Association of four metalloids in the serum and urine of individuals with major depressive disorders: a case-control study.

Background: Major depressive disorder (MDD) pathogenesis may involve metalloids in a significant way. The aim of our study was to identify potential links between MDD and metalloid elements [boron (B), germanium (Ge), arsenic (As), antimony (Sb)]. Methods: A total of 72 MDD cases and 75 healthy controls (HCs) were recruited from Zhumadian Second People's Hospital in Henan Province, China. The levels of four metallic elements (B, Ge, As, and Sb) in the serum and urine were measured using inductively coupled plasma mass spectrometry (ICP-MS). Results: In comparison to the HCs, the B, As, and Sb levels were considerably lower in the MDD group (p < 0.05) in the serum; the MDD group had significantly higher (p < 0.05) and significantly lower (p < 0.001) B and Sb levels in the urine. After adjusting for potential confounders, serum B (OR = 0.120; 95% CI, 0.048, 0.300; p < 0.001) and Sb (OR = 0.133; 95% CI, 0.055, 0.322; p < 0.001) showed a negative correlation with MDD. Urine B had a negative correlation (OR = 0.393; 95% CI, 0.193, 0.801; p = 0.01) with MDD, while urine Sb had a positive correlation (OR = 3.335; 95% CI, 1.654, 6.726; p = 0.001) with MDD. Conclusion: Our current research offers insightful hints for future investigation into the function of metalloids in connection to MDD processes.

Isolation and identification of a pigeonpox virus strain and study on the integration of reticuloendotheliosis virus sequence.

In order to study the integration of reticuloendotheliosis virus (REV) in pigeonpox virus (PPV), we collected suspected pigeonpox disease material, amplified the 4b core protein gene of PPV, the gp90 gene of REV, and the integrated sequence fragments from the end of the ORF201 segment of PPV to the beginning of the LTR of REV, and sequenced these genes. The results showed that a 4b core protein fragment of 332 bp was amplified and identified as pigeonpox virus, which was named SX/TY/LTR 01/2023. Sequence analysis showed that the pigeonpox virus isolate belonged to genotype A2, which was the closest to the domestic CVL strain, with a identity of 99.4%. A band of 1191 bp was amplified from the gp90 gene of REV, named SX/TY/PPV-REV01/2023, and sequence analysis indicated that REV belonged to genotype III. The sequence analysis showed that REV belonged to genotype III, and belonged to the same large branch as the domestic isolates JSRD0701 and LNR0801, with 99.3% identity. The integrated sequence fragment was amplified to a band of 637 bp, which determined that the REV sequence was integrated in the PPV rather than a mixed infection of the two viruses. This indicates that REV was integrated in this isolation of PPV, suggesting that pigeon farms need to prevent reticuloendotheliosis at the same time when preventing pigeonpox.

ZFP36L1 controls KLF16 mRNA stability in vascular smooth muscle cells during restenosis after vascular injury.

The RNA-binding zinc finger protein 36 (ZFP36) family participates in numerous physiological processes including transition and differentiation through post-transcriptional regulation. ZFP36L1 is a member of the ZFP36 family. This study aimed to evaluate the role of ZFP36L1 in restenosis. We found that the expression of ZFP36L1 was inhibited in VSMC-phenotypic transformation induced by TGF-ß, PDGF-BB, and FBS and also in the rat carotid injury model. In addition, we found that the overexpression of ZFP36L1 inhibited the proliferation and migration of VSMCs and promoted the expression of VSMC contractile genes; whereas ZFP36L1 interference promoted the proliferation and migration of VSMCs and suppressed the expression of contractile genes. Furthermore, the RNA binding protein immunoprecipitation and double luciferase reporter gene experiments shows that ZFP36L1 regulates the phenotypic transformation of VSMCs through the posttranscriptional regulation of KLF16. Finally, our research results in the rat carotid balloon injury animal model further confirmed that ZFP36L1 regulates the phenotypic transformation of VSMCs through the posttranscriptional regulation of KLF16 and further plays a role in vascular injury and restenosis in vivo.

Boosting Photothermocatalytic Oxidation of Toluene Over Pt/N-TiO2: The Gear Effect of Light and Heat.

