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1.
Int J Mol Sci ; 20(20)2019 Oct 16.
Artigo em Inglês | MEDLINE | ID: mdl-31623059

RESUMO

Long noncoding RNAs (lncRNAs) are involved in a diversity of biological processes. It is known that differential expression of thousands of lncRNAs occurs in host during influenza A virus (IAV) infection. However, only few of them have been well characterized. Here, we identified a lncRNA, named as interferon (IFN)-stimulated lncRNA (ISR), which can be significantly upregulated in response to IAV infection in a mouse model. A sequence alignment revealed that lncRNA ISR is present in mice and human beings, and indeed, we found that it was expressed in several human and mouse cell lines and tissues. Silencing lncRNA ISR in A549 cells resulted in a significant increase in IAV replication, whereas ectopic expression of lncRNA ISR reduced the viral replication. Interestingly, interferon-ß (IFN-ß) treatment was able to induce lncRNA ISR expression, and induction of lncRNA ISR by viral infection was nearly abolished in host deficient of IFNAR1, a type I IFN receptor. Furthermore, the level of IAV-induced lncRNA ISR expression was decreased either in retinoic acid-inducible gene I (RIG-I) knockout A549 cells and mice or by nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) inhibitor treatment. Together, these data elucidate that lncRNA ISR is regulated by RIG-I-dependent signaling that governs IFN-ß production during IAV infection, and has an inhibitory capacity in viral replication.

2.
Front Immunol ; 10: 1843, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31474976

RESUMO

Influenza A virus (IAV) remains a major public health threat in the world, as indicated by the severe pneumonia caused by its infection annually. Interleukin-6 (IL-6) involved excessive inflammatory response to IAV infection profoundly contributes to the virus pathogenesis. However, the precise mechanisms underlying such a response are poorly understood. Here we found from both in vivo and in vitro studies that IAV not only induced a surge of IL-6 release, but also greatly upregulated expression of suppressor of cytokine signaling-3 (SOCS3), the potent suppressor of IL-6-associated signal transducer and activator of transcription 3 (STAT3) signaling. Interestingly, there existed a cytokine-independent mechanism of the robust induction of SOCS3 by IAV at early stages of the infection. Furthermore, we employed SOCS3-knockdown transgenic mice (TG), and surprisingly observed from virus challenge experiments using these mice that disruption of SOCS3 expression provided significant protection against IAV infection, as evidenced by attenuated acute lung injury, a higher survival rate of infected animals and lower viral load in infected tissues as compared with those of wild-type littermates under the same condition. The activity of nuclear factor-kappa B (NFκB) and the expression of its target gene IL-6 were suppressed in SOCS3-knockdown A549 cells and the TG mice after infection with IAV. Moreover, we defined that enhanced STAT3 activity caused by SOCS3 silencing was important for the regulation of NFκB and IL-6. These findings establish a critical role for IL-6-STAT3-SOCS3 axis in the pathogenesis of IAV and suggest that influenza virus may have evolved a strategy to circumvent IL-6/STAT3-mediated immune response through upregulating SOCS3.

3.
Anal Chem ; 91(19): 12538-12545, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31476869

RESUMO

The efficient and precise delivery of antisense oligonucleotides (ASOs) to target cells is of great value in gene silencing. However, the specificity and packaging capacity of delivery system still remains challenging. Here, we designed an i-motif forming-initiated in situ bipedal hybridization chain reaction (pH-Apt-BiHCR) amplification strategy for specific target cells imaging and enhanced gene delivery of ASOs. As a proof of concept, an 8-nt ASO modified with locked nucleic acid (LNA) which is complementary to the seed region of microRNA21 (miR-21) was used for gene silencing studies. Benefiting from the design of hairpin-contained i-motif, the stimuli-responsive assembly of pH-Apt-BiHCR was successfully achieved on MCF-7 cells surface based on the specific recognition of aptamer. Using this strategy, the pH-Apt-BiHCR not only contains repeated fluorescence resonance energy transfer (FRET) units for activatable tumor imaging with high contrast but also arrays with plenty of LNA ASOs as interference molecules for cancer cells inhibition. An in vitro assay showed that this strategy presented an excellent response ability in buffer within a narrow pH range (6.0-7.0) with a transition midpoint (pHT) of 6.44 ± 0.06. Moreover, live cell studies revealed that it realized a specific activatable imaging of target cells, while the ASOs arrayed pH-Apt-BiHCR exhibited improved internalization via an endocytosis pathway and enhanced gene silencing to MCF-7 cells compared to single ASO alone. We believe that this design will inspire the development of novel probes for early diagnosis and therapy of cancer cells.

