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A 28-d experiment was conducted to investigate the effects of feed-conditioning temperature on the pellet quality, growth performance, intestinal development, and blood parameters of geese. A total of 180 one-day-old White Yuzhou goslings were randomly allotted to 5 treatment groups, with 6 replicates containing 6 birds each. Five diets were conditioned at 65, 70, 75, 80, and 85°C. Body weight and feed intake per pen basis were recorded from the arrival to the end of the trial. Blood and small intestine samples were collected on d 28 for analysis. The results showed that the pellet durability index (PDI), pellet hardness, and gelatinisation degree of starch (GDS) increased with increasing conditioning temperature (P < 0.05). The final body weight (FBW), average daily gain (ADG) and average daily feed intake (ADFI) of goslings significantly increased when conditioning temperature increased from 65 or 70°C to 80 or 85°C (P < 0.05), accompanied by unaffected feed conversion ratio (FCR) (P > 0.05). The villus height to crypt depth ratio (VH/CD) in the duodenum and ileum improved with increasing conditioning temperature (P < 0.05). Additionally, trypsin and amylase activity were enhanced when the conditioning temperature increased from 65 to 85°C (P < 0.05). No significant differences in the carcass traits and blood parameters of goslings were observed among the groups (P > 0.05). Overall, under the present experimental conditions, increasing the steam-conditioning temperature of pelleted feed improved pellet quality, growth performance, intestinal morphology, and digestive enzyme activity in goslings. Based on broken-line regression analysis, the lower critical conditioning temperature for ADG in geese from 1 to 28 d of age was 80.95°C.
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Alimentación Animal , Dieta , Gansos , Animales , Gansos/fisiología , Gansos/crecimiento & desarrollo , Gansos/sangre , Alimentación Animal/análisis , Dieta/veterinaria , Temperatura , Distribución Aleatoria , Intestinos/fisiología , Fenómenos Fisiológicos Nutricionales de los AnimalesRESUMEN
BACKGROUND: Population aging might increase the prevalence of undernutrition in older people, which increases the risk of frailty. Numerous studies have indicated that myokines are released by skeletal myocytes in response to muscular contractions and might be associated with frailty. This study aimed to evaluate whether myokines are biomarkers of frailty in older inpatients with undernutrition. METHODS: The frailty biomarkers were extracted from the Gene Expression Omnibus and Genecards datasets. Relevant myokines and health-related variables were assessed in 55 inpatients aged ≥ 65 years from the Peking Union Medical College Hospital prospective longitudinal frailty study. Serum was prepared for enzyme-linked immunosorbent assay using the appropriate kits. Correlations between biomarkers and frailty status were calculated by Spearman's correlation analysis. Multiple linear regression was performed to investigate the association between factors and frailty scores. RESULTS: The prevalence of frailty was 13.21%. The bioinformatics analysis indicated that leptin, adenosine 5'-monophosphate-activated protein kinase (AMPK), irisin, decorin, and myostatin were potential biomarkers of frailty. The frailty group had significantly higher concentrations of leptin, AMPK, and MSTN than the robust group (p < 0.05). AMPK was significantly positively correlated with frailty (p < 0.05). The pre-frailty and frailty groups had significantly lower concentrations of irisin than the robust group (p < 0.05), whereas the DCN concentration did not differ among the groups. Multiple linear regression suggested that the 15 factors influencing the coefficients of association, the top 50% were the ADL score, MNA-SF score, serum albumin concentration, urination function, hearing function, leptin concentration, GDS-15 score, and MSTN concentration. CONCLUSIONS: Proinflammatory myokines, particularly leptin, myostatin, and AMPK, negatively affect muscle mass and strength in older adults. ADL and nutritional status play major roles in the development of frailty. Our results confirm that identification of frailty relies upon clinical variables, myokine concentrations, and functional parameters, which might enable the identification and monitoring of frailty.
