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Hemiboea pterocaulis is a unique species only found in Guilin, Guangxi, China. In this study, we sequenced and assembled the complete chloroplast genome of H. pterocaulis and revealed its phylogenetic relationship with other Hemiboea species. The chloroplast genome sequence of H. pterocaulis is 153,159 bp in length and comprises a large single-copy (LSC) region of 84,178 bp, a small single-copy (SSC) region of 18,087 bp, and a pair of inverted repeat (IR) regions, each with a length of 25,447 bp. It has a total GC content of 37.6% and encodes 132 genes, including 87 protein-coding genes, 37 tRNA genes, and eight rRNA genes. The phylogenetic relationships based on the complete chloroplast genome sequences of Hemiboea taxa indicate that H. pterocaulis is most closely related to H. suiyangensis, indicating that H. pterocaulis is an independent species and is separated from the H. subcapitata complex. These results provide valuable insights into the phylogeny, species divergence, and delimitation of the Hemiboea genus.
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Protein ubiquitination is a common post-translational modification and a critical mechanism for regulating protein stability. This study aimed to explore the role and potential molecular mechanism of ubiquitin-specific peptidase 38 (USP38) in the progression of lung adenocarcinoma (LUAD). USP38 expression was significantly higher in patients with LUAD than in their counterparts, and higher USP38 expression was closely associated with a worse prognosis. USP38 silencing suppresses the proliferation of LUAD cells in vitro and impedes the tumorigenic activity of cells in xenograft mouse models in vivo. Further, we found that USP38 affected the protein stability of transcription factor Krüppel-like factors 5 (KLF5) by inhibiting its degradation. Subsequent mechanistic investigations showed that the N-terminal of USP38 (residues 1-400aa) interacted with residues 1-200aa of KLF5, thereby stabilizing the KLF5 protein by deubiquitination. Moreover, we found that PIAS1-mediated SUMOylation of USP38 was promoted, whereas SENP2-mediated de-SUMOylation of USP38 suppressed the deubiquitination effects of USP38 on KLF5. Additionally, our results demonstrated that KLF5 overexpression restored the suppression of the malignant properties of LUAD cells by USP38 knockdown. SUMOylation of USP38 enhances the deubiquitination and stability of KLF5, thereby augmenting the malignant progression of LUAD.
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Adenocarcinoma del Pulmón , Factores de Transcripción , Animales , Humanos , Ratones , Adenocarcinoma del Pulmón/genética , Proliferación Celular/genética , Factores de Transcripción de Tipo Kruppel/genética , Factores de Transcripción de Tipo Kruppel/metabolismo , Factores de Transcripción/metabolismo , Proteasas Ubiquitina-Específicas/genética , Proteasas Ubiquitina-Específicas/metabolismo , UbiquitinaciónRESUMEN
Phanera championii is a medicinal liana plant that has successfully adapted to hostile karst habitats. Despite extensive research on its medicinal components and pharmacological effects, the molecular mechanisms underlying the biosynthesis of critical flavonoids and its adaptation to karst habitats remain elusive. In this study, we performed high-coverage PacBio and Hi-C sequencing of P. championii, which revealed its high heterozygosity and phased the genome into two haplotypes: Hap1 (384.60 Mb) and Hap2 (383.70 Mb), encompassing a total of 58 612 annotated genes. Comparative genomes analysis revealed that P. championii experienced two whole-genome duplications (WGDs), with approximately 59.59% of genes originating from WGD events, thereby providing a valuable genetic resource for P. championii. Moreover, we identified a total of 112 genes that were strongly positively selected. Additionally, about 81.60 Mb of structural variations between the two haplotypes. The allele-specific expression patterns suggested that the dominant effect of P. championii was the elimination of deleterious mutations and the promotion of beneficial mutations to enhance fitness. Moreover, our transcriptome and metabolome analysis revealed alleles in different tissues or different haplotypes collectively regulate the synthesis of flavonoid metabolites. In summary, our comprehensive study highlights the significance of genomic and morphological adaptation in the successful adaptation of P. championii to karst habitats. The high-quality phased genomes obtained in this study serve as invaluable genomic resources for various applications, including germplasm conservation, breeding, evolutionary studies, and elucidation of pathways governing key biological traits of P. championii.