4.
J Agric Food Chem ; 67(40): 11005-11017, 2019 Oct 09.
Artigo em Inglês | MEDLINE | ID: mdl-31532657

RESUMO

The limited number of agrochemicals targeting plant bacterial diseases has driven us to develop highly efficient, low-cost, and versatile antibacterial alternatives. Herein, a novel type of simple furan-functionalized quinazolin-4-amines was systematically fabricated and screened for their antibacterial activity. Bioassay results revealed that compounds C1 and E4 could substantially block the growth of two frequently mentioned pathogens Xanthomonas oryzae pv oryzae and X. axonopodis pv citri in vitro, displaying appreciable EC50 values of 7.13 and 10.3 mg/L, respectively. This effect was prominently improved by comparing those of mainly used agrochemicals. An in vivo experiment against bacterial blight further illustrated their viable applications as antimicrobial ingredients. Quantitative proteomics demonstrated that C1 possessed a remarkable ability to manipulate the upregulation and downregulation of expressed proteins, which probably involved d-glucose and biotin metabolic pathways. This finding was substantially verified by parallel reaction monitoring analysis. Scanning electron microscopy images and fluorescence spectra also indicated that the designed compounds had versatile capacities for destroying the integrity of bacteria. Given these remarkable characteristics, furan-functionalized quinazoline hybrids can serve as a viable platform for developing innovative antibiotic alternatives against bacterial infections.


Assuntos
Antibacterianos/química , Antibacterianos/farmacologia , Furanos/farmacologia , Quinazolinas/farmacologia , Xanthomonas/efeitos dos fármacos , Antibacterianos/síntese química , Proteínas de Bactérias/genética , Proteínas de Bactérias/metabolismo , Furanos/química , Testes de Sensibilidade Microbiana , Estrutura Molecular , Doenças das Plantas/microbiologia , Proteômica , Quinazolinas/química , Relação Estrutura-Atividade , Xanthomonas/genética , Xanthomonas/crescimento & desenvolvimento , Xanthomonas/metabolismo
5.
Gene ; 719: 144044, 2019 Nov 30.
Artigo em Inglês | MEDLINE | ID: mdl-31400406

RESUMO

OBJECTIVE: Exosomes have been described as a messenger between cells' communication and contain various information (lipids, proteins, mRNAs, microRNAs, LncRNAs). It has been proved that Linc-ROR was enriched in exosomes released by HepG2 cells. Our aim was to investigate whether exosomes released by HepG2 cells could affect the biological behaviors of LO2 cells and whether Linc-ROR played an important role in this process. METHODS: Exosomes-derived from HepG2 cells were isolated and characterized. Real-time PCR assessed expression level of Linc-ROR in specimens of cancerous tissues and carcinoma-adjacent tissues. The Linc-ROR expression level in HepG2, Huh7, SMMC-7721, Bel-7402, LO2 cells and exosomes was detected by real-time PCR. Knockdown the expression of Linc-ROR in HepG2 by using effective siRNA. Cell counting method was used to test LO2 cells proliferative activities. Flow cytometry was performed to quantify the apoptosis rates of LO2 cells cocultured with exosomes. The expression levels of OCT4, NANOG, SOX2, P53 and CD133 were assessed by western blot. RESULTS: Linc-ROR was enriched in exosomes released by HepG2 cells. Exosomes derived from HepG2 cells promoted the proliferation and suppressed the apoptosis of LO2 cells suffering nutrient deficiency. Knockdown the expression of Linc-ROR in HepG2 or LO2 cells could significantly impaired the exosomes' effects on LO2 cells. In addition, the long-term coculture with exosomes would obviously change the biological behaviors of LO2 cells. CONCLUSIONS: Our experiments indicated the HepG2 cells could transfer its Linc-ROR to the LO2 cells via exosomes, then influenced the recipient cells.