Photothermal catalysis is extremely promising for the removal of various indoor pollutants owing to its photothermal synergistic effect, while the low light utilization efficiency and unclear catalytic synergistic mechanism hinder its practical applications. Here, nitrogen atoms are introduced, and Pt nanoparticles are loaded on TiO2 to construct Pt/N-TiO2-H2, which exhibits 3.5-fold higher toluene conversion rate than the pure TiO2. Compared to both photocatalytic and thermocatalytic processes, Pt/N-TiO2-H2 exhibited remarkable performance and stability in the photothermocatalytic oxidation of toluene, achieving 98.4% conversion and 98.3% CO2 yield under a light intensity of 260 mW cm-2. Furthermore, Pt/N-TiO2-H2 demonstrated potential practical applicability in the photothermocatalytic elimination of various indoor volatile organic compounds. The synergistic effect occurs as thermocatalysis accelerates the accumulation of carboxylate species and the degradation of aldehyde species, while photocatalysis promotes the generation of aldehyde species and the consumption of carboxylate species. This ultimately enhances the photothermocatalytic process. The photothermal synergistic effect involves the specific conversion of intermediates through the interplay of light and heat, providing novel insights for the design of photothermocatalytic materials and the understanding of photothermal mechanisms.

Associations Between Life's Essential 8 and Abdominal Aortic Calcification Among Middle-Aged and Elderly Populations.

BACKGROUND: Abdominal aortic calcification (AAC) is an independent risk factor for cardiovascular disease. We aim to examine the associations between Life's Essential 8 (LE8), the recently updated measurement of cardiovascular health (CVH), and AAC among participants aged ≥40 years. METHODS AND RESULTS: This population-based cross-sectional study used data from the National Health and Nutrition Examination Survey in 2013 to 2014. AAC (AAC score>0) and severe AAC (AAC score>6) were quantified by the Kauppila score system. Multiple linear, multivariable logistic, and restricted cubic spline models were used to assess the associations. A total of 2369 participants were included with a mean AAC score of 1.41 (0.13). Participants in the high-cardiovascular-health group had lower AAC scores, lower prevalence of AAC, and lower prevalence of severe AAC. After the adjustment of potential confounders (age, sex, race and ethnicity, education levels, marital status, poverty income ratio, estimated glomerular filtration rate, serum creatinine, serum uric acid, serum phosphorus, and serum total calcium), higher cardiovascular health was significantly associated with lower risk of AAC. Meanwhile, elevated nicotine exposure score, blood glucose score, and blood pressure score within the LE8 components were significantly associated with lower risk of AAC. Also, nonlinear dose-response relationships were observed. Subgroup analyses (age strata, sex, poverty income ratio, education levels, marital status) indicated the inverse associations of LE8 and AAC were generally similar in different populations. CONCLUSIONS: LE8 was negatively and nonlinearly related to the risk of AAC among middle-aged and older populations. Meanwhile, LE8 components should prioritize higher scores for nicotine exposure, blood glucose, and blood pressure evaluations.

Cardiotoxic and neurobehavioral effects of sucralose and acesulfame in Daphnia: Toward understanding ecological impacts of artificial sweeteners.

Artificial sweeteners are widely used in food and pharmaceuticals, but their stability and persistence raise concerns about their impact on aquatic life. Although standard toxicity tests do not reveal lethal effects, recent studies suggest a potential neurotoxic mode of action. Using environmentally relevant concentrations, we assessed the effects of sucralose and acesulfame, common sugar substitutes, on Daphnia magna focusing on biochemical (acetylcholinesterase activity; AChE), physiological (heart rate), and behavioural (swimming) endpoints. We found dose-dependent increases in AChE and inhibitory effects on heart rate and behaviour for both substances. Moreover, acesulfame induced a biphasic response in AChE activity, inhibiting it at lower concentrations and stimulating at higher ones. For all endpoints, the EC50 values were lower for acesulfame than for sucralose. Additionally, the relationship between acetylcholinesterase and heart rate differed depending on the substance, suggesting possible differences in the mode of action between sucralose and acesulfame. All observed EC50 values were at µg/l levels, i.e., within the levels reported for wastewater, with adverse effects observed at as low as 0.1 µg acesulfame /l. Our findings emphasise the need to re-evaluate risk assessment thresholds for artificial sweeteners and provide evidence for the neurotoxic effects of artificial sweeteners in the environment, informing international regulatory standards.

