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1.
Cell Biochem Funct ; 42(4): e4031, 2024 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-38760985

RESUMEN

Super-enhancers play prominent roles in driving robust pathological gene expression, but they are hidden in human genome at noncoding regions, making them difficult to explore. Leukemia inhibitory factor (LIF) is a multifunctional cytokine crucially involved in acute respiratory distress syndrome (ARDS) and lung cancer progression. However, the mechanisms governing LIF regulation in disease contexts remain largely unexplored. In this study, we observed elevated levels of LIF in the bronchoalveolar lavage fluid (BALF) of patients with sepsis-related ARDS compared to those with nonsepsis-related ARDS. Furthermore, both basal and LPS-induced LIF expression were under the control of super-enhancers. Through analysis of H3K27Ac ChIP-seq data, we pinpointed three potential super-enhancers (LIF-SE1, LIF-SE2, and LIF-SE3) located proximal to the LIF gene in cells. Notably, genetic deletion of any of these three super-enhancers using CRISPR-Cas9 technology led to a significant reduction in LIF expression. Moreover, in cells lacking these super-enhancers, both cell growth and invasion capabilities were substantially impaired. Our findings highlight the critical role of three specific super-enhancers in regulating LIF expression and offer new insights into the transcriptional regulation of LIF in ARDS and lung cancer.


Asunto(s)
Factor Inhibidor de Leucemia , Neoplasias Pulmonares , Síndrome de Dificultad Respiratoria , Humanos , Síndrome de Dificultad Respiratoria/metabolismo , Síndrome de Dificultad Respiratoria/genética , Síndrome de Dificultad Respiratoria/patología , Factor Inhibidor de Leucemia/metabolismo , Factor Inhibidor de Leucemia/genética , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patología , Líquido del Lavado Bronquioalveolar/química , Elementos de Facilitación Genéticos , Proliferación Celular , Masculino
2.
BMC Gastroenterol ; 23(1): 105, 2023 Apr 04.
Artículo en Inglés | MEDLINE | ID: mdl-37016327

RESUMEN

AIM: The aim of this study was to explore the experience and perceptions of patients with Crohn's disease in China. METHODS: Data mining was used to investigate posts in Crohn's disease online medical communities. The data were collected through the crawler code, and latent Dirichlet allocation (LDA) and grounded theory were used to mine the theme features after data cleaning. RESULTS: In analyzing the topic characteristics of online posts, LDA divided 6757 posts into 15 topics on four aspects: seeking disease information, making decisions on medication use, psychological burden, and communicating about diet and nutrition. CONCLUSION: Overall, social media is patient-centric and helps us better understand the experiences and perceptions of patients. This study can help medical staff predict the thoughts and concerns of Crohn's disease patients during the treatment process, facilitate doctor-patient communication, and assist in the formulation of medical policies.


Asunto(s)
Enfermedad de Crohn , Medios de Comunicación Sociales , Humanos , China , Relaciones Médico-Paciente , Pueblos del Este de Asia
3.
Biotechnol Lett ; 43(4): 899-907, 2021 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-33389273

RESUMEN

OBJECTIVE: To develop a new DNA assembly method based on FnCas12a and T5 exonuclease. RESULTS: We developed a method named as FnCas12a and T5 exonuclease (CT5) cloning system. FnCas12a performs site-directed cleavage to the target DNA fragments, and T5 exonuclease generates 20-30 nt single-stranded region at each end of the DNA fragments for homologous recombination-mediated DNA assembly. CT5 was applied to multi-fragment assembly and DNA cloning of large vectors (> 10 kb). The efficiencies were approximately 91.4% and 97%, respectively. In addition, CT5 cloning is also utilized for the "walking" of DNA elements, which enables subtle modification of the relative distances of DNA elements in plasmids. CONCLUSIONS: The CT5 method was a precise and exquisite DNA operating system and provided an ideal platform for the study of gene functions, genetic engineering and synthetic biology.