Assuntos
Carcinoma Hepatocelular/patologia , Exossomos/metabolismo , Neoplasias Hepáticas/patologia , RNA Longo não Codificante/genética , Apoptose , Carcinoma Hepatocelular/genética , Linhagem Celular Tumoral , Proliferação de Células , Estudos de Coortes , Feminino , Humanos , Neoplasias Hepáticas/genética , Masculino , Pessoa de Meia-Idade
6.
Exp Dermatol ; 2019 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-31461795

RESUMO

Mycosis Fungoides (MF) is the most common subtype of cutaneous T-cell lymphomas (CTCL). Shank-associated RH domain-interacting protein (SHARPIN) participates in the initiation and development of multiple tumors. However, the clinical significance of SHARPIN in MF hasn't been investigated. The c-Jun N-terminal kinases (JNKs) pathway is a member of mitogen-activated protein kinases (MAPKs). Its dysregulation is observed in various tumors including CTCL, whereas the roles of JNKs pathway in MF remain largely unknown, the relationship between SHARPIN and JNKs pathway remains elusive. Herein, we showed that upregulated expression of SHARPIN was related to poor prognosis of MF patients. In vitro experiments found increased SHARPIN expression and activation of JNKs pathway in MF cell line MyLa2059. SHARPIN induced transforming growth factor ß activated kinase-1 (TAK1) transcription, which is an upstream kinase of JNKs, NF-κB and p38 pathway, leading to activation of JNKs and NF-κB pathway. SHARPIN also promoted p38 signalling independent of TAK1 expression, by which overexpression of SHARPIN induced cell proliferation, inhibited apoptosis, enhanced migration and invasion of MyLa2059. Our work provided direct evidences for effects of SHARPIN on JNKs and NF-κB pathway, and the contributing roles of JNKs, NF-κB and p38 pathway regulated by SHARPIN in the development of MF.

7.
Poult Sci ; 98(10): 5109-5117, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31265733

RESUMO

FOXO3 belongs to the Forkhead O transcription factor family and it is an important gene in multiple biological processes, such as cell cycle control, cell proliferation, cell apoptosis, human longevity, and oxidative stress. Previous studies have shown that FOXO3 is associated with skeletal muscle growth and adipose development in mammals. However, the sequence of chicken FOXO3 is still incomplete and the cellular functions of FOXO3 in chickens are poorly understood. Thus, we obtained the full-length sequence of chicken FOXO3 by 5' rapid amplification of cDNA ends (5' RACE) and the phylogenetic tree showed that the chicken FOXO3 sequence was homologous with those in other species. Flow cytometry analysis and 5-ethynyl-2'-deoxyuridine assays showed that FOXO3 repressed cellular proliferation and induced apoptosis in a chicken hepatocellular carcinoma cell line (LMH). Mutations were screened in the second exon of FOXO3 and 13 synonymous single nucleotide polymorphisms were found in the test population. Further analysis showed that rs317670452 and rs15379317 were associated with many growth and carcass traits, such as the body weight at different ages and breast muscle weight. Our results indicate that chicken FOXO3 has similar cellular functions to those found in mammals and it is significantly associated with chicken growth.