Targeting H3K27me3 demethylase to inhibit Shh signaling and cholesterol metabolism in medulloblastoma growth.

Previously we uncovered the epigenetic regulation of medulloblastoma that low levels of H3K27me3 are required for Shh target gene expression and medulloblastoma growth. Since Jmjd3, an H3K27me3 demethylase, is responsible for maintaining low H3K27me3 at Shh target genes, targeting Jmjd3 could be an efficient way to inhibit Shh signaling and medulloblastoma growth. Here we show that the small molecule GSK-J4, an inhibitor of Jmjd3, significantly inhibited the expression of Shh target genes in Shh responsive cell models and primary cerebellar granule neuron precursors. GSK-J4 also significantly reduced the growth of primary Shh medulloblastoma cultures. Treating human medulloblastoma cell line DaoY by GSK-J4 led to cell cycle arrest at G0/G1 phase with decreased cells in S-phase. Tumor cell proliferation was significantly inhibited by GSK-J4 treatment. Gene expression analyses showed that GSK-J4 additionally constrained the expression of key genes in cholesterol biosynthesis. Our results highlight the possibility that targeting H3K27me3 demethylase Jmjd3 with GSK-J4 to inhibit Shh signaling and cholesterol metabolism is a potential application to treat Shh medulloblastoma.

Genome-Wide Identification of Immune-Related Alternative Splicing and Splicing Regulators Involved in Abdominal Aortic Aneurysm.

The molecular mechanism of AAA formation is still poorly understood and has not been fully elucidated. The study was designed to identify the immune-related genes, immune-RAS in AAA using bioinformatics methods. The GSE175683 datasets were downloaded from the GEO database. The DEseq2 software was used to identify differentially expressed genes (DEGs). SUVA pipeline was used to quantify AS events and RAS events. KOBAS 2.0 server was used to identify GO terms and KEGG pathways to sort out functional categories of DEGs. The CIBERSORT algorithm was used with the default parameter for estimating immune cell fractions. Nine samples from GSE175683 were used to construct the co-disturbed network between expression of SFs and splicing ratio of RAS events. PCA analysis was performed by R package factoextra to show the clustering of samples, and the pheatmap package in R was used to perform the clustering based on Euclidean distance. The results showed that there were 3,541 genes significantly differentially expressed, of which 177 immune-related genes were upregulated and 48 immune-related genes were downregulated between the WT and WTA group. Immune-RAS events were mainly alt5P and IR events, and about 60% of it was complex splicing events in AAA. The WT group and the WTA group can be clearly distinguished in the first principal component by using the splicing ratio of immune-RAS events. Two downregulated genes, Nr4a1 and Nr4a2, and eight upregulated genes, Adipor2, Akt2, Bcl3, Dhx58, Pparg, Ptgds, Sytl1, and Vegfa were identified among the immune-related genes with RAS and DEGs. Eighteen differentially expressed SFs were identified and displayed by heatmap. The proportion of different types of cells and ratio of the average ratio of different cells were quite different. Both M1 and M2 types of macrophages and plasma cells were upregulated, while M0 type was downregulated in AAA. The proportion of plasma cells in the WTA group had sharply increased. There is a correlation between SF expression and immune cells/immune-RAS. Sf3b1, a splicing factor with significantly different expression, was selected to bind on a mass of immune-related genes. In conclusion, our results showed that immune-related genes, immune-RAS, and SFs by genome-wide identification were involved in AAA.

Single-cell transcriptome in silico analysis reveals conserved regulatory programs in macrophages/monocytes of abdominal aortic aneurysm from multiple mouse models and human.