Asunto(s)
Proteínas Bacterianas/genética , Proteínas Asociadas a CRISPR/genética , Clonación Molecular/métodos , Endodesoxirribonucleasas/genética , Exodesoxirribonucleasas/genética , Proteínas Bacterianas/metabolismo , Proteínas Asociadas a CRISPR/metabolismo , Endodesoxirribonucleasas/metabolismo , Escherichia coli/genética , Escherichia coli/crecimiento & desarrollo , Exodesoxirribonucleasas/metabolismo , Ingeniería Genética , Plásmidos/genética , Recombinación Genética , Biología Sintética
4.
Pharmacol Res ; 161: 105290, 2020 11.
Artículo en Inglés | MEDLINE | ID: mdl-33181320

RESUMEN

The coronavirus disease 2019 (COVID-19) epidemic has been almost controlled in China under a series of policies, including "early diagnosis and early treatment". This study aimed to explore the association between early treatment with Qingfei Paidu decoction (QFPDD) and favorable clinical outcomes. In this retrospective multicenter study, we included 782 patients (males, 56 %; median age 46) with confirmed COVID-19 from 54 hospitals in nine provinces of China, who were divided into four groups according to the treatment initiation time from the first date of onset of symptoms to the date of starting treatment with QFPDD. The primary outcome was time to recovery; days of viral shedding, duration of hospital stay, and course of the disease were also analyzed. Compared with treatment initiated after 3 weeks, early treatment with QFPDD after less than 1 week, 1-2 weeks, or 2-3 weeks had a higher likelihood of recovery, with adjusted hazard ratio (HR) (95 % confidence interval [CI]) of 3.81 (2.65-5.48), 2.63 (1.86-3.73), and 1.92 (1.34-2.75), respectively. The median course of the disease decreased from 34 days to 24 days, 21 days, and 18 days when treatment was administered early by a week (P < 0.0001). Treatment within a week was related to a decrease by 1-4 days in the median duration of hospital stay compared with late treatment (P<0.0001). In conclusion, early treatment with QFPDD may serve as an effective strategy in controlling the epidemic, as early treatment with QFPDD was associated with favorable outcomes, including faster recovery, shorter time to viral shedding, and a shorter duration of hospital stay. However, further multicenter, prospective studies with a larger sample size should be conducted to confirm the benefits of early treatment with QFPDD.


Asunto(s)
Tratamiento Farmacológico de COVID-19 , Medicamentos Herbarios Chinos/uso terapéutico , Adulto , Anciano , Anciano de 80 o más Años , China , Estudios de Cohortes , Femenino , Estudios de Seguimiento , Humanos , Tiempo de Internación , Masculino , Persona de Mediana Edad , Tiempo de Tratamiento , Resultado del Tratamiento , Adulto Joven
5.
PLoS Pathog ; 13(9): e1006600, 2017 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-28898289

RESUMEN

Toll-like receptor (TLR)-mediated signaling are critical for host defense against pathogen invasion. However, excessive responses would cause harmful damages to the host. Here we show that deficiency of the E3 ubiquitin ligase TRIM32 increases poly(I:C)- and LPS-induced transcription of downstream genes such as type I interferons (IFNs) and proinflammatory cytokines in both primary mouse immune cells and in mice. Trim32-/- mice produced higher levels of serum inflammatory cytokines and were more sensitive to loss of body weight and inflammatory death upon Salmonella typhimurium infection. TRIM32 interacts with and mediates the degradation of TRIF, a critical adaptor protein for TLR3/4, in an E3 activity-independent manner. TRIM32-mediated as well as poly(I:C)- and LPS-induced degradation of TRIF is inhibited by deficiency of TAX1BP1, a receptor for selective autophagy. Furthermore, TRIM32 links TRIF and TAX1BP1 through distinct domains. These findings suggest that TRIM32 negatively regulates TLR3/4-mediated immune responses by targeting TRIF to TAX1BP1-mediated selective autophagic degradation.