8.
Toxicol Lett ; 314: 18-26, 2019 Oct 10.
Artigo em Inglês | MEDLINE | ID: mdl-31299270

RESUMO

Epidemiological investigations indicate that effects related to prenatal adverse environments on the organs of the offspring could continue to adulthood. This study intends to confirm that prenatal nicotine exposure (PNE) increases the susceptibility of osteoarthritis (OA) in the male offspring, and to explore the potential intrauterine programming mechanism. During pregnancy, rats were divided into a PNE group and a control group. After birth, rats were given a high-fat diet for 6 months and long-distance running for 6 weeks. The rats were euthanized at 18 months after birth (PM18) and on gestational day 20 (GD20), respectively. Knee joints were collected for histochemistry, immunohistochemistry, and quantitative polymerase chain reaction (qPCR) assays. Histological analyses and the Mankin's score showed increased cartilage destruction and accelerated OA progression in adult offspring from the PNE group. Immunohistochemistry results showed decreased expression of transforming growth factor beta (TGFß) signaling pathway. Furthermore, the expression of apoptosis factors (caspase-3 and caspase-8), inflammatory factors [interleukin (IL)-1, IL-6] and matrix degradation enzymes [matrix metalloproteinase (MMP)-3, MMP-13] were also significantly increased. Traced back to the intrauterine period, it was found that the number of chondrocytes and the contents of Col2A1 and aggrecan in the matrix in the PNE group were decreased. And, the expression of the TGFß signaling pathway was inhibited. These results suggested that PNE enhanced the susceptibility of OA in male elderly offspring rats by down-regulating TGFß signaling, which increased articular cartilage local inflammation, matrix degradation, and cell apoptosis. This study confirmed the developmental origin of OA, and clarified the congenital and the living environment impact on the occurrence and development of OA. Our findings provide a theoretical and experimental basis for OA early prevention.


Assuntos
Articulações/efeitos dos fármacos , Nicotina/toxicidade , Agonistas Nicotínicos/toxicidade , Osteoartrite/induzido quimicamente , Efeitos Tardios da Exposição Pré-Natal , Transdução de Sinais , Fator de Crescimento Transformador beta/metabolismo , Fatores Etários , Agrecanas/metabolismo , Animais , Apoptose/efeitos dos fármacos , Caspase 3/metabolismo , Caspase 8/metabolismo , Condrócitos/efeitos dos fármacos , Condrócitos/metabolismo , Condrócitos/patologia , Condrogênese/efeitos dos fármacos , Colágeno Tipo II/metabolismo , Feminino , Idade Gestacional , Interleucina-1/metabolismo , Interleucina-6/metabolismo , Articulações/metabolismo , Articulações/patologia , Masculino , Exposição Materna , Metaloproteinase 13 da Matriz/metabolismo , Metaloproteinase 3 da Matriz/metabolismo , Osteoartrite/metabolismo , Osteoartrite/patologia , Gravidez , Ratos Wistar , Fatores de Risco , Fatores Sexuais
9.
Chemistry ; 25(54): 12497-12501, 2019 Sep 25.
Artigo em Inglês | MEDLINE | ID: mdl-31343787

RESUMO

N-Substituted naphthalimides (NNIs) have been shown to exhibit highly efficient and persistent room-temperature phosphorescence from an NNI-localized triplet excited state, when the N-substitution is a sufficiently strong donor and mediates an intramolecular charge-transfer (ICT) state upon photo-excitation. This work shows that, when the electron-donating ability of the N-substitution is further increased in the presence of a carbanion or phenoxide, spontaneous electron transfer (ET) occurs and results in radical anions, verified with electron-paramagnetic resonance (EPR) spectroscopy. However, the EPR-active anion is surprisingly persistent and impervious to nucleophilic and radical reactions under anionic conditions. The stability is thought to originate from an intramolecular spin pairing between the N-donor and the NI acceptor post ET, which is demonstrated in supramolecular chemistry.