Abdominal aortic aneurysm (AAA) is a life-threatening disease and there is currently a lack of effective treatment to prevent it rupturing. ScRNA-seq studies of AAA are still lacking. In the study, we analyzed the published AAA scRNA-seq datasets from the mouse elastase-induced model, CaCl2 treatment model, Ang II-induced model and human by using bioinformatic approaches and in silico analysis. A total of 26 cell clusters were obtained and 11 cell types were identified from multiple mouse AAA models. Also, the proportion of Mφ/Mo increased in the AAA group and Mφ/Mo was divided into seven subtypes. There were significant differences in transcriptional regulation patterns of Mφ/Mo in different AAA models. The enrichment pathways of upregulated or downregulated genes from Mφ/Mo in the three mouse datasets were different. The actived regulons of Mφ/Mo had strong specificity and the repressed regulons showed high consistency. The co-upregulated genes as well as actived regulons and co-downregulated genes as well as repressed regulons were closely correlated and formed regulatory networks. Mφ/Mo from human AAA dataset was divided into five subtypes. The proportion of three macrophage subpopulations increased but the proportion of two monocyte subpopulations decreased. In the AAA group, the upregulated or downregulated genes of Mφ/Mo were enriched in different pathways. After further analyzing the genes in Mφ/Mo of both mouse and human scRNA-seq datasets, two genes were upregulated in the four datasets, IL-1B and THBS1. In conclusion, in silico analysis of scRNA-seq revealed that Mφ/Mo and their regulatory related genes as well as interaction networks played an important role in the pathogenesis of AAA.

Metformin protects cardiomyocytes against oxygen-glucose deprivation injury by promoting autophagic flux through AMPK pathway.

Metformin has been shown to protect myocardial ischaemia/reperfusion or hypoxia/reoxygenation injury. In our current study, we investigated the effects of metformin on autophagy and its possible underlying mechanisms in in vivo myocardial infarction (MI) model and in vitro oxygen-glucose deprivation (OGD) model. A rat model of MI was made by ligating coronary artery in vivo study. Metformin (200 mg/kg/day) could improve cardiac function, prevent rats from MI-induced injury by reducing myocardial infarct size and apoptosis. Moreover, metformin furtherly promoted autophagy by increasing the protein expression of LC3-II, ATG5, ATG7 and Beclin1, and by involving AMPK pathway during MI. H9c2 cells were treated with metformin (4 mM) in vitro study to assess its effects after exposure to OGD. Metformin increased cell viability and inhibited OGD-induced LDH synthesis and cell apoptosis. Furthermore, metformin increased autophagosome formations as well as expression of autophagy-related proteins, promoted autophagic flux. In addition, metformin augmented the protein level of Bcl-2 and diminished the protein levels of Bax and cleaved caspase-3. Metformin also upregulated p-AMPK expression. Nevertheless, the above-mentioned effects of metformin on H9c2 cells were remarkably eliminated by compound C (an AMPK inhibitor). In summary, we displayed that metformin protected cardiomyocytes against OGD-induced injury and apoptosis by promoting autophagic flux through the AMPK pathway.

Numerical Analysis of Signal Response Characteristic of Piezoelectric Energy Harvesters Embedded in Pavement.

Piezoelectric pavement energy harvesting is a technological approach to transform mechanical energy into electrical energy. When a piezoelectric energy harvester (PEH) is embedded in asphalt pavements or concrete pavements, it is subjected to traffic loads and generates electricity. The wander of the tire load and the positioning of the PEH affect the power generation; however, they were seldom comprehensively investigated until now. In this paper, a numerical study on the influence of embedding depth of the PEH and the horizontal distance between a tire load and the PEH on piezoelectric power generation is presented. The result shows that the relative position between the PEH and the load influences the voltage magnitude, and different modes of stress state change voltage polarity. Two mathematic correlations between the embedding depth, the horizontal distance, and the generated voltage were fitted based on the computational results. This study can be used to estimate the power generation efficiency, and thus offer basic information for further development to improve the practical design of PEHs in an asphalt pavement.

Congenital fibrinogen disorders with repeated thrombosis.

Congenital dysfibrinogenemia is characterized with undetectable or low fibrinogen level by Clauss assay complicated by bleeding and/or thrombosis. These may lead to a diagnostic problem to some clinicians unfamiliar with this disease. We reported a case of congenital dysfibrinogenemia manifested as hemorrhage, repeated thrombosis, low fibrinogen levels through Clauss assay and but normal levels of fibrinogen through PT-derived tests. In conclusion, to patients with thrombosis complicated by decreased fibrinogen level, clinicians and laboratory physicians should be alert to the possibility of congenital dysfibrinogenemia.