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Genoma de Planta , Genómica , Haplotipos , Análisis de Secuencia de ADN , Genoma de Planta/genética , Flavonoides/genéticaRESUMEN
In this study, we sequenced and assembled the complete chloroplast genome of Chloranthus nervosus Collett ex Hemsl. 1890. The total length of the complete chloroplast sequence was found to be 158,002 bp. It consisted of a large single-copy (LSC) region of 87,127 bp, a small single-copy (SSC) region of 18,541 bp, and a pair of inverted repeat (IR) regions, each with a length of 26,167 bp. The overall GC content of the complete chloroplast genome was 38.9%, with the LSC region, SSC region, and IR regions exhibiting GC contents of 37.4%, 34.1%, and 43.1%, respectively. The annotation of the chloroplast genome revealed a total of 131 genes, comprising 86 protein-coding genes, 37 tRNA genes, and eight rRNA genes. Phylogenetic analysis revealed that the seven sampled species of Chloranthus were divided into two clades. Within the clade characterized by long filamentous anther connectives, C. nervosus showed the closest relation to C. japonicus. These findings validated the previous preliminary results on the phylogenetic relationships of the seven species of Chloranthus with strong support.
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Investigating the role of ubiquitin-specific peptidase 10 (USP10) in triple-negative breast cancer (TNBC). Analyzed USP10 expression levels in tumors using public databases. Detected USP10 mRNA and protein levels in cell lines. Examined USP10 expression in tumor tissues from breast cancer patients. Conducted USP10 knockdown experiments and analyzed changes in cell proliferation and metastasis. Confirmed protein-protein interactions with USP10 through mass spectrometry, Co-IP, and fluorescence experiments. Assessed impact of USP10 on transcription factor 4 (TCF4) ubiquitination and validated TCF4's influence on TNBC cells. We initially identified a pronounced overexpression of USP10 across multiple tumor types, including TNBC. Subsequently, we observed a conspicuous upregulation of USP10 expression levels in breast cancer cell lines compared to normal breast epithelial cells. However, upon subsequent depletion of USP10 within cellular contexts, we noted a substantial attenuation of malignant proliferation and metastatic potential in TNBC cells. In subsequent experimental analyses, we elucidated the physical interaction between USP10 and the transcription factor TCF4, whereby USP10 facilitated the deubiquitination modification of TCF4, consequently promoting its protein stability and contributing to the initiation and progression of TNBC. Collectively, this study demonstrates that USP10 facilitated the deubiquitination modification of TCF4, consequently promoting its protein stability and contributing to the initiation and progression of TNBC.
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Neoplasias de la Mama Triple Negativas , Humanos , Neoplasias de la Mama Triple Negativas/metabolismo , Factor de Transcripción 4/genética , Factor de Transcripción 4/metabolismo , Ubiquitinación , Células Epiteliales/metabolismo , Regulación hacia Arriba , Línea Celular Tumoral , Proliferación Celular , Regulación Neoplásica de la Expresión Génica , Ubiquitina Tiolesterasa/genéticaRESUMEN
Nickel compounds are widely used in industries and daily life as important industrial products. Long-term exposure to nickel compounds has been associated with increased incidence and poor prognosis of lung cancer. However, the molecular mechanism by which exposure to nickel compounds induces the malignant phenotype of lung cancer cells remains unclear. In this study, we confirmed that nickel chloride (NiCl2) exposure promotes invasion and metastasis through IL-6/STAT3 both in vitro and vivo. Mechanistically, we found that NiCl2 mediated the transcriptional regulation of E3 ubiquitin ligase TRIM31 by SATAT3 phosphorylation, and promoted its up-regulation. Overexpression TRIM31 is an independent risk factor for lung cancer patients, and it promotes the invasion and metastasis of lung cancer cells. In addition, E3 ubiquitination ligase TRIM31 binds to its substrate TP53 protein in the RING region and accelerates TP53 protein ubiquitination and degradation. Functional recovery experiments showed that NiCl2 exposure promotes the invasion and metastasis ability of lung cancer and ubiquitination-mediated degradation of TP53 protein through the STAT3/TRIM31 axis. These findings reveal the role and mechanism of NiCl2 in lung cancer progression, indicating that STAT3 and TRIM31 may be promising targets for the treatment of lung cancer.
