RESUMEN
Piglet diarrhea is one of the primary factors that affects the benefits of the swine industry. Recent studies have shown that exon 2 of the swine leukocyte antigen-DQA gene is associated with piglet resistance to diarrhea; however, the contributions of additional exon coding regions of this gene remain unclear. Here, we detected and sequenced variants in the exon 3 region and examined their associations with diarrhea infection in 425 suckling piglets using the polymerase chain reaction-single-strand conformational polymorphism and sequencing analysis. The results revealed that exon 3 of the swine leukocyte antigen-DQA gene is highly polymorphic and pivotal to both diarrhea susceptibility and resistance in piglets. We identified 14 genotypes (AA, AB, BB, BC, CC, EE, EF, BE, BF, CF, DD, DH, GG, and GF) and eight alleles (A-H) that were generated by 14 nucleotide variants, eight of which were novel, and three nucleotide deletions. Statistical analyses revealed that the genotypes AB and EF were associated with resistance to diarrheal disease (P < 0.05), and the genotype DD may contribute to diarrhea susceptibility but was unique to Large White pigs (P > 0.05). These results elucidate the genetic and immunological background to piglet diarrhea, and provide useful information for resistance breeding programs.
Asunto(s)
Diarrea/veterinaria , Antígenos de Histocompatibilidad Clase II/genética , Sus scrofa/genética , Enfermedades de los Porcinos/genética , Secuencia de Aminoácidos , Animales , Secuencia de Bases , Cruzamiento , Diarrea/genética , Resistencia a la Enfermedad , Exones , Femenino , Estudios de Asociación Genética , Predisposición Genética a la Enfermedad , Antígenos de Histocompatibilidad Clase I , Masculino , Polimorfismo Conformacional Retorcido-Simple , PorcinosRESUMEN
Recent data have indicated that inflammation may have an important correlation with obstructive sleep apnea (OSA). Studies have indicated a relationship between OSA and TNF-α gene polymorphisms. Zinc finger protein 36 (ZFP36) regulates TNF-α mRNAs. However, ZFP36 gene polymorphisms have not been investigated in OSA. Therefore, we conducted the present case-control study to assess whether variances in ZFP36 gene polymorphisms account for differences in TNF-α levels in patients with moderate-to-severe OSA. This case-control study aims to investigate the relationship between genetic variations in the ZFP36 gene and moderate-to-severe OSA. Three common single nucleotide polymorphisms of the ZFP36 gene (rs251864, rs3746083, and rs17879933) were evaluated in a group of patients with moderate-to-severe OSA (N = 408) and in a control group (N = 394) by using TaqMan polymerase chain reaction analysis. The moderate-to-severe OSA group and the control group exhibited significant differences in the distributions of rs251864 and rs17879933 genotypes and alleles (P < 0.05). TNF-α levels were significantly different not only among the three rs251864 genotypes but also between the II genotype and the DD + ID genotypes of rs17879933. However, no significant differences in sleep apnea parameters in the three ZFP36 gene polymorphisms were observed. Logistic regression analyses demonstrated that TNF-α and the three ZFP36 gene polymorphisms were not independently associated with OSA. ZFP36 might be involved in TNF-α regulation. However, ZFP36 gene variants were not independent risk factors for moderate-to-severe OSA.