Asunto(s)
Proteínas Adaptadoras del Transporte Vesicular/metabolismo , Autofagia , Inmunidad Innata , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Proteínas de Neoplasias/metabolismo , Receptor Toll-Like 3/metabolismo , Receptor Toll-Like 4/metabolismo , Factores de Transcripción/metabolismo , Proteínas de Motivos Tripartitos/metabolismo , Ubiquitina-Proteína Ligasas/metabolismo , Proteínas Adaptadoras Transductoras de Señales/metabolismo , Citocinas/metabolismo , Humanos , Inmunidad Innata/efectos de los fármacos , Inmunidad Innata/inmunología , Péptidos y Proteínas de Señalización Intracelular/genética , Lipopolisacáridos/farmacología , Macrófagos/inmunología , Proteínas de Neoplasias/genética , Receptor Toll-Like 3/genética
6.
EMBO Rep ; 16(4): 447-55, 2015 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-25736436

RESUMEN

Toll-like receptors (TLRs) are pattern recognition receptors that sense a variety of pathogens, initiate innate immune responses, and direct adaptive immunity. All TLRs except TLR3 recruit the adaptor MyD88 to ultimately elicit inflammatory gene expression, whereas TLR3 and internalized TLR4 use TIR-domain-containing adaptor TRIF for the induction of type I interferon and inflammatory cytokines. Here, we identify the WD repeat and FYVE-domain-containing protein WDFY1 as a crucial adaptor protein in the TLR3/4 signaling pathway. Overexpression of WDFY1 potentiates TLR3- and TLR4-mediated activation of NF-κB, interferon regulatory factor 3 (IRF3), and production of type I interferons and inflammatory cytokines. WDFY1 depletion has the opposite effect. WDFY1 interacts with TLR3 and TLR4 and mediates the recruitment of TRIF to these receptors. Our findings suggest a crucial role for WDFY1 in bridging the TLR-TRIF interaction, which is necessary for TLR signaling.


Asunto(s)
Proteínas Adaptadoras del Transporte Vesicular/genética , Proteínas Nucleares/genética , Receptor Toll-Like 3/genética , Receptor Toll-Like 4/genética , Factores de Transcripción/genética , Proteínas Adaptadoras Transductoras de Señales , Proteínas Adaptadoras del Transporte Vesicular/inmunología , Secuencias de Aminoácidos , Citocinas/genética , Citocinas/inmunología , Regulación de la Expresión Génica , Células HEK293 , Humanos , Inductores de Interferón/farmacología , Factor 3 Regulador del Interferón/genética , Factor 3 Regulador del Interferón/inmunología , Interferón Tipo I/genética , Interferón Tipo I/inmunología , Datos de Secuencia Molecular , Factor 88 de Diferenciación Mieloide/genética , Factor 88 de Diferenciación Mieloide/inmunología , FN-kappa B/genética , FN-kappa B/inmunología , Proteínas Nucleares/antagonistas & inhibidores , Proteínas Nucleares/inmunología , Plásmidos/química , Plásmidos/inmunología , Poli I-C/farmacología , ARN Interferente Pequeño/genética , ARN Interferente Pequeño/metabolismo , Transducción de Señal , Receptor Toll-Like 3/inmunología , Receptor Toll-Like 4/inmunología , Factores de Transcripción/antagonistas & inhibidores , Factores de Transcripción/inmunología , Transfección
7.
PLoS Pathog ; 10(9): e1004358, 2014 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-25254379

RESUMEN

Viral infection triggers induction of type I interferons (IFNs), which are critical mediators of innate antiviral immune response. Mediator of IRF3 activation (MITA, also called STING) is an adapter essential for virus-triggered IFN induction pathways. How post-translational modifications regulate the activity of MITA is not fully elucidated. In expression screens, we identified RING finger protein 26 (RNF26), an E3 ubiquitin ligase, could mediate polyubiquitination of MITA. Interestingly, RNF26 promoted K11-linked polyubiquitination of MITA at lysine 150, a residue also targeted by RNF5 for K48-linked polyubiquitination. Further experiments indicated that RNF26 protected MITA from RNF5-mediated K48-linked polyubiquitination and degradation that was required for quick and efficient type I IFN and proinflammatory cytokine induction after viral infection. On the other hand, RNF26 was required to limit excessive type I IFN response but not proinflammatory cytokine induction by promoting autophagic degradation of IRF3. Consistently, knockdown of RNF26 inhibited the expression of IFNB1 gene in various cells at the early phase and promoted it at the late phase of viral infection, respectively. Furthermore, knockdown of RNF26 inhibited viral replication, indicating that RNF26 antagonizes cellular antiviral response. Our findings thus suggest that RNF26 temporally regulates innate antiviral response by two distinct mechanisms.