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Neoplasias Pulmonares , Metástasis de la Neoplasia , Níquel , Ubiquitina-Proteína Ligasas , Humanos , Interleucina-6/metabolismo , Neoplasias Pulmonares/inducido químicamente , Níquel/efectos adversos , Factor de Transcripción STAT3/metabolismo , Proteínas de Motivos Tripartitos/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Ubiquitina-Proteína Ligasas/genética , Ubiquitina-Proteína Ligasas/metabolismo , UbiquitinaciónRESUMEN
Growing studies have linked metal exposure to diabetes risk. However, these studies had inconsistent results. We used a multiple linear regression model to investigate the sex-specific and dose-response associations between urinary metals (cobalt (Co) and molybdenum (Mo)) and diabetes-related indicators (fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), homeostasis model assessment for insulin resistance (HOMA-IR), and insulin) in a cross-sectional study based on the United States National Health and Nutrition Examination Survey. The urinary metal concentrations of 1423 eligible individuals were stratified on the basis of the quartile distribution. Our results showed that the urinary Co level in males at the fourth quartile (Q4) was strongly correlated with increased FPG (ß = 0.61, 95% CI: 0.17-1.04), HbA1c (ß = 0.31, 95% CI: 0.09-0.54), insulin (ß = 8.18, 95% CI: 2.84-13.52), and HOMA-IR (ß = 3.42, 95% CI: 1.40-5.44) when compared with first quartile (Q1). High urinary Mo levels (Q4 vs. Q1) were associated with elevated FPG (ß = 0.46, 95% CI: 0.17-0.75) and HbA1c (ß = 0.27, 95% CI: 0.11-0.42) in the overall population. Positive linear dose-response associations were observed between urinary Co and insulin (Pnonlinear = 0.513) and HOMA-IR (Pnonlinear = 0.736) in males, as well as a positive linear dose-response relationship between urinary Mo and FPG (Pnonlinear = 0.826) and HbA1c (Pnonlinear = 0.376) in the overall population. Significant sex-specific and dose-response relationships were observed between urinary metals (Co and Mo) and diabetes-related indicators, and the potential mechanisms should be further investigated.
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Diabetes Mellitus , Resistencia a la Insulina , Adulto , Glucemia , Cobalto , Estudios Transversales , Femenino , Hemoglobina Glucada , Humanos , Insulina , Resistencia a la Insulina/fisiología , Masculino , Metales , Molibdeno , Encuestas Nutricionales , Estados UnidosRESUMEN
TNBC is a malignant tumor that easily relapses and metastasizes, with a poor prognosis in women. Ubiquitination plays a key role in promoting the tumor process. In various tumors, TRIM65 can affect malignant biological tumor behavior by ubiquitination of related proteins. We aimed to investigate TRIM65 expression in TNBC and whether it promotes malignant biological behavior in TNBC cells using Cell Counting Kit-8, colony formation, and transwell assays. Mechanically, we confirmed that TRIM65 promoted TNBC invasion and metastasis by ubiquitination of LATS1 protein through Co-IP, CHX, and endogenous ubiquitination experiments. The expression of TRIM65 was abnormally high and accelerated the proliferation, invasion, and migration of MDA-MB-231 and MDA-MB-453 cells. In vivo animal experiments also revealed that TRIM65 accelerated TNBC cell proliferation. Mechanistically, TRIM65 degraded LATS1 protein expression through ubiquitination in the Co-IP, CHX, and endogenous ubiquitination experiments. Rescue assays confirmed that TRIM65 degraded LATS1 protein expression, accelerating the proliferation, invasion, and migration ability of TNBC cells. Our results show that TRIM65 is upregulated in TNBC, and TRIM65 degrades LATS1 protein expression through ubiquitination and promotes malignant biological behavior in TNBC cells. TRIM65 may play an important role as a new oncogene in TNBC.
