Expression of Ferroptosis-Related Proteins Glutathione Peroxidase 4, Nuclear Factor Erythroid 2-Related Factor 2, and Solute Carrier Family 7 Member 11 in Gastric Cancer Patients.

BACKGROUND/AIMS: The aim of this study was to investigate the expression of ferroptosis-related targets glutathione peroxidase 4, nuclear factor erythroid 2-related factor 2, and solute carrier family 7 member 11 in gastric cancer and the correlation between their expression and the clinicopathological characteristics and prognosis of gastric cancer patients. MATERIALS AND METHODS: Forty-two gastric cancer samples and paracancerous samples were included, and all cases were detected with glutathione peroxidase 4, nuclear factor erythroid 2-related factor 2, and solute carrier family 7 member 11 by immunohistochemistry. Six gastric cancer cell lines and 1 normal gastric epithelial cell were stably cultured, and the expression of target genes of different cell lines was detected using western blot and polymerase chain reaction. Public data were downloaded from the database, and analyses were performed by software including Statistical Package for the Social Sciences and Prism. RESULTS: A high glutathione peroxidase 4 expression level was found in 7 (16.67%) cancer tissues and 0 (0.00%) paracancerous tissues (P = .012). Nuclear factor erythroid 2-related factor 2 was upregulated in 23 (54.76%) cancer tissues and 2 (4.76%) paracancerous tissues (P < .001). Solute carrier family 7 member 11 showed increased expression in 4 (9.52%) cancer tissues and 1 (2.38%) paracancerous tissue (P = .356). No significant association existed between their expression and the clinicopathological characteristics and prognosis of gastric cancer patients. Glutathione peroxidase 4 and nuclear factor erythroid 2-related factor 2 expressions were higher in all 6 gastric cancer cell lines compared to normal gastric epithelial cells. CONCLUSION: Glutathione peroxidase 4 and nuclear factor erythroid 2-related factor 2 expressions were significantly higher in gastric cancer, which may be potential biomarkers of gastric cancer.

The influencing factors of infectious complications after percutaneous nephrolithotomy: a systematic review and meta-analysis.

Infection is the most common complications of percutaneous nephrolithotomy (PCNL) in treating urinary calculi. However, the risk factors for developing infectious complications after surgery have not been clarified, and the predictive value of some factors is controversial. This study aimed to assess the risk factors for postoperative infectious complications of PCNL. We performed a systematic search of PubMed, Web of Science, Cochrane Library, and EMBASE to obtain studies reporting risk factors for postoperative infection complications after PCNL. In this review, demographic factors, laboratory test factors, and perioperative factors were evaluated. The odds ratio (OR) or mean difference (MD) with a 95% confidence interval (CI) was calculated to assess the risk factors. A total of 18 studies were included, with a total of 7161 study patients with a mean age of 46.4 to 55.5 years and an incidence of infectious complications after PCNL ranging from 2.4% to 40.4%. Twelve factors were identified as independent risk factors for post-PCNL infection complications (P < 0.05), female (OR = 1.60, 95% CI 1.23-2.07), positive urine culture (UC) (OR = 3.16, 95% CI 2.11-4.74), positive renal pelvis urine culture (RPUC) (OR = 5.81, 95% CI 1.75-19.32), positive stone culture (SC) (OR = 5.11, 95% CI 1.46-17.89), positive urine leukocyte (OR = 3.61, 95% CI 2.45-5.34), infected stones (OR = 7.00, 95% CI 1.27-38.55), elevated blood leukocyte (MD = 0.71, 95% CI 0.31-1.10), elevated neutrophil-to-lymphocyte ratio (NLR) (MD = 0.55, 95% CI 0.43-0.66), preoperative stenting (OR = 1.55, 95% CI 1.10-2.20), multiple puncture access (OR = 2.58, 95% CI 1.75-3.82), prolonged operative time (MD = 10 20, 95% CI 4.80-15.60), and postoperative residual stone (OR = 1.56, 95% CI 1.24-1.98). Female, UC positivity, RPUC positivity, SC positivity, urine leukocyte positivity, infected stones, elevated peripheral blood leukocytes, elevated NLR, preoperative stent implantation, multiple puncture channels, prolonged operation time, and postoperative residual stones were identified as independent risk factors for infection complications after PCNL.

