Delayed neutrophil apoptosis may enhance NET formation in ARDS.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is a neutrophil-associated disease. Delayed neutrophil apoptosis and increased levels of neutrophil extracellular traps (NETs) have been described in ARDS. We aimed to investigate the relationship between these phenomena and their potential as inflammation drivers. We hypothesized that delayed neutrophil apoptosis might enhance NET formation in ARDS. METHOD: Our research was carried out in three aspects: clinical research, animal experiments, and in vitro experiments. First, we compared the difference between neutrophil apoptosis and NET levels in healthy controls and patients with ARDS and analyzed the correlation between neutrophil apoptosis and NET levels in ARDS. Then, we conducted animal experiments to verify the effect of neutrophil apoptosis on NET formation in Lipopolysaccharide-induced acute lung injury (LPS-ALI) mice. Furthermore, this study explored the relationship between neutrophil apoptosis and NETs at the cellular level. Apoptosis was assessed using morphological analysis, flow cytometry, and western blotting. NET formation was determined using immunofluorescence, PicoGreen assay, SYTOX Green staining, and western blotting. RESULTS: ARDS neutrophils lived longer because of delayed apoptosis, and the cyclin-dependent kinase inhibitor, AT7519, reversed this phenomenon both in ARDS neutrophils and neutrophils in bronchoalveolar lavage fluid (BALF) of LPS-ALI mice. Neutrophils in a medium containing pro-survival factors (LPS or GM-CSF) form more NETs, which can also be reversed by AT7519. Tissue damage can be reduced by promoting neutrophil apoptosis. CONCLUSIONS: Neutrophils with extended lifespan in ARDS usually enhance NET formation, which aggravates inflammation. Enhancing neutrophil apoptosis in ARDS can reduce the formation of NETs, inhibit inflammation, and consequently alleviate ARDS.

The Modulation of Interferon Regulatory Factor-1 via Caspase-1-Mediated Alveolar Macrophage Pyroptosis in Ventilator-Induced Lung Injury.

Background: To examine the role of interferon regulatory factor-1 (IRF-1) and to explore the potential molecular mechanism in ventilator-induced lung injury. Methods: Wild-type C57BL/6 mice and IRF-1 gene knockout mice/caspase-1 knockout mice were mechanically ventilated with a high tidal volume to establish a ventilator-related lung injury model. The supernatant of the alveolar lavage solution and the lung tissues of these mice were collected. The degree of lung injury was examined by hematoxylin and eosin staining. The protein and mRNA expression levels of IRF-1, caspase-1 (p10), and interleukin (IL)-1ß (p17) in lung tissues were measured by western blot and quantitative real-time polymerase chain reaction, respectively. Pyroptosis of alveolar macrophages was detected by flow cytometry and western blotting for active caspase-1 and cleaved GSDMD. An enzyme-linked immunosorbent assay was used to measure the levels of IL-1ß, IL-18, IL-6, TNF-α, and high mobility group box protein 1 (HMGB-1) in alveolar lavage fluid. Results: IRF-1 expression and caspase-1-dependent pyroptosis in lung tissues of wild-type mice were significantly upregulated after mechanical ventilation with a high tidal volume. The degree of ventilator-related lung injury in IRF-1 gene knockout mice and caspase-1 knockout mice was significantly improved compared to that in wild-type mice, and the levels of GSDMD, IL-1ß, IL-18, IL-6, and HMGB-1 in alveolar lavage solution were significantly reduced (P < 0.05). The expression levels of caspase-1 (p10), cleaved GSDMD, and IL-1ß (p17) proteins in lung tissues of IRF-1 knockout mice with ventilator-related lung injury were significantly lower than those of wild-type mice, and the level of pyroptosis of macrophages in alveolar lavage solution was significantly reduced. Conclusions: IRF-1 may aggravate ventilator-induced lung injury by regulating the activation of caspase-1 and the focal death of alveolar macrophages.

Clinical characteristics, treatment and outcomes of acute postpartum inflammatory sacroiliitis: a retrospective study.