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Fragilidad , Desnutrición , Humanos , Anciano , Proteínas Quinasas Activadas por AMP , Fibronectinas , Fragilidad/diagnóstico , Fragilidad/epidemiología , Pacientes Internos , Leptina , Mioquinas , Miostatina , Estudios Prospectivos , Desnutrición/diagnóstico , Desnutrición/epidemiología , BiomarcadoresRESUMEN
OBJECTIVE: This study aimed to investigate the relationship between different dietary patterns and diabetic microvascular complications in patients with type 2 diabetes mellitus. PATIENTS AND METHODS: This study was conducted based on the Chinese Chronic Disease and its Risk Factor Surveillance System. A multi-stage stratified sampling method was used to randomly select two districts (Henghualing District, Taiyuan City, and Yuzi District, Jinzhong City) and two counties (Huguan County, Changzhi City, and Jiang County, Yuncheng City) from the chronic disease surveillance sites in Shanxi Province to collect general information, dietary records, physical measurements, and laboratory tests. In total, 1,227 patients were enrolled according to the study criteria. Factor analysis was performed to construct six dietary patterns, and the relationship between dietary pattern scores and type 2 diabetic microvascular complications was analysed using binary logistic regression after correcting for confounders. RESULTS: (1) Regarding the prevalence of type 2 diabetic microvascular complications and dietary characteristics, the prevalence of microvascular complications in patients with type 2 diabetes mellitus was 55.3% and was higher in urban than in rural areas. The prevalence of diabetic kidney disease (DKD), diabetic retinopathy, and diabetic peripheral neuropathy (DPN) were 21.4%, 12.7%, and 38.0%, respectively. (2) Six dietary patterns were constructed, namely, 'animal protein', 'coarse grains and plant protein', 'nuts and fruits', 'refined grains and vegetables', 'dairy', and 'added sugars', with factor contributions of 15.42%, 9.99%, 8.23%, 8.16%, 7.56%, and 7.28% respectively, explaining 56.64% of the total dietary variation. (3) After adjusting for confounding variables, the results of binary logistic regression indicated that patients in the highest quartile of dietary pattern scores for 'nuts and fruits' experienced a 43.3% lower risk of DKD compared to those in the lowest quartile [odds ratio (OR) = 0.567; 95% confidence interval (CI), 0.359-0.894; p < 0.001]. Similarly, patients in the highest quartile of dietary pattern scores for 'animal protein' had a 42.8% lower risk of DPN compared with those in the lowest quartile (OR = 0.572; 95% CI, 0.388-0.843; p < 0.05). CONCLUSIONS: The results of this study suggest that in patients with type 2 diabetes mellitus, a 'nuts and fruits' dietary pattern reduces the risk of DKD and an 'animal protein' dietary pattern reduces the risk of DPN.
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Diabetes Mellitus Tipo 2 , Nefropatías Diabéticas , Retinopatía Diabética , Animales , Humanos , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/epidemiología , Frutas , Factores de RiesgoRESUMEN
Enhanced osseointegration and a shortened healing time are required for dental implant treatment. The aim of this study was to evaluate whether topical application of the osteogenic inducer (OI) sustained-release system over the implant promotes early bone remodeling around the implant. The mandibular canines of 15 New Zealand White rabbits were extracted. After 3 months of healing, implants coated with poly(lactic-co-glycolic acid) (PLGA)+OI, PLGA alone, or no material (control) were inserted into the canine sites. After 4 weeks, specimens were harvested from the three groups and evaluated. Implant stability recorded by Periotest revealed significantly higher values for the PLGA + OI group (-2.61 ± 0.43) than for the PLGA (-1.47 ± 0.45) and control groups (-1.08 ± 0.19) (P < 0.001). Moreover, the PLGA+OI group had improved bone volume and structural parameters around the implants at 4 weeks, as shown by significantly increased BV/TV, BSA/BV, Tb.Th, and BIC (P < 0.05), as well as decreased Tb.Sp (P = 0.010) compared with the other groups. The histological results showed more trabecular bone and bone matrix around the implants in the PLGA+OI group. Therefore, local application of the OI sustained-release system might be able to promote early bone remodeling around titanium implants and facilitate faster and better osseointegration.