Tumor expression of CXCL12 and survival of patients with colorectal cancer: A meta-analysis.

C-X-C motif chemokine ligand 12 (CXCL12) has been suggested as a possible biomarker of poor prognosis in patients with various malignancies. However, the association between tumor expression of CXCL12 and survival of patients with colorectal cancer (CRC) remains to be comprehensively analyzed. A meta-analysis to systematically evaluate this association was performed in the present study. Relevant cohort studies were retrieved by searching the PubMed, Embase and Web of Science databases from inception to March 22, 2022. A conservative random-effect model incorporating the possible influence of between-study heterogeneity was used to pool the results. A total of 14 cohort studies that included 2,060 patients with CRC contributed to the meta-analysis, and 1,055 (51.2%) of them had higher tumor expression levels of CXCL12. Pooled results showed that a higher tumor expression level of CXCL12 was associated with poor overall survival [hazard ratio (HR), 1.74; 95% confidence interval (CI), 1.29-2.34; P<0.001; I2, 33%] and progression-free survival (HR, 2.00; 95% CI, 1.47-2.73; P<0.001; I2, 33%). Subgroup analyses showed that the association between higher cancer expression levels of CXCL12 and poor survival in patients with CRC was not significantly affected by the country of the study, the location of the tumor, the cancer stage or the methods used for measuring tumor CXCL12 levels (all P>0.05). In conclusion, the study found that a higher tumor expression level of CXCL12 was associated with the poor survival of patients with CRC. Studies are warranted to determine if CXCL12-targeted intervention could improve the prognosis of patients with CRC.

Blue Light Signaling Regulates Escherichia coli W1688 Biofilm Formation and l-Threonine Production.

Escherichia coli biofilm may form naturally on biotic and abiotic surfaces; this represents a promising approach for efficient biochemical production in industrial fermentation. Recently, industrial exploitation of the advantages of optogenetics, such as simple operation, high spatiotemporal control, and programmability, for regulation of biofilm formation has garnered considerable attention. In this study, we used the blue light signaling-induced optogenetic system Magnet in an E. coli biofilm-based immobilized fermentation system to produce l-threonine in sufficient quantity. Blue light signaling significantly affected the phenotype of E. coli W1688. A series of biofilm-related experiments confirmed the inhibitory effect of blue light signaling on E. coli W1688 biofilm. Subsequently, a strain lacking a blue light-sensing protein (YcgF) was constructed via genetic engineering, which substantially reduced the inhibitory effect of blue light signaling on biofilm. A high-efficiency biofilm-forming system, Magnet, was constructed, which enhanced bacterial aggregation and biofilm formation. Furthermore, l-threonine production was increased from 10.12 to 16.57 g/L during immobilized fermentation, and the fermentation period was shortened by 6 h. IMPORTANCE We confirmed the mechanism underlying the inhibitory effects of blue light signaling on E. coli biofilm formation and constructed a strain lacking a blue light-sensing protein; this mitigated the aforementioned effects of blue light signaling and ensured normal fermentation performance. Furthermore, this study elucidated that the blue light signaling-induced optogenetic system Magnet effectively regulates E. coli biofilm formation and contributes to l-threonine production. This study not only enriches the mechanism of blue light signaling to regulate E. coli biofilm formation but also provides a theoretical basis and feasibility reference for the application of optogenetics technology in biofilm-based immobilized fermentation systems.

Successful management of life-threatening aortoesophageal fistula: A case report and review of the literature.