10.
Biomed Res Int ; 2019: 3739086, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31281837

RESUMO

Acne is the eighth most frequent disease worldwide. Inflammatory response runs through all stages of acne. It is complicated and is involved in innate and adaptive immunity. This study aimed to explore the candidate genes and their relative signaling pathways in inflammatory acne using data mining analysis. Microarray data GSE6475 and GSE53795, including 18 acne lesion tissues and 18 matched normal skin tissues, were obtained. Differentially expressed genes (DEGs) were filtered and subjected to functional and pathway enrichment analyses. Protein-protein interaction (PPI) network and module analyses were also performed based on the DEGs. In this work, 154 common DEGs, including 145 upregulated and 9 downregulated, were obtained from two microarray profiles. Gene Ontology and pathway enrichment of DEGs were clustered using significant enrichment analysis. A PPI network containing 110 nodes/DEGs was constructed, and 31 hub genes were obtained. Four modules in the PPI network, which mainly participated in chemokine signaling pathway, cytokine-cytokine receptor interaction, and Fc gamma R-mediated phagocytosis, were extracted. In conclusion, aberrant DEGs and pathways involved in acne pathogenesis were identified using bioinformatic analysis. The DEGs included FPR2, ITGB2, CXCL8, C3AR1, CXCL1, FCER1G, LILRB2, PTPRC, SAA1, CCR2, ICAM1, and FPR1, and the pathways included chemokine signaling pathway, cytokine-cytokine receptor interaction, and Fc gamma R-mediated phagocytosis. This study could serve as a basis for further understanding the pathogenesis and potential therapeutic targets of inflammatory acne.

11.
ACS Appl Mater Interfaces ; 11(32): 28781-28790, 2019 Aug 14.
Artigo em Inglês | MEDLINE | ID: mdl-31252501

RESUMO

Despite their inherent efficacy in significantly accelerating the rate of chemical reactions in biological processes, the applicability of natural enzymes is often hindered because of their intrinsic limitations such as high sensitivity, poor operational stability, and relatively high cost for purification as well as preparation. Thus, the fabrication of catalytically active nanomaterials as artificial enzymes (nanozymes) has become a newly burgeoning area of research in bionic chemistry, aiming in designing functional nanomaterials that mimic various inherent properties of natural enzymes. To address these issues, we present the supercritical fluid (SCF)-assisted fabrication of discrete, monodisperse, and uniform-sized manganese (III) oxide (Mn2O3)-based hollow containers as high-efficiency nanozymes for glucose sensing characteristics. Initially, the core-shell nanoreactors based on polyvinylpyrrolidone (PVP)-encapsulated manganese (III) acetylacetonate (Mn(acac)3) as precursors are fabricated using the SCF technology and subsequent calcination resulted in the Mn2O3 hollow nanoparticles (MHNs). This eco-friendly approach has resulted in the PVP-coated Mn(acac)3 nanoreactors with an average diameter of 220 nm and subsequent calcined hollow products are about one-fifth to that of the precursor. Such MHNs conveniently catalyzed 3,3',5,5'-tetramethylbenzidine (TMB) in the presence of hydrogen peroxide (H2O2) as a prominent peroxidase mimic, resulting in the oxidation products (TMB*+) at a specific absorption (UV-vis) maxima of 652 nm. Following typical Michaelis-Menten theory, this approach is further utilized to develop visual nonenzymatic sensing of glucose in a linear range of 0.1-1 mM at a detection limit of 2.31 µM. Collectively, this reliable as well as a cost-effective system with high precision potentially allows rapid detection of analytes, providing a convenient way for its utilization in diverse fields.

12.
Talanta ; 202: 152-158, 2019 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-31171163

RESUMO

Colorectal cancer (CRC) is the third most commonly diagnosed cancer in the world, which can lead to considerably high mortality rate. It was reported that the prognosis is extremely poor and survival is often measured in months once CRC metastases become clinically evident. Therefore, the development of effective approach for metastatic CRC cells detection and imaging may potentially be significant and helpful for CRC prognosis and treatment. Therefore, we proposed a sensitive and specific approach for high-metastatic CRC LoVo cells detection and imaging by using terminal deoxynucleotidyl transferase (TdT)-initiated molecule beacons (MBs) arrayed fluorescent aptamer probes (denoted as TMAP). In this approach, the aptamer W3 targeting high-metastatic CRC LoVo cells was elongated to form W3-poly A at the 3'-hydroxyl terminus with repeated A bases in the presence of TdT and dATP. The MBs designed with poly T sequence in the loop were then hybridized with the poly A in the aptamer W3. The TMAP was easily constructed without the need of aptamer modification. It was demonstrated that this approach could specifically detect and image the high-metastatic CRC LoVo cells from the mixture of high-metastatic CRC LoVo cells and non-metastatic HCT-8 cells. Compared with 6-carboxyfluorescein (6-FAM) labeled aptamer W3, the TMAP was demonstrated to have a much stronger fluorescence signal on the target cells, realizing a 4-fold increase in signal-to-background ratio (SBR). Determination by flow cytometry allowed for detection of as low as 23 CRC LoVo cells in 200 µL cell culture medium. The high sensitivity and the capability for using in complicate biological samples imply that this approach holds considerable potential for metastatic CRC detection and therapy.