Asunto(s)
Antivirales/metabolismo , Inmunidad Innata/inmunología , Factor 3 Regulador del Interferón/metabolismo , Interferón Tipo I/metabolismo , Proteínas de la Membrana/metabolismo , Proteínas de Neoplasias/metabolismo , Ubiquitina-Proteína Ligasas/metabolismo , Virus/inmunología , Western Blotting , Células Cultivadas , Humanos , Técnicas para Inmunoenzimas , Inmunoprecipitación , Factor 3 Regulador del Interferón/genética , Interferón Tipo I/genética , Proteínas de la Membrana/genética , Proteínas de Neoplasias/antagonistas & inhibidores , Proteínas de Neoplasias/genética , Procesamiento Proteico-Postraduccional , ARN Mensajero/genética , ARN Interferente Pequeño/genética , Reacción en Cadena en Tiempo Real de la Polimerasa , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Transducción de Señal , Ubiquitina-Proteína Ligasas/antagonistas & inhibidores , Ubiquitina-Proteína Ligasas/genética , Ubiquitinación , Activación Viral , Virosis/inmunología , Virosis/virología , Replicación Viral
8.
J Biol Chem ; 289(18): 12876-85, 2014 May 02.
Artículo en Inglés | MEDLINE | ID: mdl-24634218

RESUMEN

The transcription factor NF-κB plays a pivotal role in a broad range of physiological and pathological processes, including development, inflammation, and immunity. How NF-κB integrates activating signals to expression of specific sets of target genes is of great interest. Here, we identified Krüppel-like factor 6 (KLF6) as a co-activator of NF-κB after TNFα and IL-1ß stimulation. Overexpression of KLF6 enhanced TNFα- and IL-1ß-induced activation of NF-κB and transcription of a subset of downstream genes, whereas knockdown of KLF6 had opposite effects. KLF6 interacted with p65 in the nucleus and bound to the promoters of target genes. Upon IL-1ß stimulation, KLF6 was recruited to promoters of a subset of NF-κB target genes in a p65-dependent manner, which was in turn required for the optimal binding of p65 to the target gene promoters. Our findings thus identified KLF6 as a previously unknown but essential co-activator of NF-κB and provided new insight into the molecular regulation of p65-dependent gene expression.


Asunto(s)
Factores de Transcripción de Tipo Kruppel/metabolismo , FN-kappa B/metabolismo , Proteínas Proto-Oncogénicas/metabolismo , Factor de Transcripción ReIA/metabolismo , Transcripción Genética , Transporte Activo de Núcleo Celular/efectos de los fármacos , Transporte Activo de Núcleo Celular/genética , Apoptosis/efectos de los fármacos , Apoptosis/genética , Western Blotting , Núcleo Celular/metabolismo , Regulación de la Expresión Génica/efectos de los fármacos , Células HCT116 , Células HEK293 , Humanos , Interleucina-1beta/farmacología , Factor 6 Similar a Kruppel , Factores de Transcripción de Tipo Kruppel/genética , FN-kappa B/genética , Regiones Promotoras Genéticas/genética , Unión Proteica/efectos de los fármacos , Unión Proteica/genética , Proteínas Proto-Oncogénicas/genética , Interferencia de ARN , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factor de Transcripción ReIA/genética , Factor de Necrosis Tumoral alfa/farmacología
9.
Eur J Immunol ; 43(4): 1034-41, 2013 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-23322406