BACKGROUND: Aortoesophageal fistula (AEF) is a rare but life-threatening cause of upper gastrointestinal bleeding. Only a handful of cases of successful management of AEF caused by esophageal cancer have been reported. The purpose of this study is to report a case of AEF managed by endovascular aortic repair and review the relevant literature. CASE SUMMARY: A 66-year-old man with upper gastroenterology bleeding presented at the Emergency Department of our hospital complaining of chest pain, fever and hematemesis for 6 h. He had vomited 400 mL of bright-red blood and experienced severe chest pain 6 h prior. He had a past medical history of advanced esophageal cancer. He received chemoradiotherapy but stopped 8 mo prior because of intolerance. A chest contrast computed tomographic scan revealed communication between the esophagus and the descending aorta as well as a descending aortic pseudoaneurysm. According to the symptoms and imaging findings, AEF was our primary consideration. The patient underwent aortic angiography, which indicated AEF and descending aortic pseudoaneurysm. Emergency percutaneous thoracic endovascular aortic repair (TEVAR) of the descending aorta was performed, and bleeding was controlled after TEVAR. He received antibiotics and was discharged after treatment. However, he died 2 mo after the TEVAR due to cancer progression. CONCLUSION: Although AEF is a lethal condition, timely diagnosis and TEVAR may successfully control bleeding.

Aberrant Intraregional Brain Activity and Functional Connectivity in Patients With Diarrhea-Predominant Irritable Bowel Syndrome.

BACKGROUND AND PURPOSE: The appearance and aggravation of diarrhea-predominant irritable bowel syndrome (IBS-D) have proven to be closely related to psychosocial factors. We aimed to measure altered spontaneous brain activity and functional connectivity (FC) in patients with IBS-D using resting-state functional magnetic resonance imaging (RS-fMRI) and to analyze the relationship between these parameters and emotional symptoms. METHODS: Thirty-six adult IBS-D patients and thirty-six demographic-matched healthy controls (HCs) underwent RS-fMRI scans. After processing RS-fMRI data, the values of the amplitude of low-frequency fluctuation (ALFF) and regional homogeneity (ReHo) of the two groups were compared. The abnormal regions were selected as the regions of interest to compare whole-brain seed-based FC between the groups. The relationships between RS-fMRI data and mood and gastrointestinal symptoms were analyzed using correlation and mediation analyses. RESULTS: Compared with HCs, IBS-D patients showed increased ALFF in the right cerebellum posterior lobe, the right lingual gyrus/calcarine, the right postcentral gyrus, the right superior frontal gyrus (SFG), and middle frontal gyrus (MFG), with decreased ALFF in the right inferior parietal lobule, the right striatum, the right anterior cingulated cortex, the right insula, the right hippocampus, the right thalamus, the right midbrain, and the left precuneus. IBS-D patients showed increased ReHo in the bilateral lingual gyrus/calcarine, the bilateral SFG, the right MFG, and the right postcentral gyrus, with decreased ReHo in the orbital part of the left inferior frontal gyrus and the right supplementary motor area. Patients showed enhanced FC between the left precuneus and the bilateral orbitofrontal cortex (OFC). There was a positive correlation between increased ALFF values in the right midbrain and anxiety-depression symptoms in IBS-D patients, and the mediating effect of gastrointestinal symptoms indirectly caused this correlation. CONCLUSION: IBS-D patients had dysregulated spontaneous activity and FC in regions related to pain regulation and emotional arousal involved in prefrontal-limbic-midbrain circuit and somatosensory processing. The development of mood disorders in IBS-D patients may be partly related to the dysfunction of components in the dopamine pathway (especially the midbrain, OFC) due to visceral pain.

BZW2/5MP1 acts as a promising target in hepatocellular carcinoma.

Basic leucine zipper and W2 domain 2 (BZW2), also known as 5MP1, is a protein related to translation regulation. Evidence from previous studies indicates that BZW2 is involved in tumorigenesis in several cancers. However, little is known about the role of BZW2 in hepatocellular carcinoma (HCC). In this study, we first analyzed the gene expression profile of BZW2 in multiple HCC datasets. Next, we explored the biological effects of BZW2 in HCC cell lines. BZW2 was overexpressed in different HCC cohorts. Multivariate analysis confirmed that increased BZW2 expression is an independent prognostic indicator of shorter overall survival. BZW2 coexpressed genes were mainly enriched in the biological processes of ribonucleoprotein complex biogenesis, rRNA metabolism, translational initiation, and negative regulation of metabolic processes. BZW2 depletion reduced proliferation, clonality, and invasion and increased apoptosis in MHCC97-H cells. Furthermore, BZW2 overexpression or knockdown enhanced or impaired c-Myc expression, respectively. Overall, these findings identified BZW2 as a biomarker of HCC and provided novel insight that the effect of BZW2 on the translatome is a potential mechanism that promotes HCC progression via the c-Myc pathway.

