 mutation and suffering from Epilepsy.

Epilepsy is a chronic neurological disease. Here we describe the generation of induced pluripotent stem cells (iPSCs) from a patient diagnosed as epilepsy caused by ATP1A2 gene mutation. Induced pluripotent stem cells (iPSCs) were developed using non-integrating episomal vectors containing OCT4, SOX2, KLF4, BCL-XL and C-MYC. The established iPSC line (SDCHi007-A) displayed pluripotent cell morphology, high expression levels of pluripotency markers, differentiation potential in vitro, normal karyotype, and remaining the original ATP1A2 gene mutation.

Epileptic seizures as an initial symptom for Sturge­Weber syndrome type III: A report of two cases.

Sturge-Weber syndrome (SWS) type III, a rare neurocutaneous disorder, presents diagnostic challenges due to its variable clinical manifestations. The present study focuses on enhancing the understanding of this syndrome by conducting a detailed analysis of two pediatric cases and providing a comprehensive review of the existing literature. The cases, managed at the Children's Hospital Affiliated to Shandong University (Jinan, China), highlight the diverse clinical presentations and successful management strategies for SWS type III. In the first case, a 4-year-old male patient exhibited paroxysmal hemiplegia, epileptic seizures and cerebral angiographic findings indicative of left pia mater and venous malformation. The second case involved a 2.5-year-old male patient presenting with recurrent seizures and angiographic findings on the right side. Both cases underscore the importance of considering epileptic seizures, acquired and transient hemiplegia and cognitive impairments in the diagnosis of SWS type III. The present study provides insights into the effective use of both pharmacological and surgical interventions, drawing from the positive outcomes observed in these cases. The findings emphasize the need for heightened awareness and a meticulous approach in diagnosing and treating SWS type III, contributing to the better management and prognosis of this condition.

[Retracted] lncRNA ROR promotes the progression of renal cell carcinoma through the miR­206/VEGF axis.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell invasion and migration assay data shown in Fig. 2D and F on p. 3786 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes, which had already been published. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 20: 3782­3792, 2019; DOI: 10.3892/mmr.2019.10636].

Vagus nerve stimulation for treating developmental and epileptic encephalopathy in young children.

Objective: To investigate the clinical variables that might predict the outcome of developmental and epileptic encephalopathy (DEE) after vagus nerve stimulation (VNS) therapy and identify the risk factors for poor long-term outcome. Patients and methods: We retrospectively studied 32 consecutive children with drug-resistant DEE who had undergone VNS surgery from April 2019 to July 2021, which were not suitable for corpus callosotomy. In spite of combining valproic acid, levetiracetam, lamotrigine, topiramate, etc. (standard anti-seizure medicine available in China) it has not been possible to effectively reduce seizures in the population we investigate (Cannabidiol and brivaracetam were not available in China). A responder was defined as a frequency reduction decrease > 50%. Seizure freedom was defined as freedom from seizures for at least 6 months. Sex, electroencephalograph (EEG) group, neurodevelopment, time lag, gene mutation, magnetic resonance imaging (MRI), and epilepsy syndrome were analyzed with Fisher's exact test, The age at onset and age at VNS therapy were analyzed with Kruskal-Wallis test, statistical significance was defined as p < 0.05. And used the effect size to correction. Results: Among the 32 patients, the median age at VNS implantation was 4.7 years (range: 1-12 years). At the most recent follow-up, five children (15.6%) were seizure-free and 22 (68.8%) were responders. Univariate analysis demonstrated that the responders were significantly associated with mild development delay/intellectual disability (p = 0.044; phi coefficient = 0.357) and a multifocal EEG pattern (p = 0.022; phi coefficient = -0.405). Kaplan-Meier survival analyses demonstrated that a multifocal EEG pattern (p = 0.049) and DEE without epileptic spasm (ES) (p = 0.012) were statistically significant (p = 0.030). Multivariate analysis demonstrated that DEE with ES had significant predictive value for poor long-term outcome (p = 0.014, hazard ratio = 5.433, confidence interval = 1.402-21.058). Conclusions: Our study suggested that VNS was a generally effective adjunct treatment for DEE. Although the predictive factors for VNS efficacy remain unclear, it should be emphasized that patients with ES are not suitable candidates for epilepsy surgery. Further investigations are needed to validate the present results.