PURPOSE: We performed this research to report the clinical characteristics and clinical therapeutic strategies of acute postpartum inflammatory sacroiliitis. METHODS: We retrospectively analyzed the data of patients diagnosed with acute postpartum inflammatory sacroiliitis from 2014 to 2020. All their clinical details including clinical symptoms and signs, laboratory tests, radiologic examination, diagnosis and treatment process and clinical outcomes were obtained and analyzed in this retrospective analysis. RESULTS: Eleven patients diagnosed with acute postpartum inflammatory sacroiliitis complain of low back pain. Magnetic resonance imaging (MRI) is useful in diagnosing acute postpartum inflammatory sacroiliitis. The systemic non-steroidal anti-inflammatory drugs (NSAIDs) administration, sacroiliac joint injection, and physical therapy effectively alleviated the pain with symptoms disappearing, and the abnormal signal reduced in MRI. CONCLUSION: Acute postpartum inflammatory sacroiliitis is an uncommon disease with atypical symptoms. MRI examination may be the best diagnostic method. General NSAIDs and sacroiliac joint injections of local anesthetic plus corticosteroid under the guidance of fluoroscopy or ultrasound can achieve safe and effective treatment. This retrospective study was approved by the Committee on the Ethics of our hospital (No. 202101023). TRIAL REGISTRY: Trial registration was performed in the Chinese Clinical Trial Registry ( http://www.chictr.org.cn , No. ChiCTR2100045656).

A new survival model based on ion channel genes for prognostic prediction in hepatocellular carcinoma.

Accumulating studies revealed the vital role of ion channels in cancers, but the prognosis role of ion channels in hepatocellular carcinoma (HCC) remains limited. Here, we developed and validated an ion channel signature for prognostic prediction of HCC patients. In total, 35 differential expressed ion channel genes (DEChannelGs) were identified in HCC and a novel ion channel risk model was established for HCC prognosis prediction using the TCGA cohort, which was validated using the ICGC cohort. Moreover, this risk model was an independent prognostic factor and was associated with the immune microenvironment in HCC. Finally, the mRNA and protein levels of ANO10 and CLCN2 were prominently up-regulated and were related to the poor prognosis of HCC patients. Taken together, these results indicated a novel ion channel risk model as a prognostic biomarker for HCC patients and provided further insight into its immunoregulatory mechanism in HCC progression.

Genetic variation of YWHAE gene-"Switch" of disease control. / YWHAEåŸºå› é—ä¼ å˜å¼‚­­ç–¾ç— 控制"å¼€å ³".

YWHAE gene is located on chromosome 17p13.3, and its product 14-3-3epsilon protein belongs to 14-3-3 protein family. As a molecular scaffold, YWHAE participates in biological processes such as cell adhesion, cell cycle regulation, signal transduction and malignant transformation, and is closely related to many diseases. Overexpression of YWHAE in breast cancer can increase the ability of proliferation, migration and invasion of breast cancer cells. In gastric cancer, YWHAE acts as a negative regulator of MYC and CDC25B, which reduces their expression and inhibits the proliferation, migration, and invasion of gastric cancer cells, and enhances YWHAE-mediated transactivation of NF-κB through CagA. In colorectal cancer, YWHAE lncRNA, as a sponge molecule of miR-323a-3p and miR-532-5p, can compete for endogenous RNA through direct interaction with miR-323a-3p and miR-532-5p, thus up-regulating K-RAS/ERK/1/2 and PI3K-AKT signaling pathways and promoting the cell cycle progression of the colorectal cancer. YWHAE not only mediates tumorigenesis as a competitive endogenous RNA, but also affects gene expression through chromosome variation. For example, the FAM22B-YWHAE fusion gene caused by t(10; 17) (q22; p13) may be associated with the development of endometrial stromal sarcoma. At the same time, the fusion transcript of YWHAE and NUTM2B/E may also lead to the occurrence of endometrial stromal sarcoma. To understand the relationship between YWHAE, NUTM2A, and NUTM2B gene rearrangement/fusion and malignant tumor, YWHAE-FAM22 fusion gene/translocation and tumor, YWHAE gene polymorphism and mental illness, as well as the relationship between 17p13.3 region change and disease occurrence. It provides new idea and basis for understanding the effect of YWHAE gene molecular mechanism and genetic variation on the disease progression, and for the targeted for the diseases.

NETs promote ALI/ARDS inflammation by regulating alveolar macrophage polarization.