Clinical Diagnosis and Treatment of Internal Jugular Venous Aneurysms.

BACKGROUND: The aneurysms of internal jugular vein (IJV) are very rare and hence scarcely described in the literature. Owing to the lack of guidelines on the treatment paradigm of this condition, management strategies vary. METHODS: Six patients presenting in our institution with internal jugular venous aneurysms from September 2007 to August 2017 were retrospectively analyzed. RESULTS: IJV aneurysms were confirmed in all 6 patients. For 3 of them, a surgical treatment was deemed necessary. These were 2 patients with intravenous thrombosis and 1 patient with progressive aneurysmal enlargement during the initial monitoring period. The choice of surgical technique was based on aneurysm morphology: 2 patients with saccular aneurysms underwent tangential aneurysmectomy with lateral venorrhaphy, and a patient presenting a fusiform aneurysm underwent its total excision followed by IJV ligation. Three remaining patients were managed conservatively, with one of them fully regressing and the other 2 remaining asymptomatic. CONCLUSIONS: IJV aneurysms are very rare and usually of benign natural history. For asymptomatic patients, conservative treatment with close follow-up is generally recommended. If any accompanying signs or symptoms are present, such as pain, swelling, evidence of thrombosis, progressive enlargement, or severe psychological stress, timely and appropriate surgical intervention should ensue.

FOXC2-AS1 regulates phenotypic transition, proliferation and migration of human great saphenous vein smooth muscle cells.

OBJECTIVES: In varicose veins, vascular smooth muscle cells (VSMCs) often shows phenotypic transition and abnormal proliferation and migration. Evidence suggests the FOXC2-Notch pathway may be involved in the pathogenesis of varicose veins. Here, this study aimed to explore the role of long non-coding RNA FOXC2-AS1 (FOXC2 antisense RNA 1) in phenotypic transition, proliferation, and migration of varicose vein-derived VSMCs and to explore whether the FOXC2-Notch pathway was involved in this process. METHODS: The effect of FOXC2-AS1 on the proliferation and migration of human great saphenous vein smooth muscle cells (SV-SMCs) was analyzed using MTT assay and Transwell migration assay, respectively. The levels of contractile marker SM22α and synthetic marker osteopontin were measured by immunohistochemistry and Western blot to assess the phenotypic transition. RESULTS: The human varicose veins showed thickened intima, media and adventitia layers, increased synthetic VSMCs, as well as upregulated FOXC2-AS1 and FOXC2 expression. In vitro assays showed that FOXC2-AS1 overexpression promoted phenotypic transition, proliferation, and migration of SV-SMCs. However, the effect of FOXC2-AS1 overexpression could be abrogated by both FOXC2 silencing and the Notch signaling inhibitor FLI-06. Furthermore, FOXC2-AS1 overexpression activated the Notch pathway by upregulating FOXC2. CONCLUSION: FOXC2-AS1 overexpression promotes phenotypic transition, proliferation, and migration of SV-SMCs, at least partially, by activating the FOXC2-Notch pathway.

Neuroprotective effects of an Nrf2 agonist on high glucose-induced damage in HT22 cells.

BACKGROUND: Oxidative stress is the hallmark of diabetic encephalopathy, which may be caused by hyperglycaemic toxicity. We aimed to discover pharmacologic targets to restore redox homeostasis. We identified the transcription factor Nrf2 as such a target. METHODS: HT22 cells were cultured in 25 or 50 mM D-glucose with various concentrations of sulforaphane (SFN) (from 1.25 to 5.0 µM). Cell viability was tested with the Cell Counting Kit-8 assay. Reactive oxygen species (ROS) production was detected with an inverted fluorescence microscope using the dichlorodihydrofluorescein-diacetate fluorescent probe. The expression of NF-E2-related factor 2 (Nrf2), haem oxygenase-1 (HO-1) and nuclear factor-κB (NF-κB) at the mRNA and protein levels was detected by reverse transcription quantitative polymerase chain reaction and western blotting. RESULT: We found that a high glucose concentration (50 mM) increased the generation of ROS, downregulated the expression of Nrf2/HO-1 and upregulated the expression of NF-κB. Moreover, HT22 cell viability significantly decreased after culture in high-glucose medium for 24, 48 and 72 h, whereas the activation of the Nrf2/HO-1 pathway using a pharmacological Nrf2 activator abrogated this high-glucose-induced toxicity. CONCLUSION: This study suggests that the activation of the Nrf2-ARE signalling pathway might be a therapeutic target for the treatment of diabetic encephalopathy.