A Resting-state Functional Magnetic Resonance Imaging Study of Whole-brain Functional Connectivity of Voxel Levels in Patients With Irritable Bowel Syndrome With Depressive Symptoms.

BACKGROUND/AIMS: Depressive symptom is one of the most common symptoms in patients with irritable bowel syndrome (IBS), but its pathogenetic mechanisms remain unclear. As a voxel-level graph theory analysis method, degree centrality (DC) can provide a new perspective for exploring the abnormalities of whole-brain functional network of IBS with depressive symptoms (DEP-IBS). METHODS: DC, voxel-wise image and clinical symptoms correlation and seed-based functional connectivity (FC) analyses were performed in 28 DEP-IBS patients, 21 IBS without depressive symptoms (nDEP-IBS) patients and 36 matched healthy controls (HC) to reveal the abnormalities of whole brain FC in DEP-IBS. RESULTS: Compared to nDEP-IBS patients and HC, DEP-IBS patients showed significant decrease of DC in the left insula and increase of DC in the left precentral gyrus. The DC's z-scores of the left insula negatively correlated with depression severity in DEP-IBS patients. Compared to nDEP-IBS patients, DEP-IBS patients showed increased left insula-related FC in the left inferior parietal lobule and right inferior occipital gyrus, and decreased left insula-related FC in the left precentral gyrus, right supplementary motor area (SMA), and postcentral gyrus. In DEP-IBS patients, abstracted clusters' mean FC in the right SMA negatively correlated with depressive symptoms. CONCLUSIONS: DEP-IBS patients have abnormal FC in brain regions associated with the fronto-limbic and sensorimotor networks, especially insula and SMA, which explains the vicious circle between negative emotion and gastrointestinal symptoms in IBS. Identification of such alterations may facilitate earlier and more accurate diagnosis of depression in IBS, and development of effective treatment strategies.

[Relationships Between Expression level of MicroRNA-146a, STAT1 Protein and Clinical Characteristics in Children with Acute Lymphoblastic Leukemia].

OBJECTIVE: To analyze the relationships between expression levels of serum microRNA-146a, STAT1 protein and clinical characteristics in children with acute lymphoblastic leukemia (ALL). METHODS: A total of 102 children diagnosed as ALL in our hospital from June 2014 to June 2016 were enrolled, and were compared by into groups according to clinical characteristics including sex, age, lymphocyte type, disease risk, chemotherapy stage and gene mutation. Fifty healthy children were chosen as control group. The relative expression of microRNA-146a and STAT1 gene was detected by real-time RT-PCR and the relative level of STAT1 protein was detected by Western blot. The difference of microRNA-146a and STAT1 protein levels between clinical factors and laboratory indexs were compared. Followed-up for 3 years, The difference of overall survival (OS) rates between ALL children with different microRNA-146a and STAT1 protein were compared. RESULTS: The levels of microRNA-146a, STAT1 mRNA and protein in ALL children were significantly higher than those in control group (P＜0.05), but there were no significantly differences in sex, age and lymphocyte type grouping in ALL children (P＞0.05). There were significantly differences in different disease risk, chemotherapy stage and gene mutation groups in ALL children (P＜0.05). Followed-up for 3 years, the OS rate of ALL children with high microRNA-146a and STAT1 protein levels were better than those with low microRNA-146a and STAT1 protein levels (P＜0.05). CONCLUSION: The up-regulation of microRNA-146a and STAT1 protein may be involved in occurrence and development of ALL, which closely relates to clinical characteristics in ALL children, such as disease risk, chemotherapy stage and gene mutation.

lncRNA Mtss1 promotes inflammatory responses and secondary brain injury after intracerebral hemorrhage by targeting miR-709 in mice.