Neutrophils activated during acute lung injury (ALI) form neutrophil extracellular traps (NETs) to capture pathogens. However, excessive NETs can cause severe inflammatory reactions. Macrophages are classified as M1 macrophages with proinflammatory effects or M2 macrophages with anti-inflammatory effects. During ALI, alveolar macrophages (AMs) polarize to the M1 phenotype. This study tested the hypothesis that NETs may aggravate ALI or acute respiratory distress syndrome (ARDS) inflammation by promoting alveolar macrophage polarization to the M1 type. Our research was carried out in three aspects: clinical research, animal experiments and in vitro experiments. We determined that NET levels in ARDS patients were positively correlated with M1-like macrophage polarization. NET formation was detected in murine ALI tissue and associated with increased M1 markers and decreased M2 markers in BALF and lung tissue. Treatment with NET inhibitors significantly inhibitor NETs generation, downregulated M1 markers and upregulated M2 markers. Regardless of LPS pre-stimulation, significant secretion of proinflammatory cytokines and upregulated M1 markers were detected from bone marrow-derived macrophages (M0 and M2) cocultured with high concentrations of NETs; conversely, M2 markers were downregulated. In conclusion, NETs promote ARDS inflammation during the acute phase by promoting macrophage polarization to the M1 phenotype. We propose that NETs play an important role in the interaction between neutrophils and macrophages during the early acute phase of ALI.

Epidemiology of pediatric eye injuries requiring hospitalization in rural areas of Wenzhou and Changsha, China: a 10-year retrospective study.

BACKGROUND: The aim of this study was to review the demographic and characteristic distribution data of serious rural pediatric eye injuries in Wenzhou and Changsha, located in Zhejiang Province in East China and Hunan Province in Central China. METHODS: This retrospective study included hospitalized pediatric patients aged < 18 years with eye injuries at the Eye Hospital of Wenzhou Medical University and Xiangya Hospital of Central South University from January 2008 to December 2017. Demographic data, injury types, injury causes, and initial and final visual acuity (VA) were recorded and analyzed. The ocular trauma score (OTS) was calculated to assess the severity of injury and evaluate the prognosis. All patient data were obtained from the medical record systems. RESULTS: In total, 1125 children were hospitalized during the 10-year period; 830 (73.8%) were males and 295 (26.2%) were females. The majority of the patients were aged 3 to 8 years (57.4%, n = 646). Among mechanical injuries (n = 1007), penetrating injury was the most common (68.4%, n = 689), followed by contusion (17.2%, n = 173) and rupture (8.1%, n = 82). Overall, the top three injury causes were sharp objects (n = 544, 48.4%), blunt objects (n = 209, 18.6%) and fireworks (n = 121, 10.8%). In Wenzhou, eye injuries occurred mostly in summer (n = 136, 29.1%), and sharp object-related eye injuries accounted for the highest proportion (n = 98, 72.1%). In Changsha, eye injuries occurred mostly in winter (n = 272, 41.3%), and firecracker- and fireworks-associated eye injury accounted for the highest proportion (n = 73, 26.8%). The final VA was positively correlated with the initial VA (r = 0.641, P < 0.001) and the OTS (r = 0.582, P < 0.001). CONCLUSION: The age range of the susceptible pediatric population from rural areas was 3-8 years. Most eye injuries were penetrating, and the main cause of injury was a sharp object. Notably, the differences in the characteristics of eye injuries in the two areas were related to regional features.

Knowledge, attitude, and practice survey regarding coronavirus disease 2019 among residents in Hunan Province. / æ¹–å—çœå± æ°‘2019å† çŠ¶ç— æ¯’ç— çŸ¥è¯†ã€æ€åº¦ä¸Žåº”å¯¹è¡Œä¸º.