Modified Naples prognostic score for evaluating the prognosis of patients with obstructive colorectal cancer.

BACKGROUND: Inflammatory, immune, and nutritional status are key factors in obstructive colorectal cancer (OCRC). This study aims to investigate the value of modified Naples prognostic score (M-NPS) in evaluating OCRC prognosis. METHODS: A total of 196 OCRC patients were retrospectively analyzed to construct M-NPS based on serum albumin (ALB), total cholesterol (CHOL), neutrophil:lymphocyte ratio (NLR), and lymphocyte:monocyte ratio (LMR), and then they were divided into three groups. The Kaplan-Meier (KM) method and Cox proportional hazard regression analysis were performed for overall survival (OS) and disease-free survival (DFS) of OCRC patients. RESULTS: Patients with high M-NPS had worse OS and DFS (P = 0.0001, P = 0.0011). Multivariate COX analysis showed that M-NPS was an independent prognostic factor for OCRC patients. Patients in the M-NPS 2 group had significantly worse OS (hazard ratio [HR] = 4.930 (95% confidence interval [95% CI], 2.217-10.964), P < 0.001) and DFS (HR = 3.508 (95% CI, 1.691-7.277), P < 0.001) than those in the 0 group. CONCLUSION: M-NPS was an independent prognostic factor for OCRC patients; it might provide a potential reference for immunonutritional intervention in patients with obstruction.

Surfactant-mediated colorimetric assay assisted with in-situ rolling circle amplification on magnetic beads.

Gold nanoparticles (AuNPs) with localized surface plasmon resonance effect have been widely used for colorimetric detection based on the interparticle plasmon coupling during AuNPs aggregation. However, it is still challenging to develop portable and quantitative methods with good sensitivity and excellent selectivity. In this study, a smartphone-based colorimetric assay is developed on the principle of surfactant-mediated AuNPs aggregation assisted with rolling circle amplification (RCA) on magnetic beads (MBs). The detection of adenosine is demonstrated as an example. The cetyl trimethyl ammonium bromide (CTAB) causes the negatively charged AuNPs to aggregate, which results in the color change from red to blue. When adenosine is in solution, the RCA process is triggered on the MBs because of specific adenosine-aptamer recognition, resulting in prolongation of single-stranded nucleic acid (ssDNA). The solution color remains red due to the electrostatic interaction between CTAB and ssDNA. Using this method, the limit of detection (LOD) for adenosine can be as low as 16 pM. Besides, it also works well in human serum. In addition, a portable device integrated with in-situ RGB analysis software is developed for the detection with a smartphone. This study offers a new strategy to improve the sensitivity and selectivity for the AuNPs-based colorimetric assay, taking advantages of specific aptamer recognition, in-situ RCA on MBs, magnetic separation, and smartphone-based portable device.

Abnormal expression of long non-coding RNA FGD5-AS1 affects the development of ovarian cancer through regulating miR-107/RBBP6 axis.