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Implantes Dentales , Titanio , Animales , Remodelación Ósea , Preparaciones de Acción Retardada/farmacología , Oseointegración , Osteogénesis , Conejos , Titanio/química , Titanio/farmacologíaRESUMEN
Purpose The aim of the present study was to elucidate the functional role of hsa-miR-328-3p/STAT3 pathway in the effects of propofol on gastric cancer proliferation. Methods Bioinformatics was used to analyze the molecular expression differences of hsa-miR-328-3p/STAT3 axis in stomach adenocarcinoma (n = 435) and normal samples (n = 41) from TCGA database. The expression of the above molecules in gastric cancer cells SGC-7901 and normal gastric mucosal cells GES-1 was verified via qPCR. The dual-luciferase assay was carried out to confirm the interaction between hsa-miR-328-3p and STAT3. Subsequently, the cell proliferation and the expression of the above molecules in SGC-7901 and GES-1 cells were evaluated after 10 μM propofol treatment. Finally, we analyzed whether propofol still inhibited the proliferation of gastric cancer by suppressing STAT3 pathway after hsa-miR-328-3p down-regulation. Results Compared with normal samples, the expression of hsa-miR-328-3p was significantly down-regulated in stomach adenocarcinoma samples, while the expression of STAT3 and downstream target genes (MMP2, CCND1 and COX2) was up-regulated. The results were consistent with those in GES-1 and SGC-7901 cell lines. Meanwhile, we found that hsa-miR-328-3p can bind to the 3′-UTR of the potential target gene STAT3. Furthermore, propofol significantly inhibited the proliferation of gastric cancer cell line SGC-7901, where hsa-miR-328-3p was up-regulated and the expression of STAT3 and downstream proliferation-related target genes were down-regulated. However, the growth inhibition of propofol on SGC-7901 cell was significantly reversed after the inhibition of hsa-miR-328-3p. Conclusions To sum up, propofol suppressed the STAT3 pathway via up-regulating hsa-miR-328-3p to inhibit gastric cancer proliferation (AU)
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Humanos , Neoplasias Gástricas/patología , Adenocarcinoma/patología , Proliferación Celular/efectos de los fármacos , MicroARNs/metabolismo , Propofol/farmacología , Factor de Transcripción STAT3/metabolismo , Regiones no Traducidas 3' , Adenocarcinoma/metabolismo , Línea Celular Tumoral , Biología Computacional , Ciclina D1/metabolismo , Ciclooxigenasa 2/metabolismo , Regulación hacia Abajo , Mucosa Gástrica/metabolismo , Factor de Transcripción STAT3/genética , Neoplasias Gástricas/metabolismoRESUMEN
PURPOSE: The aim of the present study was to elucidate the functional role of hsa-miR-328-3p/STAT3 pathway in the effects of propofol on gastric cancer proliferation. METHODS: Bioinformatics was used to analyze the molecular expression differences of hsa-miR-328-3p/STAT3 axis in stomach adenocarcinoma (n = 435) and normal samples (n = 41) from TCGA database. The expression of the above molecules in gastric cancer cells SGC-7901 and normal gastric mucosal cells GES-1 was verified via qPCR. The dual-luciferase assay was carried out to confirm the interaction between hsa-miR-328-3p and STAT3. Subsequently, the cell proliferation and the expression of the above molecules in SGC-7901 and GES-1 cells were evaluated after 10 µM propofol treatment. Finally, we analyzed whether propofol still inhibited the proliferation of gastric cancer by suppressing STAT3 pathway after hsa-miR-328-3p down-regulation. RESULTS: Compared with normal samples, the expression of hsa-miR-328-3p was significantly down-regulated in stomach adenocarcinoma samples, while the expression of STAT3 and downstream target genes (MMP2, CCND1 and COX2) was up-regulated. The results were consistent with those in GES-1 and SGC-7901 cell lines. Meanwhile, we found that hsa-miR-328-3p can bind to the 3'-UTR of the potential target gene STAT3. Furthermore, propofol significantly inhibited the proliferation of gastric cancer cell line SGC-7901, where hsa-miR-328-3p was up-regulated and the expression of STAT3 and downstream proliferation-related target genes were down-regulated. However, the growth inhibition of propofol on SGC-7901 cell was significantly reversed after the inhibition of hsa-miR-328-3p. CONCLUSIONS: To sum up, propofol suppressed the STAT3 pathway via up-regulating hsa-miR-328-3p to inhibit gastric cancer proliferation.