Secondary brain injuries following intracerebral hemorrhage (ICH) are mediated by inflammatory pathway activation. The present study aimed to characterize long noncoding RNAs (lncRNAs) that are differentially expressed in cerebral tissues during ICH pathogenesis and to investigate their pathogenic functions. An ICH mouse model established by collagenase injection was used to obtain differentially expressed lncRNAs for deep sequencing. A cellular inflammation model was established by treating mouse microglia with lipopolysaccharide. Expression of lncRNA and miRNA was assessed by quantitative RT-PCR, and protein abundance was measured by western blot. Cytokine levels in mouse serum and cell culture supernatants were analyzed using enzyme-linked immunosorbent assay. Cerebral injury was evaluated by hematoxylin-eosin and Nissl staining, the ratio of brain dry weight/brain wet weight, and neurobehavior scoring. Ionized calcium-binding adaptor molecule 1 (IBA1) expression in the brain sections was assessed using immunohistochemistry. A total of 3681 lncRNAs were differentially expressed in the brain tissue of the ICH mice group compared with the Sham group. Of these, lncRNA metastasis suppressor-1 (Mtss1) expression was increased. Mtss1 knockdown by siRNA in the cellular model strongly suppressed TIR-domain-containing adapter-inducing interferon-ß (TRIF) expression, P65 phosphorylation, and tumor necrosis factor (TNF)-α and interleukin (IL)-1ß secretion. Mtss1 knockdown in ICH mice inhibited secondary brain injury and decreased IBA1, TNF-α, and IL-1ß. Mtss1 was predicted to bind miR-709, and Mtss1 knockdown elevated miR-709 expression in the cellular inflammation model and ICH mice. High expression of Mtss1 promoted inflammatory brain injuries after ICH by enhancing inflammatory cytokine secretion and targeting miR-709 expression.

The emerging role of ferroptosis in inflammation.

Ferroptosis is a newly discovered type of cell death triggered by intracellular phospholipid peroxidation that is morphologically, biologically and genetically distinct from other types of cell death. Ferroptosis is classified as regulated necrosis and is more immunogenic than apoptosis. To date, compelling evidence indicates that ferroptosis plays an important role in inflammation, and several antioxidants functioning as ferroptosis inhibitors have been shown to exert anti-inflammatory effects in experimental models of certain diseases. Our review provides an overview of the link between ferroptosis and inflammation; a better understanding of the mechanisms underlying ferroptosis and inflammation may hasten the development of promising therapeutic strategies involving ferroptosis inhibitors to address inflammation.

Convergent syndromic atrophy of pain and emotional systems in patients with irritable bowel syndrome and depressive symptoms.

Irritable bowel syndrome (IBS) is a brain-gut disorder that is often accompanied by psychiatric comorbidities, particularly depression. However, the neuroanatomical substrates of IBS with depressive symptoms (DEP-IBS) and how depressive symptoms and brain morphology modulate IBS symptoms remain unknown. In this study, structural MRI data were processed using a voxel-based morphometry technique and one-way analysis of covariance (ANCOVA) and post-hoc t-tests were performed to compare gray matter volume (GMV) among 28 patients with DEP-IBS, 21 patients with IBS who lacked depressive symptoms (nDEP-IBS), and 36 healthy controls (HC). Correlation and mediation analyses were performed to evaluate the relationship between differing GMV in DEP-IBS and clinical variables. We found that GMV in the bilateral prefrontal, insular, and dorsal striatal areas, as well as the left temporal pole, were significantly lower in the DEP-IBS group than in the HC group. Moreover, compared with the nDEP-IBS group, the DEP-IBS group exhibited decreased GMV in the bilateral medial, dorsolateral prefrontal, and orbitofrontal cortices, bilateral dorsal striatum, and left insular cortices. Correlation analysis revealed that GMV in these atrophic brain areas of the DEP-IBS group was negatively correlated with depression, gastrointestinal symptoms, and disease duration. Our results further revealed that depressive symptoms served as a mediator between gastrointestinal symptoms and GMV in the left insula, right medial prefrontal cortex, and right middle frontal gyrus, while gastrointestinal symptoms served as a mediator between depression and GMV in these regions. Our results suggest convergent syndromic atrophy in the pain and emotional systems of patients with DEP-IBS.

PCDH17 increases the sensitivity of colorectal cancer to 5-fluorouracil treatment by inducing apoptosis and autophagic cell death.