Long non-coding RNAs (lncRNAs) are important players in cancer development. LncRNA FGD5-AS1 has been reported as a potential oncogene in ovarian cancer (OC). The present paper focused on the action mechanism of FGD5-AS1 in OC. Clinical OC samples were collected for expression analyses of FGD5-AS1, RBBP6, and miR-107. The expression of FGD5-AS1, RBBP6, and miR-107 in OC cells was altered by transfection. OC cell proliferation was assessed by MTT and colony formation assays, and angiogenesis of human umbilical vein endothelial cells (HUVECs) cultured with OC cell supernatants by matrigel angiogenesis assay. The interactions among FGD5-AS1, miR-107, and RBBP6 were detected by luciferase reporter assay. FGD5-AS1 and RBBP6 were strongly expressed and miR-107 was poorly expressed in clinical OC samples and OC cell lines. FGD5-AS1 or RBBP6 overexpression in Hey and SKOV3 cells could potentiate OC cell proliferation and HUVEC angiogenesis, while FGD5-AS1 or RBBP6 knockdown in OC cells inhibited the above cellular processes. FGD5-AS1 targeted miR-107 to positively regulate RBBP6 expression. Additionally, miR-107 overexpression or RBBP6 knockdown in SKOV3 cells partially reversed the FGD5-AS1-dependent stimulation of OC cell proliferation and HUVEC angiogenesis. FGD5-AS1 may act as a promoter of OC via miR-107/RBBP6 axis.

Paper-Based Flow Sensor for the Detection of Hyaluronidase via an Enzyme Hydrolysis-Induced Viscosity Change in a Polymer Solution.

Hyaluronidase (HAase) is implicated in inflammation, cancer development, and allergic reaction. The detection of HAase is significantly important in clinical diagnosis and medical treatment. Herein, we propose a new principle for the development of equipment-free and label-free paper-based flow sensors based on the enzymatic hydrolysis-induced viscosity change in a stimuli-responsive polymer solution, which increases the water flow distance on the pH indicator paper. The detection of HAase is demonstrated as an example. This facile and versatile method can overcome the potential drawbacks of traditional hydrogel-based sensors, including complex preparation steps, slow response time, or low sensitivity. Moreover, it can also avoid the use of specialized instruments, labeled molecules, or functionalized nanoparticles in the sensors developed using the polymer solutions. Using this strategy, the detection of HAase is achieved with a limit of detection as low as 0.2 U/mL. Also, it works well in human urine. Additionally, the detection of tannic acid, which is an inhibitor of HAase, is also fulfilled. Overall, a simple, efficient, high-throughput, and low-cost detection method is developed for the rapid and quantitative detection of HAase and its inhibitor without the use of labeled molecules, synthetic particles, and specialized instruments. As only minimal reagents of HAase, HA, and paper are used, it is very promising in the development of commercial kits for point-of-care testing.

UBA2 promotes the progression of renal cell carcinoma by suppressing the p53 signaling.

BACKGROUND: Renal cell carcinoma or RCC is a type of malignancy commonly occurred in the human kidney especially in the adults. The pathogenesis of RCC involves the complex networking of multiple signaling pathways, and the underlying molecular mechanisms remain largely unclear. OBJECTIVES: This study aimed to elucidate the regulatory functions of UBA2 and explore its potential downstream molecules during the tumor progression in RCC. METHODS: In this paper, the expression of UBA2 and associated molecules was examined by RT-qPCR and western blotting. The proliferative activity of RCC cells was determined using CCK-8 assay and immunofluorescence staining of proliferation-related marker Ki-67. Moreover, the cell distribution and apoptosis were evaluated by flow cytometry. RESULTS: Our results revealed the upregulation of UBA2 in RCC tissues and cells, and the high-expression of UBA2 was also associated with bigger tumor size, more advanced stage, and poorer overall survival in RCC patients. In addition, UBA2 knockdown was able to suppress the growth of RCC cells and induced cell cycle arrest at G0/G1 phase. Furthermore, the p53 signaling could be the novel target of UBA2 in RCC, and UBA2 affected the biological behaviors of RCC cells in a p53-dependent manner. CONCLUSION: In summary, UBA2 was able to enhance the proliferation, inhibit the apoptosis, and suppress cell cycle arrest in RCC cells by targeting the p53 pathway.

Disruption of Jmjd3/p16Ink4a Signaling Pathway Causes Bizarre Parosteal Osteochondromatous Proliferation (BPOP)-like Lesion in Mice.