RESUMEN

Ag receptor engagement triggers lymphocyte activation and proliferation by activating several transcription factors including NF-κB. Caspase recruitment domain (CARD) containing membrane-associated guanylate kinase (MAGUK) protein 1 (CARMA1) is an essential adaptor protein that links Ag receptors to NF-κB activation. Here, we identify stress-induced-phosphoprotein 1 homology and U-box containing protein 1 (STUB1) as a CARMA1-associated protein. STUB1 constitutively interacted with CARMA1, and the interaction was intensified by TCR stimulation. Downregulation of STUB1 expression by RNAi markedly diminished TCR-induced canonical NF-κB activation and IL-2 production. Furthermore, overexpression of STUB1 enhanced the ubiquitination of CARMA1, whereas knockdown of STUB1 abolished the endogenous ubiquitination of CARMA1 induced by TCR stimulation. Subsequently, the ubiquitination of CARMA1 catalyzed by STUB1 was identified as Lys-27 linked, which is important for CARMA1-mediated NF-κB activation. These data provide the first evidence that ubiquitination of CARMA1 by STUB1 promotes TCR-induced NF-κB signaling.


Asunto(s)
Proteínas Adaptadoras de Señalización CARD/metabolismo , Guanilato Ciclasa/metabolismo , Activación de Linfocitos/inmunología , Linfocitos T/inmunología , Linfocitos T/metabolismo , Ubiquitina-Proteína Ligasas/metabolismo , Catálisis , Línea Celular , Activación Enzimática , Humanos , Interleucina-2/biosíntesis , FN-kappa B/metabolismo , Unión Proteica , Receptores de Antígenos de Linfocitos T/metabolismo , Ubiquitina-Proteína Ligasas/genética , Ubiquitinación
10.
Viruses ; 16(4)2024 03 30.
Artículo en Inglés | MEDLINE | ID: mdl-38675882

RESUMEN

As a mosquito-borne flavivirus, Zika virus (ZIKV) has been identified as a global health threat. The virus has been linked to severe congenital disabilities, including microcephaly and other congenital malformations, resulting in fatal intrauterine death. Therefore, developing sensitive and specific methods for the early detection and accurate diagnosis of the ZIKV is essential for controlling its spread and mitigating its impact on public health. Herein, we set up a novel nucleic acid detection system based on Pyrococcus furiosus Argonaute (PfAgo)-mediated nucleic acid detection, targeting the non-structural protein 5 (NS5) region of the ZIKV genome (abbreviated ZIKV-PAND). Without preamplification with the polymerase chain reaction (PCR), the minimum detection concentration (MDC) of ZIKV-PAND was about 10 nM. When introducing an amplification step, the MDC can be dramatically decreased to the aM level (8.3 aM), which is comparable to qRT-PCR assay (1.6 aM). In addition, the diagnostic findings from the analysis of simulated clinical samples or Zika virus samples using ZIKV-PAND show a complete agreement of 100% with qRT-PCR assays. This correlation can aid in the implementation of molecular testing for clinical diagnoses and the investigation of ZIKV infection on an epidemiological scale.


Asunto(s)
Pyrococcus furiosus , Proteínas no Estructurales Virales , Infección por el Virus Zika , Virus Zika , Virus Zika/genética , Virus Zika/aislamiento & purificación , Infección por el Virus Zika/diagnóstico , Infección por el Virus Zika/virología , Humanos , Proteínas no Estructurales Virales/genética , Pyrococcus furiosus/genética , Proteínas Argonautas/genética , Sensibilidad y Especificidad , ARN Viral/genética , Técnicas de Diagnóstico Molecular/métodos , Técnicas de Amplificación de Ácido Nucleico/métodos , Genoma Viral
11.
J Biol Chem ; 287(24): 20081-7, 2012 Jun 08.
Artículo en Inglés | MEDLINE | ID: mdl-22528498