OBJECTIVES: To evaluate residents' knowledge, attitude and behavior towards coronavirus disease 2019 (COVID-19) in Hunan Province, and to explore the factors influencing behaviors. METHODS: A self-designed questionnaire was used to conduct an online survey for 4 139 Hunan residents. The contents included general population information, residents' knowledge, attitude and practice to COVID-19. RESULTS: Mean scores of knowledge, attitude, and behavior were 29.82±3.16, 6.71±1.12, and 14.93±1.45, respectively. Residents had the highest score of major symptoms of COVID-19 (3.96±0.39), but the lowest was the main transmission routes (3.47±0.89). A total of 22.68% of the residents were very or relatively afraid of the outbreak, but 95.22% of the residents had confidence in defeating COVID-19. In behavior dimension, "handling of suspicious symptoms" had the lowest score (3.58±0.75). The behavior implementation rate of "keep the surfaces of household items clean" (80.50%), "doing more exercise, reasonable diet, working and resting regularly" (84.59%), and "avoid hand contacting with eyes, mouth or nose" (89.51%) were relatively low. Pearson correlation coefficient showed that the knowledge, attitude, and practices score were correlated with each other (knowledge vs behavior: r=0.366; knowledge vs attitude: r=0.041; attitude vs behavior: r=0.100; all P<0.05). Multiple linear regression analysis showed that the knowledge, attitude and behavior on COVID-19 were mostly influenced by education background (all P<0.05), and the independent factors affecting behavior included knowledge and attitude, gender, permanent residence, education background (all P<0.05). CONCLUSIONS: Residents in Hunan Province have a good knowledge, attitude, and behavior to COVID-19. Nevertheless there are still weak links to be improved in all dimensions. It is necessary to strengthen knowledge and behavior of family protection, and care for residents' psychological health, especially persons with low education degree, male and rural residents.

Retraction Note: Upregulation of the long non-coding RNA AFAP1-AS1 affects the proliferation, invasion and survival of tongue squamous cell carcinoma via the Wnt/ß-catenin signaling pathway.

The authors have retracted this article [1] because there are errors in Figures 4a and 4b.

PKR suppress NLRP3-pyroptosis pathway in lipopolysaccharide-induced acute lung injury model of mice.

To explore the effect of double-stranded RNA-dependent kinase (PKR) in acute lung injury (ALI) and resultant acute respiratory distress syndrome (ARDS). A mouse model of lipopolysaccharide (LPS)-induced ALI was used to evaluate the levels of phosphorylated (p)-PKR and NLRP3 in lung tissue, and the protective effects of a PKR inhibitor on lung injury. And in vitro, macrophages were incubated with LPS, with or without PKR inhibitor pre-treatment. It was observed that the levels of p-PKR protein and NLRP3 protein were significantly increased compared with those in control tissues after LPS administration. Meanwhile, treatment with PKR inhibitor decreased inflammation, injury score, wet/dry weight ratio, bronchoalveolar lavage fluid (BALF) protein levels, neutrophil count in BALF, myeloperoxidase activity and expression of high-mobility group box1(HMGB1) and interleukin(IL)-1ß in the lungs of LPS-challenged mice. In vitro, we demonstrated that the levels of p-PKR and NLRP3, and cell mortality rate were increased in macrophages which were incubated with LPS compared with those without LPS administration, and PKR inhibitor significantly suppressed the level of NLRP3, caspase-1, HMGB1 and IL-1ß. These results indicate that PKR plays a key role in ALI through NLRP3-pyrotosis pathway and pharmacological inhibition of PKR may have potential therapeutic effects in the treatment of patients with ALI and ARDS.

The antimicrobial cathelicidin peptide hlF(1-11) attenuates alveolar macrophage pyroptosis induced by Acinetobacter baumannii in vivo.

Acinetobacter baumannii is a Gram-negative coccobacillus found primarily in hospital settings that has recently emerged as a source of hospital-acquired infections, including bacterial pneumonia. The hLF(1-11) peptide comprising the first 11 N-terminal residues of human lactoferrin exerts antimicrobial activity in vivo and was highly effective against multidrug-resistant A. baumannii strains in vitro and in vivo. Pyroptosis is a caspase-1-dependent inflammatory cell death process and is induced by various microbial infections. In the present study, we investigated the molecular mechanisms that regulate pyroptosis induced by A. baumannii in macrophages. Our results revealed that A. baumannii induced pyroptosis through caspase-1 activation and IL-1ß production. We also found that caspase-1 activation and IL-1ß maturation in A. baumannii-triggered pyroptotic cell death were reduced by hLF(1-11) treatment. Moreover, hLF(1-11) inhibited the A. baumannii-induced caspase-1 activation and pyroptosis of pulmonary alveolar macrophages in vivo.

Upregulation of the long non-coding RNA AFAP1-AS1 affects the proliferation, invasion and survival of tongue squamous cell carcinoma via the Wnt/ß-catenin signaling pathway.