5-Fluorouracil (5-FU) is known as a first-line chemotherapeutic agent against colorectal cancer (CRC), but drug resistance occurs frequently and significantly limits its clinical success. Our previous study showed that the protocadherin 17 (PCDH17) gene was frequently methylated and functioned as a tumor suppressor in CRC. However, the relationship between PCDH17 and 5-FU resistance in CRC remains unclear. Here, we revealed that PCDH17 was more highly expressed in 5-FU-sensitive CRC tissues than in 5-FU-resistant CRC tissues, and high expression of PCDH17 was correlated with high BECN1 expression. Moreover, this expression profile contributed to superior prognosis and increased survival in CRC patients. Restoring PCDH17 expression augmented the 5-FU sensitivity of CRC in vitro and in vivo by promoting apoptosis and autophagic cell death. Furthermore, autophagy played a dominant role in PCDH17-induced cell death, as an autophagy inhibitor blocked cell death to a greater extent than the pancaspase inhibitor Z-VAD-FMK. PCDH17 inhibition by siRNA decreased the autophagy response and 5-FU sensitivity. Mechanistically, we showed that c-Jun NH2-terminal kinase (JNK) activation was a key determinant in PCDH17-induced autophagy. The compound SP600125, an inhibitor of JNK, suppressed autophagy and 5-FU-induced cell death in PCDH17-reexpressing CRC cells. Taken together, our findings suggest for the first time that PCDH17 increases the sensitivity of CRC to 5-FU treatment by inducing apoptosis and JNK-dependent autophagic cell death. PCDH17 may be a potential prognostic marker for predicting 5-FU sensitivity in CRC patients.

LncRNA GAS5 regulates the proliferation, migration, invasion and apoptosis of brain glioma cells through targeting GSTM3 expression. The effect of LncRNA GAS5 on glioma cells.

INTRODUCTION: To investigate the effects of lncRNA GAS5 on the proliferation, migration, invasion and apoptosis of brain glioma cells. METHODS: The expression levels of lncRNA GAS5 and GSTM3 in normal glial cells (HEB) and glioma cells (U251 and U87) were detected by RT-qPCR and western blot, respectively. Glioma cells were transfected with ctrl vector, pcDNA-GAS5, siRNA ctrl (siNC) or GSTM3 siRNA and the effects of lncRNA GAS5 and GSTM3 on the proliferation, migration, invasion and apoptosis of glioma cells were detected by CCK-8 assay, transwell assay and Caspase 3/7 activity assay, respectively. RESULTS: The expression of lncRNA GAS5 was significantly decreased in glioma cell lines U251 and U87 compared with normal glial cells HEB (p < 0.01). In addition, overexpression of lncRNA GAS5 inhibited the proliferation, migration and invasion of U251 and U87 cells, and promoted cell apoptosis as demonstrated by the increased activity of Caspase 3/7. Furthermore, GSTM3 was predicted as a target gene of lncRNA GAS5 by bioinformatics analysis and its expression was increased in glioma cells compared with the normal cells as indicated by western blotting and RT-qPCR experimental results. Silencing of GSTM3 with GSTM3 siRNA decreased the proliferation, migration and invasion but increased the apoptosis of glioma cell lines U251 and U87, which was similar to that the effect lncRNA GAS5 over-expression. CONCLUSION: lncRNA GAS5 can effectively inhibit the proliferation, migration and invasion of glioma cells and promote cell apoptosis through targeting GSTM3 expression.

Circ-U2AF1 promotes human glioma via derepressing neuro-oncological ventral antigen 2 by sponging hsa-miR-7-5p.