RESUMEN

T-cell receptor (TCR)-induced T-cell activation is a critical event in adaptive immune responses. The engagement of TCR complex by antigen along with the activation of the costimulatory receptors trigger a cascade of intracellular signaling, in which caspase recruitment domain-containing membrane-associated guanylate kinase 1 (CARMA1) is a crucial scaffold protein. Upon stimulation, CARMA1 recruits downstream molecules including B-cell CLL/lymphoma 10 (Bcl10), mucosa-associated lymphoid tissue lymphoma translocation gene 1 (MALT1), and TRAF6 to assemble a specific TCR-induced signalosome that triggers NF-κB and JNK activation. In this report, we identified protein kinase Cδ (PKCδ) as a CARMA1-associated protein by a biochemical affinity purification approach. PKCδ interacted with CARMA1 in TCR stimulation-dependent manner in Jurkat T cells. Overexpression of PKCδ inhibited CARMA1-mediated NF-κB activation, whereas knockdown of PKCδ potentiated TCR-triggered NF-κB activation and IL-2 secretion in Jurkat T cells. Reconstitution experiments with PKCδ kinase-dead mutant indicated that the kinase activity of PKCδ was dispensable for its ability to inhibit TCR-triggered NF-κB activation. Furthermore, we found that PKCδ inhibited the interaction between MALT1 and TRAF6, but not the association of CARMA1 with PKCθ, Bcl10, or MALT1. These observations suggest that PKCδ is a negative regulator in T cell activation through inhibiting the assembly of CARMA1 signalosome.


Asunto(s)
Proteínas Adaptadoras de Señalización CARD/metabolismo , Guanilato Ciclasa/metabolismo , Activación de Linfocitos/fisiología , FN-kappa B/metabolismo , Proteína Quinasa C-delta/metabolismo , Receptores de Antígenos de Linfocitos T/metabolismo , Transducción de Señal/fisiología , Linfocitos T/enzimología , Proteínas Adaptadoras Transductoras de Señales/genética , Proteínas Adaptadoras Transductoras de Señales/metabolismo , Proteína 10 de la LLC-Linfoma de Células B , Proteínas Adaptadoras de Señalización CARD/genética , Caspasas/genética , Caspasas/metabolismo , Guanilato Ciclasa/genética , Células HEK293 , Humanos , Interleucina-2/genética , Interleucina-2/metabolismo , Células Jurkat , Proteína 1 de la Translocación del Linfoma del Tejido Linfático Asociado a Mucosas , FN-kappa B/genética , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/metabolismo , Proteína Quinasa C-delta/genética , Receptores de Antígenos de Linfocitos T/genética , Factor 6 Asociado a Receptor de TNF/genética , Factor 6 Asociado a Receptor de TNF/metabolismo
12.
Life Sci ; 326: 121792, 2023 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-37211344

RESUMEN

AIMS: We aim to explore the possibility and mechanism of SH3PXD2B as a reliable biomarker for gastric cancer (GC). MAIN METHODS: We used public databases to analyze the molecular characteristics and disease associations of SH3PXD2B, and KM database for prognostic analysis. The TCGA gastric cancer dataset was used for single gene correlation, differential expression, functional enrichment and immunoinfiltration analysis. SH3PXD2B protein interaction network was constructed by the STRING database. And the GSCALite database was used to explore sensitive drugs and perform SH3PXD2B molecular docking. The impact of SH3PXD2B silencing and over-expression by lentivirus transduction on the proliferation and invasion of human GC HGC-27 and NUGC-3 cells was determined. KEY FINDINGS: The high expression of SH3PXD2B in gastric cancer was related to the poor prognosis of patients. It may affect the progression of gastric cancer by forming a regulatory network with FBN1, ADAM15 and other molecules, and the mechanism may involve regulating the infiltration of Treg, TAM and other immunosuppressive cells. The cytofunctional experiments verified that it significantly promoted the proliferation and migration of gastric cancer cells. In addition, we found that some drugs were sensitive to the expression of SH3PXD2B such as sotrastaurin, BHG712 and sirolimus, and they had strong molecular combination of SH3PXD2B, which may provide guidance for the treatment of gastric cancer. SIGNIFICANCE: Our study strongly suggests that SH3PXD2B is a carcinogenic molecule that can be used as a biomarker for GC detection, prognosis, treatment design, and follow-up.