BACKGROUND: Long non-coding RNA (lncRNA) actin filament associated protein 1 antisense RNA1 (AFAP1-AS1) is oriented in an antisense direction to the protein-coding gene AFAP1 in the opposite strand. Previous studies showed that lncRNA AFAP1-AS1 was upregulated and acted as an oncogene in a variety of tumors. However, the expression and biological functions of lncRNA AFAP1-AS1 in tongue squamous cell carcinoma (TSCC) are still unknown. METHODS: The expression level of AFAP1-AS1 was measured in 103 pairs of human TSCC tissues and corresponding adjacent normal tongue mucous tissues. The correlation between AFAP1-AS1 and the clinicopathological features was evaluated using the chi-square test. The effects of AFAP1-AS1 on TSCC cells were determined via a CCK-8 assay, clone formation assay, flow cytometry, wound healing assay and transwell assay. Furthermore, the effect of AFAP1-AS1 knockdown on the activation of the Wnt/ß-catenin signaling pathway was investigated. Finally, CAL-27 cells with AFAP1-AS1 knockdown were subcutaneously injected into nude mice to evaluate the effect of AFAP1-AS1 on tumor growth in vivo. RESULTS: In this study, we found that lncRNA AFAP1-AS1 was increased in TSCC tissues and that patients with high AFAP1-AS1 expression had a shorter overall survival. Short hairpin RNA (shRNA)-mediated AFAP1-AS1 knockdown significantly decreased the proliferation of TSCC cells. Furthermore, AFAP1-AS1 silencing partly inhibited cell migration and invasion. Inhibition of AFAP1-AS1 decreased the activity of the Wnt/ß-catenin pathway and suppressed the expression of EMT-related genes (SLUG, SNAIL1, VIM, CADN, ZEB1, ZEB2, SMAD2 and TWIST1) in TSCC cells. In addition, CAL-27 cells with AFAP1-AS1 knockdown were injected into nude mice to investigate the effect of AFAP1-AS1 on tumorigenesis in vivo. Downregulation of AFAP1-AS1 suppressed tumor growth and inhibited the expression of EMT-related genes (SLUG, SNIAL1, VIM, ZEB1, NANOG, SMAD2, NESTIN and SOX2) in vivo. CONCLUSIONS: Taken together, our findings present a road map for targeting the newly identified lncRNA AFAP1-AS1 to suppress TSCC progression, and these results elucidate a novel potential therapeutic strategy for TSCC.

Activation of Bombesin Receptor Subtype-3 Promotes Antigen-Presenting Action in Human Bronchial Epithelial Cells.

BACKGROUND: Bombesin receptor subtype-3 (BRS-3) is a member of the bombesin-like peptide receptor family. Our previous studies demonstrated that activation of the human BRS-3 plays a protective role in oxidation-injured human bronchial epithelial cells (HBEC). The present study was designed to determine the role of BRS-3 activation in the antigen-presenting action of HBEC and the corresponding proliferation and differentiation of T cells. MATERIALS AND METHODS: In vivo, an asthma animal model was established and the expression and distribution of BRS-3 were analyzed by immunocytochemistry. In vitro, 2 kinds of B7 costimulatory molecules, i.e., B7H1 and B7DC, on HBEC were analyzed by flow cytometry. The antigen uptake by HBEC was examined by confocal microscopy and flow cytometry. The antigen-presenting-action-induced proliferation of T cells was determined by MTT assays. IFN-γ and IL-4 levels were measured by ELISA. All studies were performed in the absence or presence of the synthetic peptide P3513. RESULTS: BRS-3 expression was induced in asthma animal models and mainly distributed in bronchial epithelial cells. HBEC express the costimulatory molecules B7H1 and B7DC. BRS-3 activation increased B7H1 expression but decreased B7DC expression on HBEC. BRS-3 activation also increased the antigen uptake by HBEC and the subsequent T cell proliferation. In addition, BRS-3 activation promoted the releases of IFN-γ, but not IL-4, in the supernatant of cocultured HBEC and T cells. CONCLUSION: These data suggest that HBEC can present antigen to T cells and BRS-3 activation promotes the process of antigen presentation and subsequent T cell proliferation and Th1 differentiation.

Facile hierarchical assembly of gold particle decorated conductive polymer nanofibers for electrochemical sensing.