Bizarre parosteal osteochondromatous proliferation (BPOP), or Nora's lesion, is a rare benign osteochondromatous lesion. At present, the molecular etiology of BPOP remains unclear. JMJD3(KDM6B) is an H3K27me3 demethylase and counteracts polycomb-mediated transcription repression. Previously, Jmjd3 was shown to be critical for bone development and osteoarthritis. Here, we report that conditional deletion of Jmjd3 in chondrogenic cells unexpectedly resulted in BPOP-like lesion in mice. Biochemical investigations revealed that Jmjd3 inhibited BPOP-like lesion through p16Ink4a . Immunohistochemistry and RT-qPCR assays indicated JMJD3 and p16INK4A level were significantly reduced in human BPOP lesion compared with normal subjects. This was further confirmed by Jmjd3/Ink4a double-gene knockout mice experiments. Therefore, our results indicated the pathway of Jmjd3/p16Ink4a may be essential for the development of BPOP in human. © 2021 American Society for Bone and Mineral Research (ASBMR).

EZH2-mediated lncRNA ABHD11-AS1 promoter regulates the progression of ovarian cancer by targeting miR-133a-3p.

Long-chain noncoding RNAs (lncRNAs) are involved in a wide range of biological and pathological processes in ovarian cancer. The purpose of this study was to investigate the effects of EZH2-mediated ABHD11-AS1 promoter on the pathogenesis of ovarian cancer. The expression levels of EZH2, ABHD11-AS1 and miR-133a-3p were examined in ovarian cancer tissues using reverse transcription-quantitative PCR. Cell proliferation was evaluated using cell counting kit 8 assay, and cell invasion/migration was determined using a Transwell assay. Cell apoptosis was evaluated using flow cytometry. Dual luciferase assay was performed to confirm the interaction between ABHD11-AS1 and miR-133a-3p. The binding site of H3K27me3 on ABHD11-AS1 promoter was confirmed by ChIP. The expression of ABHD11-AS1 was significantly upregulated in ovarian cancer samples, and its levels were closely associated with lymph node metastasis, tumor stage and 3-year survival rate. Furthermore, interference of ABHD11-AS1 suppressed the proliferation, migration and invasion of ovarian cancer cells, while cell apoptosis was promoted. Additionally, miR-133a-3p could be a novel target of ABHD11-AS1, and EZH2-mediated H3K27me3 protein might bind to ABHD11-AS1 promoter directly. Moreover, rescue experiments indicated that the effects caused by ABHD11-AS1 knockdown on the malignant characteristics of ovarian cancer cells were notably enhanced by miR-133a-3p mimics, whereas the influences on cell growth and metastasis induced by overexpressed ABHD11-AS1 were abrogated by the restoration of miR-133a-3p expression. In summary, EZH2-mediated enrichment of H3K27me3 on ABHD11-AS1 promoter could regulate the progression of ovarian cancer via miR-133a-3p. Therefore, EZH2/ABHD11-AS1/miR-133a-3p axis might be a putative candidate for targeted treatment of ovarian cancer.

Prognostic Significance of Pretreatment Prognostic Nutritional Index (PNI) in Patients with Nasopharyngeal Carcinoma: A Meta-Analysis.