Asunto(s)
Polimorfismo de Nucleótido Simple , ARN Mensajero/genética , Apnea Obstructiva del Sueño/genética , Tristetraprolina/genética , Factor de Necrosis Tumoral alfa/genética , Adulto , Alelos , Estudios de Casos y Controles , Femenino , Regulación de la Expresión Génica , Frecuencia de los Genes , Genotipo , Humanos , Inflamación , Modelos Logísticos , Masculino , Persona de Mediana Edad , Polisomnografía , ARN Mensajero/metabolismo , Factores de Riesgo , Índice de Severidad de la Enfermedad , Transducción de Señal , Apnea Obstructiva del Sueño/metabolismo , Apnea Obstructiva del Sueño/patología , Tristetraprolina/metabolismo , Factor de Necrosis Tumoral alfa/metabolismoRESUMEN
Accumulating evidence has indicated the importance of cancer stem cells in carcinogenesis. The goal of the present study was to determine the effect of low-dose cisplatin on enriched liver cancer stem cells (LCSCs). Human hepatoblastoma HepG2 cells were treated with concentrations of cisplatin ranging from 1 to 5 μg/mL. Cell survival and proliferation were evaluated using a tetrazolium dye (MTT) assay. LCSCs were identified using specific markers, namely aldehyde dehydrogenase-1 (ALDH1) and CD133. The percentage of ALDH1+ or CD133+ cells was examined by flow cytometric analysis. The expression of ALDH1 and/or CD133 in HepG2 cells was determined by immunocytochemical analysis. Low-dose cisplatin treatment significantly decreased cell survival in HepG2 cells after 24 or 72 h. However, the percentage of LCSCs in the surviving cells was greatly increased. The percentage of ALDH1+ or CD133+ cells was increased in a time- and dose-dependent manner after treatment with 1-4 μg/mL cisplatin, whereas 5 μg/mL cisplatin exposure slightly reduced the number of positive cells. These findings indicate that low-dose cisplatin treatment may efficiently enrich the LCSC population in HepG2 cells.
Asunto(s)
Humanos , Antineoplásicos/administración & dosificación , Proliferación Celular/efectos de los fármacos , Cisplatino/administración & dosificación , Hepatoblastoma/tratamiento farmacológico , Neoplasias Hepáticas/tratamiento farmacológico , Células Madre Neoplásicas/efectos de los fármacos , Antígenos CD/análisis , Línea Celular Tumoral , Carcinogénesis/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Cisplatino/uso terapéutico , Citometría de Flujo , Glicoproteínas/análisis , Hepatoblastoma/patología , Inmunohistoquímica , Isoenzimas/análisis , Neoplasias Hepáticas/patología , Células Madre Neoplásicas/citología , Péptidos/análisis , Retinal-Deshidrogenasa/análisis , Sales de Tetrazolio , Biomarcadores de Tumor/análisisRESUMEN
BACKGROUND: Lung cancer in never smokers presents predominately as adenocarcinoma and in females. MicroRNA-183 (miR-183) has various expression patterns in types of human cancers. In the present study, we evaluated the expression of miR-183-3p in female lung adenocarcinoma and adjacent noncancerous tissues and explored its relationship with clinicopathological characteristics and prognosis. METHODS: In the present study, a hundred female nonsmoking patients who were newly diagnosed and histologically confirmed as lung adenocarcinoma at Tianjin Medical University Cancer Hospital were included. miR-183-3p expression of surgically removed NSCLC tissues and their corresponding normal lung tissues was measured by qRT-PCR assay. Associations of miR-183-3p expression with clinicopathological features were determined using the Student's t test. Log-rank test, and Cox proportional hazards model were used for survival analysis. RESULTS: At first, miR-183-3p was up-regulated in lung cancer tissues when compared with the corresponding noncancerous lung tissues. Moreover, the expression of miR-183-3p in tumor tissue was found to be associated with lymph node metastasis (P = 0.043), clinical stage (P = 0.015), and EGFR mutation (P = 0.003). At last, high miR-183-3p expression was also associated with both poor overall survival and progression-free survival of women with lung adenocarcinoma (P = 0.005 and P = 0.010, respectively). CONCLUSION: This study suggested that miR-183-3p expression might be involved in lung cancer pathogenesis and progression, and could be used as a potential prognostic biomarker of female lung adenocarcinoma.