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Adenocarcinoma/patología , Anestésicos Intravenosos/farmacología , Proliferación Celular/efectos de los fármacos , MicroARNs/metabolismo , Propofol/farmacología , Factor de Transcripción STAT3/metabolismo , Neoplasias Gástricas/patología , Regiones no Traducidas 3' , Adenocarcinoma/metabolismo , Línea Celular Tumoral , Biología Computacional , Ciclina D1/genética , Ciclina D1/metabolismo , Ciclooxigenasa 2/genética , Ciclooxigenasa 2/metabolismo , Regulación hacia Abajo , Mucosa Gástrica/efectos de los fármacos , Mucosa Gástrica/metabolismo , Humanos , Luciferasas/metabolismo , Metaloproteinasa 2 de la Matriz/genética , Metaloproteinasa 2 de la Matriz/metabolismo , MicroARNs/antagonistas & inhibidores , Factor de Transcripción STAT3/genética , Neoplasias Gástricas/metabolismo , Regulación hacia ArribaRESUMEN
OBJECTIVE: Neuropathic pain (NP) is one of the most intractable complications of spinal cord injury (SCI). This study aims to explore the role of long non-coding RNA (lncRNA) SNHG1 in influencing SCI-induced NP. MATERIALS AND METHODS: After establishment of the spinal nerve ligation (SNL) model in rats, spinal tissues were extracted. SNHG1 level in rat spinal tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The role of SNHG1 in the development of NP was explored by assessing paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) in model rats. The interaction between SNHG1 and CDK4 was explored by Luciferase assay and RIP (RNA-Binding Protein Immunoprecipitation). Enzyme-linked immunosorbent assay (ELISA) and qRT-PCR were conducted to determine inflammatory factor levels in rat spinal tissues. RESULTS: SNHG1 was upregulated in rats undergoing SNL. Knockdown of SNHG1 alleviated the development of NP and overexpression of SNHG1 was capable of inducing NP symptoms in uninjured rats. SNHG1 induced NP by directly regulating CDK4 level. CONCLUSIONS: SNHG1 is a novel target in the treatment of NP associated with neuroinflammation.
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Quinasa 4 Dependiente de la Ciclina/metabolismo , Neuralgia/metabolismo , ARN Largo no Codificante/metabolismo , Traumatismos de la Médula Espinal/metabolismo , Animales , Quinasa 4 Dependiente de la Ciclina/genética , Masculino , Neuralgia/patología , Células PC12 , ARN Largo no Codificante/genética , Ratas , Ratas Sprague-Dawley , Traumatismos de la Médula Espinal/patología , Células Tumorales CultivadasRESUMEN
Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA PCAT-1 promoted ovarian cancer cell proliferation and invasion by suppressing KLF6, by H.-P. Liu, D. Lv, J.-Y. Wang, Y. Zhang, J.-F. Chang, Z.-T. Liu, N. Tang, published in Eur Rev Med Pharmacol Sci 2019; 23 (11): 4650-4655-DOI: 10.26355/eurrev_201906_18044-PMID: 31210290" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18044.
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Triple-negative breast cancer (TNBC) is the most aggressive breast cancer, and thus, has limited treatment options. Neuropilin1 (NRP1) is a multi-functional transmembrane protein that interacts with a number of signaling receptors and plays an important role in cancer progression. Previous studies demonstrated that the expression of NRP1 is activated and promotes the progression of breast cancer particularly in TNBC compared to other molecular subtypes; however, whether or not the level of NRP1 expression is related to the progression of TNBC warrants further study. In the current study, we determined the expression and function of NRP1 and evaluated the clinical significance of NRP1 in patients with TNBC. In addition, we determined whether or not an NRP1 antagonist potentiates the inhibitory effects of paclitaxel (PTX) in patients with TNBC. In our clinical study, NRP1 had higher expression in TNBC tissues than non-TNBC tissues at the same stage, and NRP1 was an independent prognostic factor. Specifically, the high expression of NRP1 was associated with shorter survival in TNBC patients. In addition, TNBC cells treated with NRP1 antagonist significantly potentiated the effect of PTX on cell proliferation, cell migration, and apoptosis. Our findings suggest that NRP1 expression can act as an independent prognostic factor for TNBC patients, and the combination of PTX and an NRP1 antagonist may be an effective treatment regimen for TNBC.