Sodium ferulate attenuates high-glucose-induced oxidative injury in HT22 hippocampal cells.

The aim of the present study was to investigate the protective effects of sodium ferulate (SF) on HT22 hippocampal cells under a high glucose concentration. Cells were cultured in normal glucose (25 mM D-glucose) or high glucose (50 mM D-glucose) with various concentrations of SF (50, 100, 250 or 500 µM) for 0, 48 and 72 h. Cell viability was tested using a Cell Counting Kit-8 assay. Reactive oxygen species (ROS) production was detected using flow cytometry. The expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and nuclear factor-κB (NF-κB) at the mRNA and protein levels were detected using a reverse transcription-quantitative polymerase chain reaction analysis and western blotting. HT22 hippocampal cell viability was revealed to be substantially decreased following culturing in high glucose medium (50 mM) for 48 and 72 h. The addition of 100 µM SF abrogated this high-glucose-induced toxicity, but higher concentrations of SF (250 and 500 µM) were harmful to the cells. Furthermore, a high glucose concentration increased the generation of ROS, downregulated the expression of Nrf2/HO-1 and upregulated the expression of NF-κB subsequent to culturing for 72 h, whereas the addition of the appropriate concentration of SF attenuated these effects. To the best of our knowledge, the present study is the first to report such results and provide evidence that SF protects HT22 cells from high glucose-induced toxicity by activating the Nrf2/HO-1 pathway and inhibiting the expression of NF-κB, which may be of therapeutic value in diabetic encephalopathy.

Exosomes derived from oxLDL-stimulated macrophages induce neutrophil extracellular traps to drive atherosclerosis.

This study aimed to investigate the role and underlying mechanism of exosomes secreted by oxidized low-density lipoprotein (oxLDL)-stimulated macrophages in the progression of atherosclerosis (AS). Exosomes from peripheral blood of AS patients or oxLDL-treated macrophages were co-cultured with human neutrophils. Neutrophil extracellular traps (NETs) were detected by immunofluorescence staining. The levels of inflammatory cytokines were quantified by enzyme-linked immunosorbent assay (ELISA). The expression levels of miR-146a and superoxide dismutase 2 (SOD2) were determined by quantitative real-time PCR (qRT-PCR) and western blot. The generation of intracellular reactive oxygen species (ROS) was observed by using dichlorofluorescin diacetate (DCFH-DA). ApoE-deficient mice were fed with high-fat diet (HFD) to induce AS. Atherosclerotic plaques were evaluated by Oil red O (ORO) and hematoxylin-eosin (HE) staining. Our results showed that miRNA-146a was enriched in serum-derived exosomes of AS patients and oxLDL-treated macrophage THP-1-derived exosomes. Importantly, exosomal miR-146a secreted by oxLDL-treated macrophages promoted ROS and NETs release via targeting SOD2. In addition, intravenous administration of oxLDL-treated THP-1 cells-derived exosomes into AS mice significantly deteriorated AS in vivo. Our findings indicate that exosomal miR-146a derived from oxLDL-treated macrophages promotes NETs formation via inducing oxidative stress, which might provide a novel scientific basis for the understanding of AS progression.

LncRNA GAS8-AS1 suppresses papillary thyroid carcinoma cell growth through the miR-135b-5p/CCND2 axis.