Asunto(s)
Carcinoma , Neoplasias Gástricas , Humanos , Proteínas ADAM , Biomarcadores , Biología Computacional , Proteínas de la Membrana , Simulación del Acoplamiento Molecular , Neoplasias Gástricas/patología
13.
Front Psychol ; 13: 1093723, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36726510

RESUMEN

Emotional labor claims its significance as the key indicator both of the psychological health of contemporary employees, and the productivity of service-based businesses depending upon genuine emotional input of employees. By far, research on emotional labor of employees in an organizational context is still lacking. This study aims to explore the relationships among emotional labor, organizational support, career competences and career commitment to investigate how emotional labor interacts with the organizational context and affects the career management of the employee. Data were collected from a sample of 387 frontline employees working at two luxury hotel brands in China. Structural equation modeling (SEM) was utilized to estimate the relationships among the constructs. It is demonstrated by the findings that organizational support mediates positively on emotional labor, which exerts positive influences on career competences and career commitment. Sound handling of emotional labor, boosted by a supportive organizational environment, has been ascertained to positively predict long-term career paths of the employees at the company. This study provides insights into how the tourism and hospitality industry can optimize the functions of emotional labor for in enhancing service quality and customer satisfaction, as well as promoting the psychological well-being of the employees.

14.
Nanoscale Adv ; 4(6): 1577-1586, 2022 Mar 15.
Artículo en Inglés | MEDLINE | ID: mdl-36134371

RESUMEN

The special microenvironment of a solid tumor promotes the orientation and colonization of facultative anaerobes. Intratumoral bacterial infection disrupts the local vascular system to form a thrombus, resulting in darkened tumor sites and enhanced near-infrared absorption. Based on this, we constructed thermally-induced bacteria (TIB) to express programmed cell death protein 1 (PD1) at tumor tissue sites. Under laser irradiation, the elevated temperature at the tumor site not only caused damage to tumor cells but also induced the expression of PD1. Expressed PD1 bound to the ligand of PD1 (PD-L1) on the tumor cell surface and facilitated its internalization and reduction, thereby relieving immune suppression in the tumor microenvironment. Through the combined effects of photothermal therapy and immune activation, the ingenious TIB@PD1 approach greatly inhibited the proliferation and metastasis of tumor cells. Therefore, bacteria-based photothermal immunotherapy represents an appealing method for tumor therapy with good specificity and selectivity.

15.
Cell Mol Immunol ; 18(7): 1708-1717, 2021 07.
Artículo en Inglés | MEDLINE | ID: mdl-32235916

RESUMEN

Toll-like receptor (TLR) signaling pathways need to be tightly controlled to avoid excessive inflammation and unwanted damage to the host. Myeloid differentiation primary response gene 88 (MyD88) is a critical adaptor of TLR signaling. Here, we identified the speckle-type POZ protein (SPOP) as a MyD88-associated protein. SPOP was recruited to MyD88 following TLR4 activation. TLR4 activation also caused the translocation of SPOP from the nucleus to the cytoplasm. SPOP depletion promoted the aggregation of MyD88 and recruitment of the downstream signaling kinases IRAK4, IRAK1 and IRAK2. Consistently, overexpression of SPOP inhibited the TLR4-mediated activation of NF-κB and production of inflammatory cytokines, whereas SPOP depletion had the opposite effects. Furthermore, knockdown of SPOP increased MyD88 aggregation and inflammatory cytokine production upon TLR2, TLR7 and TLR9 activation. Our findings reveal a mechanism by which MyD88 is regulated and highlight a role for SPOP in limiting inflammatory responses.


Asunto(s)
Factor 88 de Diferenciación Mieloide , Receptores Toll-Like , Humanos , Inflamación/metabolismo , Factor 88 de Diferenciación Mieloide/metabolismo , FN-kappa B/metabolismo , Proteínas Nucleares/metabolismo , Proteínas Represoras , Receptores Toll-Like/metabolismo
16.
Phytomedicine ; 81: 153433, 2021 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-33373925