OBJECTIVE: Previous studies have investigated the pretreatment prognostic nutritional index (PNI) as a prognostic factor in patients with nasopharyngeal carcinoma (NPC); however, the results remained inconsistent. We aimed to assess the prognostic value of PNI in patients with NPC through conducting meta-analysis. Methods: Pooled hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated for low PNI of overall survival (OS), progression-free survival (PFS), distant metastasis-free survival (DMFS), loco-regional recurrence-free survival (LRFS), and cancer-specific survival (CSS). Results: Totally, eight studies involving 4299 patients were included in this meta-analysis. A low pretreatment PNI was associated with poor OS (HR = 1.86, 95% CI = 1.55-2.33, P < 0.001), DMFS (HR = 2.03, 95% CI = 1.69-2.44, P < 0.001), PFS (HR = 1.57, 95% CI = 1.31-1.90, P < 0.001), and CSS (HR = 2.29, 95% CI = 1.54-3.42, P < 0.001). The subgroup analysis showed that low PNI remained a significant factor for poor OS, DMFS, and PFS irrespective of treatment, country, and cutoff value of PNI. In addition, low PNI was correlated to female gender (OR = 1.35, 95% CI = 1.12-1.62, P = 0.002), older age (OR = 1.75, 95% CI = 1.17-2.62, P = 0.007), and T3-T4 stage (OR = 1.27, 95% CI = 1.06-1.53, P = 0.011). Conclusions: A low PNI was associated with poor survival outcomes in patients with NPC. Moreover, PNI could serve as an index to help guide clinical management for older patients.

Exosomal circular RNA_400068 promotes the development of renal cell carcinoma via the miR­210­5p/SOCS1 axis.

Renal cell carcinoma (RCC) is a common type of malignancy in the kidney, which accounts for ~80% of the cases within adult patients. The pathogenesis of RCC is complicated and involves alterations at both genetic and epigenetic levels. The aim of the present study was to investigate the roles of circRNAs in the pathogenesis of RCC. In the current study, exosomes were isolated via gradient centrifugation and identified using transmission electron microscope. The expression levels of circular RNA (circ)_400068, microRNA (miR)­210­5p and suppressor of cytokine signaling 1 (SOCS1) were examined using reverse transcription­quantitative PCR. Cell proliferation was evaluated using a Cell Counting Kit­8 assay, and the apoptotic rate was determined in transfected cells using flow cytometry. The protein expression levels of proliferation­ and apoptosis­associated genes were assessed via western blot analysis. Upregulation of circ_400068 was detected in RCC plasma exosomes, tissue samples and cells. Additionally, treatment with exosomal circ_400068 promoted the proliferation and inhibited the apoptosis of healthy kidney cells, which were abrogated by short hairpin RNA­circ_400068. The results suggested that miR­210­5p was a potential downstream molecule of circ_400068, and SOCS1 was a novel target of miR­210­5p. Moreover, circ_400068 regulated the proliferation of HK­2 cells by targeting the miR­210­5p/SOCS1 axis, as the effects on cell proliferation caused by treatment using exosomes isolated from the culture media of RCC cells were abolished by miR­210­5p mimics. It was found that enhanced cell proliferation induced by miR­210­5p inhibitors was attenuated by the knockdown of SOCS1, while the influences triggered by miR­210­5p mimics were reversed by SOCS1 overexpression. Collectively, the present findings provided a novel insight into the crucial regulatory functions of circ_400068 in RCC, and the circ_400068/miR­210­5p/SOCS1 axis could be a candidate therapeutic target for the treatment of patients with RCC.

TRAF3 promotes ROS production and pyroptosis by targeting ULK1 ubiquitination in macrophages.

Disrupted mitochondrial function and reactive oxygen species (ROS) generation cause cellular damage and oxidative stress-induced macrophage inflammatory cell death. It remains unclear how mitochondrial dysfunction relates to inflammasome activation and pyroptotic cell death. In this study, we demonstrated that tumor necrosis factor receptor-associated factor 3 (TRAF3) regulates mitochondrial ROS production and promotes TLR agonist LPS plus nigericin (LPS/Ng)-induced inflammasome and pyroptosis in mouse primary macrophages and human monocyte THP-1 cells. Co-IP assays confirmed that TRAF3 forms a complex with TRAF2 and cIAP1 and mediates ubiquitin and degradation of Unc-51 like autophagy activating kinase 1 (ULK1). Moreover, knockdown of ULK1 in THP-1 cells significantly promoted LPS/Ng-induced inflammasome by activating caspase 1 and mature IL-1ß. Apoptosis inducing factor (AIF) translocation from mitochondrial to nuclear was observed in ULK1-deficient THP-1 cells under LPS/Ng stimulation, which mediates LPS/Ng-induced cell death in ULK1 deficient macrophages. In conclusion, this study identified a novel role of TRAF3 in regulation of ULK1 ubiquitination and inflammasome signaling and provided molecular mechanisms by which ubiquitination of ULK1 controls mitochondrial ROS production, inflammasome activity, and AIF-dependent pyroptosis.