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Neuropilina-1/genética , Paclitaxel/uso terapéutico , Neoplasias de la Mama Triple Negativas , Línea Celular Tumoral , Proliferación Celular , Regulación Neoplásica de la Expresión Génica , Humanos , Pronóstico , Neoplasias de la Mama Triple Negativas/tratamiento farmacológico , Neoplasias de la Mama Triple Negativas/genéticaRESUMEN
OBJECTIVE: To explore the effects of micro ribonucleic acid (miR)-188 on proliferation and apoptosis of lung adenocarcinoma (LUAD) cells, and its potential mechanism. MATERIALS AND METHODS: The expression level of miR-188 in LUAD cell lines was detected via quantitative Real Time-Polymerase Chain Reaction (PCR). The effects of miR-188 overexpression on proliferation and apoptosis of A549 cells were detected using methyl thiazolyl tetrazolium (MTT) assay, colony formation assay, and flow cytometry. The potential targets for miR-188 were predicted using the TargetScan Human database, and the interaction between miR-188 and target gene was determined through Dual-Luciferase reporter assay. Moreover, the associations of miR-188 and sine oculis homeobox homolog 1 (SIX1) with the extracellular signal-regulated kinase (ERK) pathway were detected via Western blotting. RESULTS: The expression of miR-188 significantly declined in LUAD cell lines (p<0.05). The overexpression of miR-188 significantly reduced the proliferation rate of A549 cells and increased the percentage of apoptotic A549 cells (p<0.05). Similarly, it was found in colony formation assay that the overexpression of miR-188 inhibited the colony formation ability of A549 cells most significantly (p<0.05). SIX1 was a direct target for miR-188, and its mRNA and protein expressions were downregulated by the overexpression of miR-188. The remarkable downregulation of phosphorylated ERK was observed in A549 cells overexpressing miR-188, while the decline in phosphorylated ERK was reversed in A549 cells overexpressing miR-188 and SIX1. CONCLUSIONS: The expression of miR-188 is downregulated in LUAD cell lines. The overexpression of miR-188 inhibits proliferation and promotes apoptosis of LUAD cells, whose functional mechanism may be related to its regulation on the ERK signaling pathway by targeting SIX1.
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Adenocarcinoma del Pulmón/metabolismo , Proliferación Celular/fisiología , Proteínas de Homeodominio/biosíntesis , Neoplasias Pulmonares/metabolismo , Sistema de Señalización de MAP Quinasas/fisiología , MicroARNs/biosíntesis , Células A549 , Adenocarcinoma del Pulmón/genética , Adenocarcinoma del Pulmón/patología , Apoptosis/fisiología , Proteínas de Homeodominio/genética , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patología , MicroARNs/antagonistas & inhibidores , MicroARNs/genéticaRESUMEN
OBJECTIVE: To clarify the expression pattern of miRNA-875-3p in CRC and its potential regulatory effect on the progression of CRC. MATERIALS AND METHODS: MiRNA-875-3p level in 56 matched CRC tissues and adjacent normal tissues were determined. The correlation between the miRNA-875-3p level and pathological indexes of CRC patients was analyzed. Prognostic potential of miRNA-875-3p in CRC patients was assessed by introducing the Kaplan-Meier curves. Influences of miRNA-875-3p on viability, migration, and wound closure were assessed through a series of functional experiments. The interaction between miRNA-875-3p and PLK1 in regulating the progression of CRC was finally uncovered by Dual-Luciferase reporter gene and rescue experiments. RESULTS: MiRNA-875-3p was downregulated in CRC tissues and cell lines. CRC patients with low level of miRNA-875-3p suffered a higher rate of distant metastasis and worse prognosis. Overexpression of miRNA-875-3p attenuated proliferative and migratory capacities of SW480 and HT29 cells. PLK1 was confirmed to be the target gene of miRNA-875-3p. PLK1 was upregulated in CRC tissues and cell lines, which was negatively regulated by miRNA-875-3p. MiRNA-875-3p alleviated the malignant progression of CRC via negatively regulating PLK1. CONCLUSIONS: MiRNA-875-3p is downregulated in CRC, which is closely related to distant metastasis and poor prognosis of CRC patients. MiRNA-875-3p alleviates the progression of CRC through targeting and downregulating PLK1.