The aim of the present study was to investigate the potential role of GAS8 antisense RNA 1 (GAS8-AS1) in papillary thyroid carcinoma (PTC). PcDNA3.1-GAS8-AS1 and si-GAS8-AS1, miR-135b-5p mimic and si-CCND2 were transfected into PTC cells. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8). QRT-PCR was used to determine expressions of GAS8-AS1, miR-135b-5p, and CCND2, and Western blot were detected protein level of CCND2. The miRNA target gene prediction site TargetScan was used to predict potential targets of GAS8-AS1 and miR-135b-5p. Cell cycle progression was analyzed by flow cytometry. We found that GAS8-AS1 was down-regulated in PTC cell lines and inhibited proliferation and cycle of PTC cell. GAS8-AS1 directly targets miR-135b-5p, and GAS8-AS1 could regulate a downstream target of miR-135b-5p, Cyclin G2 (CCNG2), in an miR-135b-5p-mediated manner. In addition, we also proved that overexpressed GAS8-AS1 inhibited tumor formation in vivo GAS8-AS1 suppresses PTC cell growth through the miR-135b-5p/CCND2 axis.

Diagnosis and surgical treatment of patients with femoral vein compression from hip joint synovial cyst.

OBJECTIVE: In this study, the diagnosis and treatment of patients with femoral vein compression from a synovial cyst of the hip joint were investigated. METHODS: A retrospective study was conducted to review hospital records from March 2010 to July 2017 of patients with femoral vein compression from a synovial cyst of the hip joint. The diagnostic procedure, duplex ultrasound results, computed tomography (CT), and magnetic resonance imaging (MRI) were recorded. The method and treatment outcomes were also documented. RESULTS: Fifteen patients with femoral vein compression resulting from a synovial cyst of the hip joint were identified. The mean age was 47.5 years, and nine of the patients (60%) were female. All patients had unilateral lower extremity edema. In 11 patients (73.3%), the mass in the groin area could not be palpated; 2 (13.3%) patients had venous insufficiency; and 2 (13.3%) patients had venous thrombosis. All patients received a duplex ultrasound examination, 4 (26.7%) patients received CT, and 11 (73.3%) patients received MRI. One patient received a duplex ultrasound-guided percutaneous needle aspiration; however, the cyst recurred 1 month later. The remaining 14 patients received surgical excision and had no cyst recurrence during the follow-up period (mean, 22.6 months). CONCLUSIONS: Duplex ultrasound should be selected as the first choice for screening of synovial cyst of the hip joint with femoral vein compression. Moreover, it can be used as the first choice for follow-up of these patients. MRI or CT can provide more anatomic information for surgical treatment. Surgical excision of the cyst is the preferred treatment method, with a lower rate of cyst recurrence compared with needle aspiration.

FOXC2-AS1 regulates phenotypic transition, proliferation and migration of human great saphenous vein smooth muscle cells

OBJECTIVES: In varicose veins, vascular smooth muscle cells (VSMCs) often shows phenotypic transition and abnormal proliferation and migration. Evidence suggests the FOXC2-Notch pathway may be involved in the pathogenesis of varicose veins. Here, this study aimed to explore the role of long non-coding RNA FOXC2-AS1 (FOXC2 antisense RNA 1) in phenotypic transition, proliferation, and migration of varicose vein-derived VSMCs and to explore whether the FOXC2-Notch pathway was involved in this process. METHODS: The effect of FOXC2-AS1 on the proliferation and migration of human great saphenous vein smooth muscle cells (SV-SMCs) was analyzed using MTT assay and Transwell migration assay, respectively. The levels of contractile marker SM22α and synthetic marker osteopontin were measured by immunohistochemistry and Western blot to assess the phenotypic transition. RESULTS: The human varicose veins showed thickened intima, media and adventitia layers, increased synthetic VSMCs, as well as upregulated FOXC2-AS1 and FOXC2 expression. In vitro assays showed that FOXC2-AS1 overexpression promoted phenotypic transition, proliferation, and migration of SV-SMCs. However, the effect of FOXC2-AS1 overexpression could be abrogated by both FOXC2 silencing and the Notch signaling inhibitor FLI-06. Furthermore, FOXC2-AS1 overexpression activated the Notch pathway by upregulating FOXC2. CONCLUSION: FOXC2-AS1 overexpression promotes phenotypic transition, proliferation, and migration of SV-SMCs, at least partially, by activating the FOXC2-Notch pathway.