lncRNA ROR promotes the progression of renal cell carcinoma through the miR­206/VEGF axis.

Renal cell carcinoma (RCC) is the most common kidney malignancy, responsible for ~80% of all cases in adults. The pathogenesis of RCC is complex, involving alterations at both the genetic and epigenetic levels. Numerous signaling pathways, such as PI3K/Akt/mTOR and Wnt­ß­catenin have been demonstrated to be associated with the tumorigenesis and development of RCC. Long non­coding RNAs (lncRNAs) are functional RNA molecules involved in the initiation and progression of cancer, and investigating the effects of lncRNA could facilitate the development of novel treatments. The lncRNA regulator of reprogramming (ROR) is aberrantly expressed in a variety of tumors. However, its underlying mechanisms remain largely unknown. In the present study, ROR was found to be upregulated and microRNA (miR)­206 was found to be downregulated in RCC tissues and cells. Furthermore, the knockdown of ROR inhibited the proliferation, migration and invasion of RCC cells. It was found that ROR binds to miR­206, and that ROR­induced cell proliferation and metastasis were reversed by the overexpression of miR­206. In addition, the levels of miR­206 and ROR were negatively correlated in RCC tissues. Furthermore, the overexpression of miR­206 notably suppressed the proliferation, migration and invasion of RCC cells, and these effects were enhanced by the knockdown of vascular endothelial growth factor (VEGF); cell growth and metastasis induced by miR­206 inhibitors could be reversed by the knockdown of VEGF. In addition, the expression levels of miR­206 and VEGF were inversely correlated in RCC samples. In summary, the results of the present study revealed that ROR was upregulated in RCC tissues, which promoted tumor progression by regulating the miR­206/VEGF axis. The present findings provided a novel insight into the potential functions of ROR in RCC, and the ROR/miR­206/VEGF pathway may be a promising therapeutic target for the treatment of patients with RCC.

Triphenylethylene-Coumarin Hybrid TCH-5c Suppresses Tumorigenic Progression in Breast Cancer Mainly Through the Inhibition of Angiogenesis.

BACKGROUND: Coumarins are a wide group of naturally occurring compounds which exhibit a wide range of biological properties such as anti-cancer activities. Here, we characterized the biological functions of three Triphenylethylene-Coumarin Hybrids (TCHs) both in cell culture and nude mouse model. METHODS: Cell proliferation assay was performed in the cell cultures of both EA.hy926 endothelial cell and breast cancer cell lines treated with different concentrations of compound TCH-10b, TCH-5a and TCH-5c. Flowcytometry assay and Western blotting were used to further investigate the effect and mechanism of TCH-5c on EA.hy926 cell proliferation and cell cycle. The effects of TCH-5c on endothelial cell migration and angiogenesis were determined using cytoskeleton staining, migration assay and tube formation assay. Inhibition of breast cancer cell line derived VEGF by TCH-5c was shown through ELISA and the use of conditioned media. SK-BR-3 xenograft mouse model was established to further study the anti-tumorigenic role of compound TCH-5c in vivo. RESULTS: We found that compound TCH-5c has inhibitory effects on both vascular endothelial cells and breast cancer cell lines. Compound TCH-5c inhibited proliferation, resulted in cell death, increased p21 protein expression to induce G0/G1 arrest and changed endothelial cell cytoskeleton organization and migration in EA.hy926 endothelial cells. Compound TCH-5c also inhibited breast cancer cell line derived VEGF secretion, decreased breast cancer cell-induced endothelial cell tube formation in vitro and suppressed SK-BR-3 breast cancer cell-initiated tumor formation in vivo. CONCLUSION: Our study demonstrates that the coumarin derivative TCH-5c exerts its anti-cancer effects by 1. inhibiting endothelial cell proliferation, migration. 2. suppressing tube formation and angiogenesis induced by breast cancer cells in vitro and in vivo. Our results have potential implications in developing new approaches against breast cancer.