Assuntos
Aptâmeros de Nucleotídeos/química , Técnicas Biossensoriais , Neoplasias Colorretais/diagnóstico por imagem , DNA Nucleotidilexotransferase/química , Corantes Fluorescentes/química , Neoplasias Colorretais/metabolismo , DNA Nucleotidilexotransferase/metabolismo , Corantes Fluorescentes/metabolismo , Humanos , Espectrometria de Fluorescência , Células Tumorais Cultivadas
13.
ACS Appl Mater Interfaces ; 11(26): 23144-23151, 2019 Jul 03.
Artigo em Inglês | MEDLINE | ID: mdl-31252469

RESUMO

Recently, loading TiO2 with transition-metal disulfides (TMDs) to construct dual functional heterostructures has been widely researched as an effective strategy to improve the photocatalytic performance of a TiO2 photocatalyst. For the TMD cocatalysts, the 2H-MoS2 and 1T-MoS2 have been widely studied and researched. However, they suffer from poor catalytic activity sites/low charge transfer ability and an unstable structure. In this regard, distorted 1T-phase TMDs with a stable structure are greatly fit for the cocatalyst due to their high charge transfer ability and rich catalytic sites on both the edge and basal plane. Therefore, it is highly desirable to develop distorted 1T-phase TMD/TiO2 heterostructures with well-identified interfaces for highly enhanced photocatalytic performance. Herein, we first introduce distorted 1T-ReS2 anchored on porous TiO2 nanofibers as a promising photocatalyst for achieving an excellent photocatalytic hydrogen production. The excellent performance is attributed to the strong chemical interaction of the Ti-O-Re bond between TiO2 and ReS2, the excellent electron mobility of distorted 1T-ReS2, and the abundant catalytic activity sites on both the plane and edge of the ReS2 cocatalyst.

14.
Int J Pediatr Otorhinolaryngol ; 124: 147-151, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31195308

RESUMO

OBJECTIVES: To investigate the outcomes of simultaneous cochlear implantation and repair of a cerebrospinal fluid (CSF) leak in two patients with inner ear malformations following meningitis. METHODS: In this retrospective study and review of the literature, two patients with recurrent meningitis and severe inner ear malformation underwent cochlear implantation via the round window, and repair of CSF otorrhea via a transmastoid lateral semicircular canal approach. Both patients were treated with antibiotics for 7 days after the surgery. RESULTS: Neither patient has exhibited evidence of CSF otorrhea 1 year after surgical repair. Categorical Auditory Performance (CAP) scores and the Speech Intelligibility Ratings (SIRs) were obtained before and 1 year after surgery: the scores were 0 versus 4 and 0 versus 2, respectively. Vestibular function tests of both patients were reviewed and were normal. CONCLUSION: Simultaneous repair of CSF otorrhea and cochlear implantation in patients with recurrent meningitis and severe inner ear malformation can be regarded as safe and effective.

15.
J Agric Food Chem ; 67(25): 6962-6969, 2019 Jun 26.
Artigo em Inglês | MEDLINE | ID: mdl-31150235

RESUMO

Target validation of current drugs remains the major challenge for target-based drug discovery, especially for agrochemical discovery. The bactericide 0 represents a novel lead structure and has shown potent efficacy against those diseases that are extremely difficult to control, such as rice bacterial leaf blight. However, no detailed target analysis of this bactericide has been reported. Here, we developed a panel of 0-derived probes 1-6, in which a conservative modification (alkyne tag) was introduced to keep the antibacterial activity of 0 and provide functionality for target identification via click chemistry. With these cell-permeable probes, we were able to discover dihydrolipoamide S-succinyltransferase (DLST) as an unprecedented target in living cells. The probes showed good preference for DLST, especially probe 1, which demonstrated distinct selectivity and reactivity. Also, we reported 0 as the first covalent DLST inhibitor, which has been used to confirm the involvement of DLST in the regulation of energy production.