The prognosis for human glioma, a malignant tumor of the central nervous system, is poor due to its rapid growth, genetic heterogeneity, and inadequate understanding of its underlying molecular mechanisms. Circular RNAs composed of exonic sequences, represent an understudied form of noncoding RNAs (ncRNAs) that was discovered more than a decade ago, function as microRNA sponges. We aimed to assess the relationship between circ-U2AF1 (CircRNA ID: hsa_circ_0061868) and hsa-mir-7-5p and examine their effects on proliferation, apoptosis, and the metastatic phenotype of glioma cells regulated by neuro-oncological ventral antigen 2 (NOVA2). We found that the expression levels of circ-U2AF1 and NOVA2 were upregulated, while hsa-miR-7-5p was downregulated in human glioma tissues and glioma cell lines. Our data and bioinformatic analysis indicated the association of these molecules with glioma grade, a positive correlation between circ-U2AF1 and NOVA2 expression levels and a negative correlation of hsa-miR-7-5p with both circ-U2AF1 and NOVA2, respectively. In addition, silencing of circ-U2AF1 expression resulted in increased hsa-miR-7-5p expression and decreased NOVA2 expression both in vitro and in vivo. Luciferase assay confirmed hsa-miR-7-5p as a direct target of circ-U2AF1 and NOVA2 as a direct target of hsa-miR-7-5p. Functionally, silencing of circ-U2AF1 inhibits glioma development by repressing NOVA2 via upregulating hsa-miR-7-5p both in vitro and in vivo. Thus, we assumed that circ-U2AF1 promotes glioma malignancy via derepressing NOVA2 by sponging hsa-miR-7-5p. Taken together, we suggest that circ-U2AF1 can be a prognostic biomarker and the circ-U2AF1/hsa-miR-7-5p/NOVA2 regulatory pathway may be a novel therapeutic target for treating gliomas.

miR­141 inhibits glioma vasculogenic mimicry by controlling EphA2 expression.

Human glioma is a pernicious tumor from the central nervous system; it has been reported that microRNAs (miRs) may have carcinogenic or tumor suppressor effects on human glioma. The aim of the present study was to assess miR­141 expression and functional role in human primary glioma, as well as in tumor­derived cell lines. The expression of miR­141 in primary human glioma tissues and cell lines was assessed by employing reverse transcription­quantitative polymerase chain reaction. Next, its role in cellular growth, migration, invasion and vasculogenic mimicry (VM) regulation was determined using various in vitro and in vivo assays, and on the identification its target gene(s) using luciferase assays. The results demonstrated that miR­141 expression was downregulated, and Ephrin type­A receptor 2 (EphA2) was upregulated in the primary human gliomas and human glioma­derived cell lines tested. In addition, a negative correlation existed between miR­141 and EphA2 expression levels in glioma grades II, III and IV. Furthermore, exogenous miR­141 expression resulted in decreased proliferation, migration and invasion, as well as in apoptosis and cell cycle arrest in vitro. It was also revealed that exogenous miR­141 expression resulted in in vivo inhibition of tumor growth and inhibition of the development of VM. Finally, the present study successfully confirmed that EphA2 was a direct target of miR­141 in glioma­derived cells using luciferase assays. Based on these results, it was concluded that miR­141 may regulate cell proliferation, migration, invasion and VM formation by controlling EphA2 expression; also, its target EphA2 may be a novel diagnostic/prognostic biomarker and a potential anti­VM therapeutic target.

Influencing factors of immediate angiographic results in intracranial aneurysms patients after endovascular treatment.

The purpose of this study was to analyze influencing factors associated with immediate angiographic results in intracranial aneurysms patients after endovascular treatment (EVT), providing theoretical evidence and guidance for clinical treatment of intracranial aneurysms. Totally 529 patients met the inclusive criteria, consisting of 338 males and 191 females. Gender; age; history of hypertension, diabetes, and smoking; intracranial atherosclerosis; rupture status, size and location, features of aneurysmal neck, shapes; vasospasm; treatment modality; and degree of aneurysm occlusion were all carefully and completely recorded. All data were investigated in univariate and multivariate logistic regression model to determine whether they were correlated with the degree of aneurysm occlusion. According to aneurysm size, aneurysms were classified as micro-miniature, miniature, and large aneurysms. There were 451 narrow-neck aneurysms and 78 wide-neck aneurysms. Totally 417 were regular and 112 were irregular. And 125 were un-ruptured aneurysms; 404 were ruptured aneurysms. The modalities of treatment were as follows: embolization with coil (n = 415), stent-assisted coil embolization (n = 89), and balloon-assisted coil embolization (n = 25). Univariate analysis showed that aneurysm size, feature of aneurysm neck, shape, and rupture status might affect the immediate occlusion after EVT. Multivariate logistic regression analysis indicated that ruptured aneurysm, tiny aneurysm, and wide-neck aneurysm were independent influencing factors of complete occlusion of intracranial aneurysm. Aneurysm rupture status, size, feature of aneurysmal neck, and shape might be the independent influencing factors of immediate angiographic results in intracranial aneurysm patients after EVT. Un-ruptured, micro-miniature, narrow-neck, and regular-shaped aneurysms were more probable to be occluded completely.