Grain development and endogenous hormones in summer maize (Zea mays L.) submitted to different light conditions.

Low light is a type of abiotic stress that seriously affects plant growth and production efficiency. We investigated the response mechanisms of summer maize to low light by measuring the changes in endogenous hormones in the grains and during grain filling in summer maize at different light intensities to provide a theoretical basis for the production and management of summer maize under light stress. We applied different light treatments in a field experiment as follows: S, shading from tassel stage (VT) to maturity stage (R6); CK, natural lighting in the field; and L, increasing light from VT to R6. The shading level was 60%, and the maximum illumination intensity of the increasing light treatment on cloudy days was 1600-1800 µmol m-2 s-1. Compared with the control, shading significantly increased the grain abscisic acid (ABA) content at 5-20 days after pollination and decreased the indole acetic acid (IAA), zeatin riboside (ZR), and gibberellin (GA) contents (P < 0.05). The grain-filling rate decreased under shading conditions. Meanwhile, the grain volume, grain weight, and yield all decreased; the yields in 2013 and 2014 decreased by 61 and 60%, respectively. The grain IAA, ZR, and GA contents were increased by increasing light. The grain ABA content at 5-20 days after pollination did not significantly differ from that of CK (P < 0.05). After 20 days after pollination, the ABA content decreased, the grain-filling rate and the filling duration increased, and the yield increased. However, shading after anthesis increased the grain ABA content and reduced the IAA, ZR, and GA contents. Grain growth and development were inhibited, and the yield decreased. The grain ABA content decreased; the IAA, ZR, and GA contents increased; and the yield increased after increasing light. The results indicate that different light intensities regulated the levels of grains endogenous hormones, which influenced the grain-filling rate and duration, and consequently, regulated grain weight and yield.

Predictors and outcome surgery for posterior cortex epilepsies.

OBJECTIVE: The aim of this study is to identify the prognostic role of MRI and EEG in posterior cortex epilepsies (PCES) and to characterize their clinical features. PATIENT AND METHODS: We retrospectively studied 54 consecutive patients (18 females, 36 males) from April 2011 to November 2015, who had undergone PCES surgery. Electro-clinical, pathological and surgical data were evaluated. Of the patients, 18 (33.3%) patients underwent a cortical resection (corticectomy), 10 (18.5%) lobectomy, 6 (11.1%) multilobar resection, 20 (30.1%) disconnection. RESULTS: The postoperative follow-up duration was ≥1 year in all patients (12-44 months, mean = 25). Thirty-two patients (59.3%) became seizure free (ILAE 1) and 40 (74.1%) had a good (ILAE 1, 2, 3) outcome. The most common pathological finding was focal cortical dysplasia (in 34 patients). Univariate analysis showed that regional scalp interictal epilepsy discharges (IEDs) (P = 0.031), Regional EEG onset (P = 0.027), a MRI lesion (P = 0.001) and the number of seizures that were recorded by the epilepsy monitor unit (P = 0.016) were significantly associated with freedom from seizures. Multivariate analysis confirmed that MRI positive was statistically significant (HR = 4.284, CI = 1.198-15.315). CONCLUSIONS: Surgical treatment is effective for PCES, and MRI and EEG analyses are important in presurgical evaluation of PCES.