Asunto(s)
Adenocarcinoma/genética , Biomarcadores de Tumor/genética , Neoplasias Pulmonares/genética , MicroARNs/biosíntesis , Adenocarcinoma/mortalidad , Adenocarcinoma/patología , Adenocarcinoma del Pulmón , Adulto , Anciano , Supervivencia sin Enfermedad , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Estimación de Kaplan-Meier , Neoplasias Pulmonares/mortalidad , Neoplasias Pulmonares/patología , MicroARNs/análisis , Persona de Mediana Edad , Pronóstico , Modelos de Riesgos Proporcionales , Reacción en Cadena en Tiempo Real de la Polimerasa , Fumar , Regulación hacia ArribaRESUMEN
Accumulating evidence has indicated the importance of cancer stem cells in carcinogenesis. The goal of the present study was to determine the effect of low-dose cisplatin on enriched liver cancer stem cells (LCSCs). Human hepatoblastoma HepG2 cells were treated with concentrations of cisplatin ranging from 1 to 5 µg/mL. Cell survival and proliferation were evaluated using a tetrazolium dye (MTT) assay. LCSCs were identified using specific markers, namely aldehyde dehydrogenase-1 (ALDH1) and CD133. The percentage of ALDH1+ or CD133+ cells was examined by flow cytometric analysis. The expression of ALDH1 and/or CD133 in HepG2 cells was determined by immunocytochemical analysis. Low-dose cisplatin treatment significantly decreased cell survival in HepG2 cells after 24 or 72 h. However, the percentage of LCSCs in the surviving cells was greatly increased. The percentage of ALDH1+ or CD133+ cells was increased in a time- and dose-dependent manner after treatment with 1-4 µg/mL cisplatin, whereas 5 µg/mL cisplatin exposure slightly reduced the number of positive cells. These findings indicate that low-dose cisplatin treatment may efficiently enrich the LCSC population in HepG2 cells.
Asunto(s)
Antineoplásicos/administración & dosificación , Proliferación Celular/efectos de los fármacos , Cisplatino/administración & dosificación , Hepatoblastoma/tratamiento farmacológico , Neoplasias Hepáticas/tratamiento farmacológico , Células Madre Neoplásicas/efectos de los fármacos , Antígeno AC133 , Familia de Aldehído Deshidrogenasa 1 , Antígenos CD/análisis , Biomarcadores de Tumor/análisis , Carcinogénesis/efectos de los fármacos , Línea Celular Tumoral , Supervivencia Celular/efectos de los fármacos , Cisplatino/uso terapéutico , Citometría de Flujo , Glicoproteínas/análisis , Células Hep G2 , Hepatoblastoma/patología , Humanos , Inmunohistoquímica , Isoenzimas/análisis , Neoplasias Hepáticas/patología , Células Madre Neoplásicas/citología , Péptidos/análisis , Retinal-Deshidrogenasa/análisis , Sales de TetrazolioRESUMEN
The G' (or 2D) Raman band of AB stacked bilayer graphene comes from a double resonance Raman (DRR) process and is composed of four peaks (P(11), P(12), P(21), and P(22)). In this work, the integrated areas (IA) of these four peaks are analyzed as a function of the laser power for different laser lines. We show that the dependence of the IA of each peak on temperature is different for each distinct laser excitation energy. This special dependence is explained in terms of the electron-phonon coupling and the relaxation of the photon-excited electron. In this DRR process, the electron is scattered by an iTO phonon from a K to an inequivalent K' point of the Brillouin zone. Here, we show that this electron relaxes while in the conduction band before being scattered by an iTO phonon due to the short relaxation time of the excited electron, and the carrier relaxation occurs predominantly by emitting a low-energy acoustic phonon. The different combinations of relaxation processes determine the relative intensities of the four peaks that give rise to the G' band. Some peaks show an increase of their IA at the expense of others, thereby making the IA of the peaks both different from each other and dependent on laser excitation energy and on power level. Also, we report that the IA of the G' mode excited at 532 nm, shows a resonance regime involving ZO' phonons (related to the interlayer breathing mode in bilayer graphene systems) in which a saturation of what we call the P(12) process occurs. This effect gives important information about the electron and phonon dynamics and needs to be taken into account for certain applications of bilayer graphene in the field of nanotechnology.