Assuntos
Aciltransferases/química , Antibacterianos/química , Proteínas de Bactérias/química , Oryza/microbiologia , Doenças das Plantas/microbiologia , Sulfonas/química , Xanthomonas/enzimologia , Aciltransferases/metabolismo , Antibacterianos/farmacologia , Proteínas de Bactérias/metabolismo , Xanthomonas/química , Xanthomonas/efeitos dos fármacos
16.
Clin Otolaryngol ; 44(4): 702-706, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31062523

RESUMO

OBJECTIVE: To analyse clinical information from a cohort of 877 cochlear implant (CI) surgeries performed in patients with inner ear malformations and report our experience with this procedure. METHODS: Clinical information on patients with inner ear malformation who underwent CI surgery in our department from January 2010 to April 2017 was analysed. RESULTS: Seven hundred and fifty-four CI surgeries (86.0%) were uneventful but cerebrospinal fluid gusher occurred during surgery in 118 cases (13.5%). Not including the patients lost to follow-up, postoperative Categories of Auditory Performance (CAP) and Speech Intelligibility Rating (SIR) scores were collected from 13 patients with common cavity deformity, 38 with IP-I, 11 with hypoplasia, 13 with IP-III, 285 with IP-II and 43 with cochlear nerve deficiency. The mean CAP scores were 2.55, 3.39, 3.45, 3.77, 3.98, 2.95 and 2.90, and the mean SIR scores were 1.54, 3.68, 3.72, 3.54, 3.80, 2.31 and 2.32. Patients with common cavity deformity who underwent surgery using the traditional facial recess approach or transmastoid slotted labyrinthotomy approach had significantly better post-activation scores on the CAP, SIR and Meaningful Auditory Integration Scale/Infant-Toddler Meaningful Auditory Integration Scale, with no significant differences between the two approaches. CONCLUSION: The traditional facial recess approach can be successful, and several approaches may be used for electrode insertion and gusher control in patients with a severe deformity, particularly common cavity deformity and IP-III. A gusher was the most common intraoperative finding and occurred most often in patients with IP-III. Careful consideration of the type of electrode used is important.

18.
Cell Microbiol ; 21(8): e13036, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31045320

RESUMO

Long noncoding RNAs (lncRNAs) are single-stranded RNA molecules longer than 200 nt that regulate many cellular processes. MicroRNA 155 host gene (MIR155HG) encodes the microRNA (miR)-155 that regulates various signalling pathways of innate and adaptive immune responses against viral infections. MIR155HG also encodes a lncRNA that we call lncRNA-155. Here, we observed that expression of lncRNA-155 was markedly upregulated during influenza A virus (IAV) infection both in vitro (several cell lines) and in vivo (mouse model). Interestingly, robust expression of lncRNA-155 was also induced by infections with several other viruses. Disruption of lncRNA-155 expression in A549 cells diminished the antiviral innate immunity against IAV. Furthermore, knockout of lncRNA-155 in mice significantly increased IAV replication and virulence in the animals. In contrast, overexpression of lncRNA-155 in human cells suppressed IAV replication, suggesting that lncRNA-155 is involved in host antiviral innate immunity induced by IAV infection. Moreover, we found that lncRNA-155 had a profound effect on expression of protein tyrosine phosphatase 1B (PTP1B) during the infection with IAV. Inhibition of PTP1B by lncRNA-155 resulted in higher production of interferon-beta (IFN-ß) and several critical interferon-stimulated genes (ISGs). Together, these observations reveal that MIR155HG derived lncRNA-155 can be induced by IAV, which modulates host innate immunity during the virus infection via regulation of PTP1B-mediated interferon response.