In this study, we successfully applied vapor-phase polymerization towards the synthesis of PEDOT nanofibers which were subsequently functionalized with gold particles and used as electrodes for electrochemical sensing. Two methods were used to synthesize the PEDOT nanofibers including (1) electrospinning followed by vapor-phase polymerization (EVP), and (2) one-step vapor-phase polymerization (OSVP). The average diameter of EVP fibers was approximately 350 nm, and OSVP was approximately 200 nm. Gold particles (∼500 nm) were synthesized by an oxidation-reduction reaction between gold precursors and residue EDOT monomers on the surface of the PEDOT nanofibers. In order to investigate the electrochemical performance of these electrodes, ascorbic acid was chosen as an analyte model. Our results indicated that PEDOT nanofiber electrodes showed an enhanced response with respect to bare gold electrodes. Furthermore, the OSVP PEDOT nanofibers with gold particles demonstrated the highest sensitivity at low ascorbic acid concentrations. These hierarchically assembled, gold particle-decorated, conductive polymer nanofibers were further fabricated into flexible electrodes, demonstrating a potential in advanced applications such as wearable electronics.

Sensorimotor Cortical Neuroplasticity in the Early Stage of Bell's Palsy.

Neuroplasticity is a common phenomenon in the human brain following nerve injury. It is defined as the brain's ability to reorganize by creating new neural pathways in order to adapt to change. Here, we use task-related and resting-state fMRI to investigate neuroplasticity in the primary sensory (S1) and motor cortex (M1) in patients with acute Bell's palsy (BP). We found that the period directly following the onset of BP (less than 14 days) is associated with significant decreases in regional homogeneity (ReHo), fractional amplitude of low frequency fluctuations (fALFF), and intrinsic connectivity contrast (ICC) values in the contralateral S1/M1 and in ReHo and ICC values in the ipsilateral S1/M1, compared to healthy controls. The regions with decreased ReHo, fALFF, and ICC values were in both the face and hand region of S1/M1 as indicated by resting-state fMRI but not task-related fMRI. Our results suggest that the early stages of BP are associated with functional neuroplasticity in both the face and hand regions of S1/M1 and that resting-state functional fMRI may be a sensitive tool to detect these early stages of plasticity in patient populations.

CDKN2B methylation is associated with carotid artery calcification in ischemic stroke patients.

BACKGROUND: Cyclin-dependent kinase inhibitor 2A/2B (CDKN2A/2B) near chromosome 9p21 have been associated with both atherosclerosis and artery calcification, but the underlying mechanisms remained largely unknown. Considering that CDKN2A/2B is a frequently reported site for DNA methylation, this study aimed to evaluate whether carotid artery calcification (CarAC) is related to methylation levels of CDKN2A/2B in patients with ischemic stroke. METHODS: DNA methylation levels of CDKN2A/2B were measured in 322 ischemic stroke patients using peripheral blood leukocytes. Methylation levels of 36 CpG sites around promoter regions of CDKN2A/2B were examined with BiSulfite Amplicon Sequencing. CarAC was quantified with Agatston score based on results of computed tomography angiography. Generalized liner model was performed to explore the association between methylation levels and CarAC. RESULTS: Of the 322 analyzed patients, 187 (58.1%) were classified as with and 135 (41.9%) without evident CarAC. The average methylation levels of CDKN2B were higher in patents with CarAC than those without (5.7 vs 5.4, p = 0.001). After adjustment for potential confounders, methylation levels of CDKN2B were positively correlated with cube root transformed calcification scores (ß = 0.591 ± 0.172, p = 0.001) in generalized liner model. A positive correlation was also detected between average methylation levels of CDKN2B and cube root transformed calcium volumes (ß = 0.533 ± 0.160, p = 0.001). CONCLUSIONS: DNA methylation of CDKN2B may play a potential role in artery calcification.

Up-Regulation of microRNA-183 Promotes Cell Proliferation and Invasion in Glioma By Directly Targeting NEFL.