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Proteínas de Ciclo Celular/metabolismo , Neoplasias Colorrectales/metabolismo , Progresión de la Enfermedad , MicroARNs/metabolismo , Proteínas Serina-Treonina Quinasas/metabolismo , Proteínas Proto-Oncogénicas/metabolismo , Anciano , Proteínas de Ciclo Celular/antagonistas & inhibidores , Proteínas de Ciclo Celular/genética , Neoplasias Colorrectales/genética , Neoplasias Colorrectales/patología , Femenino , Estudios de Seguimiento , Regulación Neoplásica de la Expresión Génica , Células HCT116 , Células HT29 , Humanos , Masculino , MicroARNs/genética , Persona de Mediana Edad , Proteínas Serina-Treonina Quinasas/antagonistas & inhibidores , Proteínas Serina-Treonina Quinasas/genética , Proteínas Proto-Oncogénicas/antagonistas & inhibidores , Proteínas Proto-Oncogénicas/genética , Tasa de Supervivencia/tendencias , Quinasa Tipo Polo 1RESUMEN
OBJECTIVE: To explore the association between the abnormal root morphology and bone metabolism or root development related gene polymorphism in patients with generalized aggressive periodontitis. METHODS: In the study, 179 patients with generalized aggressive periodontitis were enrolled, with an average age of (27.23±5.19) years, male / female = 67/112. The average number of teeth remaining in the mouth was (26.80±1.84). Thirteen single nucleotide polymorphisms (SNPs) of nine genes which related to bone metabolism and root development were detected by matrix assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF-MS). Root abnormalities were identified using periapical radiographs. The abnormal root morphology included cone-rooted teeth, slender-root teeth, short-rooted teeth, curved-rooted teeth, syncretic-rooted molars, and molar root abnormalities. The number of teeth and incidence of abnormal root morphology in different genotypes of 13 SNPs were analyzed. RESULTS: The constituent ratio of root with root abnormality in GAgP patients was 14.49%(695/4 798). The average number of teeth with abnormal root morphology in GAgP was (3.88±3.84). The average number of teeth with abnormal root morphology in CC, CT and TT genotypes in vitamin D receptor (VDR) rs2228570 was (4.66±4.10), (3.71±3.93) and (2.68±2.68). There was significant difference between TT genotype and CC genotype (t = 2.62, P =0.01). The average number of root morphological abnormalities in CC, CT and TT genotypes of Calcitotin Receptor (CTR) gene rs2283002 was (5.02±3.70), (3.43±3.95), and (3.05±3.12). The incidence of root morphological abnormalities in CC genotype was higher than that in the patients with CT and TT, and the difference was statistically significant(87.86% vs. 65.26% & 63.64%, P=0.006, adjusted OR =3.71, 95%CI: 1.45-9.50). There was no significant difference in the incidence of abnormal root morphology between CT and TT genotypes. CONCLUSION: VDR rs2228570 and CTR rs2283002 may be associated with the occurrence of abnormal root morphology in patients with generalized aggressive periodontitis, which is worthy of further research.
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Periodontitis Agresiva , Adulto , Periodontitis Agresiva/genética , Estudios de Casos y Controles , Femenino , Frecuencia de los Genes , Predisposición Genética a la Enfermedad , Genotipo , Humanos , Masculino , Polimorfismo de Nucleótido Simple , Receptores de Calcitriol/genética , Adulto JovenRESUMEN
BACKGROUND: Microscopic structures of the ossification centres of the odontoid process were studied from the micro-computed tomography (CT) images of the axis, and the potential influence of the ossification centres with different microscopic structures on odontoid process fractures was analysed. MATERIALS AND METHODS: Eighteen odontoid process specimens were randomly collected and scanned by micro-CT. The obtained images were then input into the software for further observation and measurement. Incomplete absorption of the ossification centres in the base was observed, along with the anatomic structure of the regions with incomplete ossification and structural parameters of the trabecular bones. RESULTS: The microscopic structures of the trabecular bones in the ossification centres in the base of the odontoid process could be clearly visualised from the micro-CT images. Among the 18 odontoid process specimens, 11 specimens were found with incomplete absorption of the ossification centres in the axis, the prevalence reaching up to 61%. Regions with incomplete ossification varied in size and morphology, and their three-dimensional morphology was predominantly oval. Of all structural parameters examined for the trabecular bones, there were only significant differences in the degree of anisotropy between the regions with incomplete absorption of ossification centres and the average vertebral trabecular bones (p < 0.05). CONCLUSIONS: Incomplete absorption of the ossification centres in the base of the odontoid process is a relatively prevalent condition. The cavitation effect of the trabecular bones may be the primary cause for odontoid process fractures.
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Anomalías Musculoesqueléticas , Apófisis Odontoides , Humanos , Apófisis Odontoides/diagnóstico por imagen , Osteogénesis , Programas Informáticos , Microtomografía por Rayos XRESUMEN
Increasing evidences have proved that circular RNAs (circRNAs), identified as a specific kind of non-coding RNAs, play a potential critical role in tumorigenesis including prostate cancer. However, the function of circRNAs in human prostate cancer remain largely unknown. In this study, we demonstrated that the expression of circZMIZ1 was higher in plasma of human prostate cancer than the paired benign prostatic hyperplasia (BPH) patients' plasma. Moreover, in cultured prostate cancer cells, knockdown of circZMIZ1 inhibited cell proliferation and caused cell cycle arrest at G1. Mechanistically, we also showed that circZMIZ1 could increase the expression of androgen receptor (AR) and androgen receptor splice variant 7 (AR-V7), which may be partly contributed to the occurrence and development of prostate cancer. In conclusion, these results revealed that circZMIZ1 might serve as a novel biomarker and a treatment target for prostate cancer treatment.