19.
Curr Neurovasc Res ; 16(2): 135-141, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30977448

RESUMO

OBJECTIVE: Gastrointestinal (GI) hemorrhage is serious during the acute phase and is reported to be related to an increased risk of death during the acute phase of acute ischemic stroke in particular. Our study was designed to investigate the relationship between GI hemorrhage and the mortality of acute ischemic stroke, assessing the influence of cerebrovascular risk factors, brain herniation and oral anticoagulation on the onset of GI hemorrhage. The identified risk factors for the occurrence of GI hemorrhage help to elucidate their respective roles in the mortality of acute ischemic stroke. METHODS: A total of 15993 consecutive patients with acute ischemic stroke, including 216 cases and 15777 controls, were enrolled in the study from October 2010 to December 2018. Basic clinical and examination data were collected at the time of study enrollment. GI hemorrhage was diagnosed according to the presence of clinical features and endoscopy. Chi-square test and multiple logistic regressions were conducted to explore the associations between the GI hemorrhage occurrence and known risk factors. Kaplan-Meier was used to assess the influence of GI hemorrhage on the age of mortality of acute ischemic stroke. RESULTS: GI hemorrhage cases among patients with acute ischemic stroke accounted for 1.35%. Male patients with ischemic stroke were more likely to have GI hemorrhage than their female counterparts (odds ratio (OR): 1.79; P = 0.000). Patients with atrial fibrillation (AF) had a higher incidence of GI hemorrhage than their counterparts without AF (3.03% vs. 1.20%; P < 0.05). Use of oral anticoagulants was related to increased risk for GI hemorrhage (OR: 1.96; P = 0.00). After adjusting for age and sex, both AF and oral anticoagulant use maintained associations with increased risk for GI hemorrhage (2.59-times and 2.02-times risk respectively; P = 0.00). Patients with hyperlipidemia had a lower incidence of GI hemorrhage than their counterparts without hyperlipidemia (0.62% vs. 1.60%; P < 0.05). Hyperlipidemia was associated with a reduced risk of GI hemorrhage (OR: 0.38, 95% confidence interval (CI): 0.25-0.58; P = 0.00), even after adjusting for age and sex (OR: 0.41; P = 0.00). Patients with brain herniation had a 6.54-times increased risk for GI hemorrhage (P = 0.00). GI hemorrhage was associated with 10.98-fold risk for mortality of acute ischemic stroke (P = 0.00). There was an interaction between GI hemorrhage and brain herniation and increased 26.91-fold risk for the mortality after acute ischemic stroke (P = 0.00). CONCLUSION: AF, oral anticoagulant use, brain herniation and male sex increase GI hemorrhage risk, while hyperlipidemia reduces risk. GI hemorrhage itself increases the risk for mortality of acute ischemic stroke. The interaction between GI hemorrhage and brain herniation increased the risk for the mortality after acute ischemic stroke.

20.
Elife ; 82019 03 12.
Artigo em Inglês | MEDLINE | ID: mdl-30860027

RESUMO

As part of the Reproducibility Project: Cancer Biology, we published a Registered Report (Li et al., 2015), that described how we intended to replicate selected experiments from the paper 'The microRNA miR-34a inhibits prostate cancer stem cells and metastasis by directly repressing CD44' (Liu et al., 2011). Here we report the results. We found the microRNA, miR-34a, was expressed at twice the level in CD44+ prostate cancer cells purified from xenograft tumors (LAPC4 cells) compared to CD44- LAPC4 cells, whereas the original study reported miR-34a was underexpressed in CD44+ LAPC4 cells (Figure 1B; Liu et al., 2011). When LAPC4 cells engineered to express miR-34a were injected into mice, we did not observe changes in tumor growth or CD44 expression; however, unexpectedly miR-34a expression was lost in vivo. In the original study, LAPC4 cells expressing miR-34a had a statistically significant reduction in tumor regeneration and reduced CD44 expression compared to control (Figure 4A and Supplemental Figures 4A,B and 5C; Liu et al., 2011). Furthermore, when we tested if miR-34a regulated CD44 through binding sites in the 3'UTR we did not find a statistically significant difference, whereas the original study reported miR-34a decreased CD44 expression that was partially abrogated by mutation of the binding sites in the CD44 3'UTR (Figure 4D; Liu et al., 2011). Finally, where possible, we report meta-analyses for each result.

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