Genetic characteristics of one highly multi-drug-resistant strain of Klebsiella ozaenae.

One highly multi-drug-resistant, mucus-producing and foul-smelling strain of Klebsiella ozaenae was isolated from a patient in the ICU of a Chinese tertiary hospital. MICs of several clinical antimicrobials against the strain were obtained using the Vitek-2 Compact System with AST-GN13 cards and resistance genes were evaluated by PCR and gene sequencing. The strain was resistant to most of the ß-lactams and quinolones tested and carried several antibiotic resistance genes, including bla(KPC-2), bla(TEM-98), bla(CTX-M-3), bla(SHV-26) and qnrS. To our knowledge, this is the first report of ß-lactam and quinolone resistance genes co-existing in a K. ozaenae strain in China.

Detection of the Smqnr quinolone protection gene and its prevalence in clinical isolates of Stenotrophomonas maltophilia in China.

The aim of this study was to detect novel variants of the Stenotrophomonas maltophilia Smqnr gene family and analyse the prevalence of Smqnr genes in clinical isolates of S. maltophilia in China. In total, 442 clinical isolates of S. maltophilia were collected from nine hospitals in four provinces in China. Antimicrobial susceptibility testing against six commonly used antibiotics was performed on these isolates. The sequences of the Smqnr genes amplified by PCR were aligned with those of known Smqnr genes in GenBank and an Smqnr database. The resistance rate against co-trimoxazole was highest at 48.6 %, followed by resistance rates against ceftazidime, chloramphenicol, ticarcillin/clavulanate and tigecycline at 28.7, 21.3, 19.0 and 16.1 %, respectively. The highest susceptibility was shown to levofloxacin, with a resistance rate of just 6.1 %. Smqnr genes were detected in 114 isolates, and comprised 11 previously identified genes and 20 new variants, bringing the total number of known Smqnr genes to 47. The 20 novel Smqnr genes were designated Smqnr28-47 and the encoded proteins showed only 1-12 amino acid differences among each other. The most common Smqnr genes in China were Smqnr8 and its variant Smqnr35 with prevalences of 17.5 % (20/114) and 13.2 % (15/114), respectively. Both the known and the novel Smqnr genes were discovered in both quinolone non-sensitive and sensitive isolates with similar frequency, suggesting that the Smqnr gene makes little contribution to quinolone resistance in this organism.

Detection of let-7a microRNA by real-time PCR in gastric carcinoma.

AIM: To establish an accurate and rapid stem-loop reverse transcriptional real-time PCR (RT-PCR) method to quantify human let-7a miRNA in gastric cancer. METHODS: According to the sequence of let-7a miRNA, the stem-loop reverse transcriptional primer, the primers and quantitative MGB probes of real-time PCR were designed and synthesized. The dynamic range and the sensitivity of quantitative reverse transcriptional real-time PCR were determined. The levels of let-7a miRNA were examined in 32 gastric carcinoma samples by stem-loop RT-PCR method. RESULTS: The dynamic range and sensitivity of the let-7a miRNA quantification scheme were evaluated, the result showed the assay could precisely detect 10 copies of mature let-7a miRNA in as few as 0.05 ng of total RNA of gastric mucosa. The results of specificity analysis showed no fluorescence signal occurred even though 50 ng of human genomic DNA was added to the reverse transcription (RT) reaction. The expression level of let-7a miRNA in gastric tumor tissues was significantly lower compared to normal tissues in 14 samples from 32 patients. CONCLUSION: The stem-loop RT-PCR is a reliable method to detect let-7a miRNA which may play an important role in the development of gastric carcinoma.