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Proliferación Celular , Neoplasias de la Próstata/patología , ARN Circular/sangre , Factores de Transcripción/sangre , Biomarcadores/sangre , Regulación Neoplásica de la Expresión Génica , Humanos , Masculino , Hiperplasia Prostática , Neoplasias de la Próstata/genética , ARN Circular/genética , Receptores Androgénicos , Factores de Transcripción/genética , Células Tumorales CultivadasRESUMEN
BACKGROUND: Epirubicin is a potent chemotherapeutic agent for the treatment of breast cancer. However, it may lead to cardiotoxicity and cardiomyopathy, and no reliable biomarker was available for the early prediction of epirubicin-induced cardiomyopathy. METHODS: Global gene expression changes of peripheral blood cells were studied using high-throughput RNA sequencing in three pair-matched breast cancer patients (patients who developed symptomatic cardiomyopathy paired with patients who did not) before and after the full session of epirubicin-based chemotherapy. Functional analysis was conducted using gene ontology and pathway enrichment analysis. RESULTS: We identified 13 significantly differentially expressed genes between patients who developed symptomatic epirubicin-induced cardiomyopathy and their paired control who did not. Among them, the upregulated Bcl-associated X protein was related to "apoptosis," while the downregulated 5'-aminolevulinate synthase 2 (ALAS2) was related to both "glycine, serine, and threonine metabolism" and "porphyrin and chlorophyll metabolism" in pathway enrichment analysis. CONCLUSIONS: ALAS2 and the metabolic pathways which were involved may play an important role in the development of epirubicin-induced cardiomyopathy. ALAS2 may be useful as an early biomarker for epirubicin-induced cardiotoxicity detection.
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5-Aminolevulinato Sintetasa/genética , Antibióticos Antineoplásicos/efectos adversos , Neoplasias de la Mama/tratamiento farmacológico , Cardiomiopatías/genética , Epirrubicina/efectos adversos , Expresión Génica , Antibióticos Antineoplásicos/sangre , Antibióticos Antineoplásicos/uso terapéutico , Neoplasias de la Mama/sangre , Neoplasias de la Mama/genética , Cardiomiopatías/sangre , Cardiomiopatías/inducido químicamente , Cardiotoxicidad , Estudios de Casos y Controles , Regulación hacia Abajo , Epirrubicina/sangre , Epirrubicina/uso terapéutico , Femenino , HumanosRESUMEN
Objective:To evaluate the influence of voice disorders on children's quality of life through the parental version of pediatric voice-related quality of lifeï¼pVRQOLï¼. Method:Three hundred and eighty-six children from August 2017 to December 2018 were enrolled in this study. A total of 214 parents of children had voice disordersï¼dysphonic groupï¼, and 172 parents of children were without voice disordersï¼control groupï¼. Both groups were filled out the questionnaire containing the parental version of pVRQOL. Result:â The most common disease in children with voice disorder was vocal fold nodule, and boys were more susceptible to voice disorder than girlsï¼71.5%, 28.5%ï¼; â¡In dysphonic group, the scores of totalï¼91.40±8.63, 97.94±4.23ï¼, physiology and functionï¼87.55±10.98, 96.99±6.10ï¼, social emotionï¼98.86 ±3.29, 99.73±1.08ï¼ were lower than those in control groupï¼P<0.01ï¼; â¢In dysphonic group, there was a correlation between the parents' overall evaluation of the children's voice quality and the three dimensions of the parental version of pVRQOLï¼total: r=-0.398, P<0.01, physical function: r=-0.448, P<0.01, social-emotion: r=-0.125, P<0.05ï¼. Conclusion:Voice disorders could cause a negative impact on children's voice related quality of life. pVRQOL could be applied to assess the voice-related quality of life in children with voice disorders.