Glioblastoma multiforme (GBM) is the most common and lethal type of primary malignant brain tumor. In recent years, increasing reports suggest that discovery of microRNAs (miRNAs) might provide a novel therapeutical target for human cancers, including GBM. The expression and roles of microRNA-183 (miR-183) has been explored in several types of human cancers, including in GBM, and plays important roles in tumor initiation and progression. However, its biological functions in GBM remain largely unknown. In this study, we demonstrated that miR-183 was significantly up-regulated in astrocytoma tissues and glioblastoma cell lines. Introduction of miR-183 mimics into U251 cells could promoted, while its antisense oligos inhibited cell proliferation and invasion. Moreover, we identified neurofilament light polypeptide (NEFL) as a novel target gene of miR-183. The expression levels of NEFL are inversely correlated with that of miR-183 in human astrocytoma clinical specimens. In addition, NEFL-siRNA could significantly attenuate the inhibitory effects of knockdown miR-183 on the proliferation and invasion of U251 cells via mTOR signaling pathway. Overall, This study revealed that miR-183 promotes glioma cell proliferation by targeting NEFL, and also demonstrated that miR-183 could be a potential target for GBM treatment.

[Effect of motivational interviewing combined with peer participation on obesity management in adolescents].

OBJECTIVE: To investigate the effect of motivational interviewing combined with peer participation on obesity management in adolescents. METHODS: A total of 100 adolescents with simple obesity were randomly divided into traditional management and peer participation groups (n=50 each). The traditional management group received traditional health management. The peer participation group received motivational interviewing performed by psychological consultants combined with peer participation through the entire process in addition to traditional health management. The physical exercise, dietary behavior, differences in body composition parameters, and effect of comprehensive intervention were compared between the two groups after intervention for half a year. RESULTS: After the health management for six months, the peer participation group showed better improvements in the control of energy intake, adjustment of dietary structure, adherence to moderate/high intensity exercise, and increase in lean body mass compared with the traditional management group (P<0.05). The peer participation group had a significantly higher attendance rate for guidance and counseling performed by a multidisciplinary team once a week than the traditional management group (89% vs 57%; P<0.05), as well as a significantly higher response rate to health management than the traditional management group (83% vs 43%; P<0.05). CONCLUSIONS: Motivational interviewing combined with peer participation for obesity management can improve the compliance and the effect of comprehensive intervention in losing weight in adolescents.

miR-25 promotes glioblastoma cell proliferation and invasion by directly targeting NEFL.

Glioblastoma multiforme (GBM) is the most malignant and common brain tumor; it is aggressive growth pattern means that GBM patients face a poor prognosis even when receiving the best available treatment modalities. In recent years, an increasing number of reports suggest that the discovery of microRNAs (miRNAs) might provide a novel therapeutic target for human cancers, including GBM. One miRNA in particular, microRNA-25 (miR-25), is overexpressed in several cancers, wherein accumulating evidence indicates that it functions as an oncogene. However, the function of miR-25 in GBM has not been totally elucidated. In this study, we demonstrated that miR-25 was significantly up-regulated in astrocytoma tissues and glioblastoma cell lines. In vitro studies further demonstrated that overexpressed miR-25 was able to promote, while its antisense oligos inhibited cell proliferation and invasion in U251 cells. Moreover, we identified neurofilament light polypeptide (NEFL) as a novel target molecule of miR-25. Also of note was the fact that NEFL was down-regulated with increased levels of miR-25 expression in human astrocytoma clinical specimens. In addition, via the mTOR signaling pathway, NEFL-siRNA could significantly attenuate the inhibitory effects of knockdown miR-25 on the proliferation and invasion of U251 cells. Overall, our results showed an important role for miR-25 in regulating NEFL expression in GBM, and suggest that miR-25 could be a potential target for GBM treatment.

Electrospun water-soluble polymer nanofibers for the dehydration and storage of sensitive reagents.

The ability to preserve and deliver reagents remains an obstacle for the successful deployment of self-contained diagnostic microdevices. In this study we investigated the ability of bacteriophage T7 to be encapsulated and preserved in water soluble nanofibers. The bacteriophage T7 was added to mixtures of polyvinylpyrrolidone and water and electrospun onto a grounded plate. Trehalose and magnesium salts were added to the mixtures to determine their effect on the infectivity of the bacteriophage following electrospinning and during storage. The loss of T7 infectivity was determined immediately following electrospinning and during storage using agar overlay plating and plaque counting. The results indicate that the addition of magnesium salts protects the bacteriophage during the relatively violent and high voltage electrospinning process, but is not as effective as a protectant during storage of the dried T7. Conversely, the addition of trehalose into the electrospinning mix has little effect on the electrospinning, but a more significant role as a protectant during storage.