RESUMEN

OBJECTIVE: Previous studies mainly reported the clinical characteristics of novel coronavirus 2019 (COVID-19) infections, but the research on clinical characteristics and treatment outcomes of COVID-19 patients with stroke is still rare. METHODS: A multi-center retrospective study was conducted at 11 hospitals in 4 provinces of China, and COVID-19 patients with stroke were enrolled from February 24 to May 4, 2020. We analyzed epidemiological, demographic, and clinical characteristics of cases as well as the laboratory test results, treatment regimens and outcomes, and the clinical characteristics and therapeutic outcomes were compared between severe and nonsevere patients, and by age group, respectively. RESULTS: A total of 27 patients [mean age: 66.41 (SD 12.1) years] were enrolled. Among them, 9 (33.3%) were severe patients and 18 (66.7%) were nonsevere patients; 17 (63.0%) were female; 19 (70.4%) were aged 60 years and above. The most common symptoms were fever [19 (70.4%)], fatigue [12 (44.4%)] and cough [11 (40.7%)], respectively. Abnormal laboratory findings of COVID-19 patients with stroke included high levels of C-reactive protein [19 (73.1%)], D-dimer [14 (58.3%)], blood glucose [14 (53.8%)], fibrinogen [13 (50.0%)], and decreased lymphocytes [12 (44.4%)]. Comparing to nonsevere cases with stroke, severe patients with stroke were likely to be older, susceptible to receiving oxygen inhalation, and had more complications (p < 0.05). In addition, there were significant differences in lymphocytes, neutrophils, lactate dehydrogenase, C-reactive protein, creatine kinase between the severe cases and nonsevere cases (p < 0.05). The older patients had a decreased platelet count and elevated fibrinogen, compared with the younger (p < 0.05). All patients (100%) received antiviral treatment, 12 (44.4%) received antibiotics treatment, 26 (96.3%) received Traditional Chinese Medicine (Lung cleansing & detoxifying decoction), and oxygen inhalation was in 18 (66.7%). The median duration of hospitalization was 16 days. By May 4, 2020, a total of 26 (96.3%) patients were cured and discharged, and 1 (3.7%) patients died. CONCLUSION: COVID-19 patients with stroke had poor indicators of coagulation system, and severe and older patients might have a higher risk of complications and unfavorable coagulation system. However, the overall treatment outcome is favorable.


Asunto(s)
COVID-19/complicaciones , COVID-19/terapia , Accidente Cerebrovascular/complicaciones , Accidente Cerebrovascular/terapia , Adulto , Factores de Edad , Anciano , Anciano de 80 o más Años , Antivirales/uso terapéutico , Trastornos de la Coagulación Sanguínea/complicaciones , Trastornos de la Coagulación Sanguínea/terapia , COVID-19/epidemiología , China/epidemiología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Terapia por Inhalación de Oxígeno , Estudios Retrospectivos , Accidente Cerebrovascular/epidemiología , Resultado del Tratamiento
17.
Cell Mol Immunol ; 15(9): 858-867, 2018 09.
Artículo en Inglés | MEDLINE | ID: mdl-28435159

RESUMEN

Interferon-induced transmembrane protein 3 (IFITM3) is a restriction factor that can be induced by viral infection and interferons (IFNs). It inhibits the entry and replication of many viruses, which are independent of receptor usage but dependent on processes that occur in endosomes. In this study, we demonstrate that IFITM3 plays important roles in regulating the RNA-virus-triggered production of IFN-ß in a negative-feedback manner. Overexpression of IFITM3 inhibited Sendai virus-triggered induction of IFN-ß, whereas knockdown of IFITM3 had the opposite effect. We also showed that IFITM3 was constitutively associated with IRF3 and regulated the homeostasis of IRF3 by mediating the autophagic degradation of IRF3. These findings suggest a novel inhibitory function of IFITM3 on the RNA-virus-triggered production of type I IFNs and cellular antiviral responses.


Asunto(s)
Autofagosomas/metabolismo , Factor 3 Regulador del Interferón/inmunología , Interferón Tipo I/inmunología , Proteínas de la Membrana/inmunología , Proteolisis , Infecciones por Virus ARN/inmunología , Virus ARN/inmunología , Proteínas de Unión al ARN/inmunología , Células HEK293 , Células HeLa , Humanos , Factor 3 Regulador del Interferón/genética , Interferón Tipo I/genética , Proteínas de la Membrana/genética , Infecciones por Virus ARN/genética , Infecciones por Virus ARN/patología , Virus ARN/genética , Proteínas de Unión al ARN/genética
18.
Science ; 371(6533): 1003, 2021 Mar 05.
Artículo en Inglés | MEDLINE | ID: mdl-33674486
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