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Calidad de Vida , Trastornos de la Voz , Niño , Femenino , Humanos , Masculino , Padres , Encuestas y Cuestionarios , Voz , Calidad de la VozRESUMEN
Objective:The aim of this study is to investigate the voice function change in patients who underwent total thyroidectomy between preoperative and the third day postoperative, Taking the result data to explore methods for voice protection and be valuable for clinical diagnose and treatment. Method:Three hundred and fifth-three patients with thyroid papillary carcinoma without preoperative vocal dysfunction were treated with total thyroidectomy and single or bilateral central cervical lymph node dissection. At preoperative and the third day postoperative, videostroboscopic, acoustic analysis, voice handicap index 10ï¼VHI-10ï¼are measured. Result: At the third day postoperative, 294 ï¼83.29%ï¼patients have voice symptomsï¼the most common voice disorder is hoarseness in 105 cases ï¼35.71%ï¼ï¼phonasthenia in 78 casesï¼26.53%ï¼ï¼unable speak louderly in 53 cases ï¼18.03%ï¼, unable speak high-pitch in 24 cases ï¼8.16%ï¼, unable speak low-pitch in 29 cases ï¼9.86%ï¼, pronunciation leakage in 5 cases ï¼1.70%ï¼. Videostroboscopic examinations are normal in all patients at the third day postoperative. The total score of VHI-10, Physiologyï¼Pï¼, Emotionï¼Eï¼ dimensions in VHI-10 between preoperative and the third day postoperative are statistically significant ï¼P<0.05ï¼. For male patients, the acoustic analysis ï¼fundamental frequency, Harmonicto Noise Ratio, Shimmer and Maximum phonation timeï¼ are statistically significant between preoperative and the third day postoperative ï¼P<0.05ï¼. For female patients, acoustic analysis ï¼fundamental frequency, Harmonicto Noise Ratio, Shimmer, Jitter and Maximum phonation timeï¼ are statistically significant between preoperative and the third day postoperative ï¼P<0.05ï¼. Conclusion:These patients who underwent total thyroidectomy with bilateral or unilateral central partment lymph node dissection may develop voice complications even their recurrent laryngealnerve be undamaged during the surgery. Changes in surgery and voice may cause changes in the patient's psychology, suggesting that clinicians need to have adequate communication between doctors and patients before surgery, pay attention to the patient's voice quality and psychological changes, and give positive intervention.
Asunto(s)
Cáncer Papilar Tiroideo/cirugía , Neoplasias de la Tiroides/cirugía , Tiroidectomía/efectos adversos , Trastornos de la Voz/etiología , Calidad de la Voz , Femenino , Humanos , Masculino , Disección del CuelloRESUMEN
OBJECTIVE: Recently, the role of long noncoding RNAs (lncRNAs) in tumor progression has caught attention in numerous researchers. In our investigation, lncRNA PCAT-1 was studied to identify how it functioned in the progression of ovarian cancer. PATIENTS AND METHODS: LncRNA PCAT-1 expression was detected by quantitative Real-time polymerase chain reaction (qRT-PCR) in both ovarian cancer cells and tissue samples. Furthermore, to identify the function of PCAT-1 in ovarian cancer, cell proliferation, transwell assay and Matrigel assay were conducted. In addition, by performing qRT-PCR and Western blot assay, the underlying mechanism was explored. RESULTS: PCAT-1 expression was remarkably higher in ovarian cancer samples when compared with that in corresponding ones. Moreover, cell proliferation, migration and invasion were inhibited after PCAT-1 was knocked down in ovarian cancer cells. Moreover, the mRNA and protein expression of KLF6 (Krüppel-like factor 6) was upregulated after PCAT-1 was knocked down. Furthermore, the KLF6 expression level was negatively related to the PCAT-1 expression level in ovarian cancer samples. CONCLUSIONS: We showed that PCAT-1 promotes the progression of ovarian cancer through enhancing cell metastasis and proliferation via suppressing KLF6, which might be a novel therapeutic strategy in ovarian cancer.
RESUMEN
OBJECTIVE: Previous studies have shown that microRNA-765 (miR-765) is involved in certain biological behaviors of human cancers. However, abnormal expression and function of miR-765 have not been reported in osteosarcoma (OS). PATIENTS AND METHODS: Changes in the expression of miR-765 and MTUS1 (Microtubule-associated tumor suppressor 1) were examined via Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. The function of miR-765 was investigated through Cell Counting Kit-8 (CCK-8) and transwell assays in OS. The target of miR-765 was identified using a Dual-Luciferase reporter assay. RESULTS: MiR-765 was upregulated in OS tissues. And upregulation of miR-765 promoted cell proliferation, migration and invasion in OS. In addition, MTUS1 was confirmed as a direct target gene of miR-765. Moreover, miR-765 promoted the progression of OS through targeting MTUS1. Furthermore, miR-765 was involved in tumorigenesis of OS through activating extracellular-signal-regulated kinase/ epithelial-mesenchymal transition (ERK/EMT) pathway. CONCLUSIONS: MiR-765 targets MTUS1 to promote the progression of OS via mediating the ERK/EMT pathway. Therefore, miR-765 may be used as a novel biomarker for the diagnosis of OS.