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Proteínas Serina-Treonina Quinasas , Proteínas de Motivos Tripartitos , Neoplasias de la Mama Triple Negativas , Animales , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Recurrencia Local de Neoplasia , Proteínas Serina-Treonina Quinasas/metabolismo , Proteínas de Motivos Tripartitos/metabolismo , Neoplasias de la Mama Triple Negativas/patología , Ubiquitina-Proteína LigasasRESUMEN
BACKGROUND: Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer. The role of the long non-coding RNA (lncRNA) LINC00958, which regulates the malignant behavior of multiple tumors, in LUAD has not been elucidated. METHODS: Tissue microarray, FISH, and qRT-PCR were used to detect the expression of LINC00958. Plasmid and viral infections were used to manipulate gene expression. The role of LINC00958 in LUAD was studied by cell proliferation analysis, cell apoptosis analysis, cell migration and invasion analysis, and subcutaneous inoculation of animal models. At the same time, RNA-Seq, RNA pull-down, ChIRP, ChIP, and luciferase reporter gene assays were performed to clarify the mechanism. RESULTS: The expression of LINC00958 in LUAD tissues was significantly upregulated when compared with that in adjacent tissues and could independently predict poor survival of patients with LUAD. LINC00958 knockdown significantly inhibited the growth and metastasis of lung cancer cells in vitro and in vivo. LINC00958 localized to the nucleus, regulated oncogenes and metabolism-related and immune response-related genes, and interacted with histones. The targets of LINC00958 were TRPV3, STAP2, and EDN2 promoters with motifs of HOXA1, NANOG, FOSL2, JUN, and ATF4. Moreover, HOXA1 overexpression mitigated the LINC00958 knockdown-induced oncogenic phenotype. MYC/MAX motif, which was detected at the cis-element of LINC00958, trans-activated the LINC00958 promoter. CONCLUSIONS: MYC/MAX-trans-activated LINC00958 promotes the malignant behavior of LUAD by recruiting HOXA1 and inducing oncogenic reprogramming.
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BACKGROUND: Triple-negative breast cancer (TNBC) is a highly malignant breast cancer subtype with a poor prognosis. The cell cycle regulator cyclin A2 (CCNA2) plays a role in tumor development. Herein, we explored the role of CCNA2 in TNBC. METHODS: We analyzed CCNA2 expression in 15 pairs of TNBC and adjacent tissues and assessed the relationship between CCNA2 expression using the tissue microarray cohort. Furthermore, we used two TNBC cohort datasets to analyze the correlation between CCNA2 and E2F transcription factor 1 (E2F1) and a luciferase reporter to explore their association. Through rescue experiments, we analyzed the effects of E2F1 knockdown on CCNA2 expression and cellular behavior. RESULTS: We found that CCNA2 expression in TNBC was significantly higher than that in adjacent tissues with similar observations in MDA-MB-231 and MDA-MB-468 cells. E2F1 was highly correlated with CCNA2 as observed through bioinformatics analysis (R= 0.80, P< 0.001) and through TNBC tissue verification analysis (R= 0.53, P< 0.001). We determined that E2F1 binds the +677 position within the CCNA2 promoter. Moreover, CCNA2 overexpression increased cell proliferation, invasion, and migration owing to E2F1 upregulation in TNBC. CONCLUSION: Our data indicate that E2F1 promotes TNBC proliferation and invasion by upregulating CCNA2 expression. E2F1 and CCNA2 are potential candidates that may be targeted for effective TNBC treatment.
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Neoplasias de la Mama Triple Negativas , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Ciclina A2/metabolismo , Factor de Transcripción E2F1/genética , Regulación Neoplásica de la Expresión Génica , Humanos , Neoplasias de la Mama Triple Negativas/patología , Regulación hacia ArribaRESUMEN
This study evaluated the relationships between parity and the age at menopause and menopausal syndrome among Chinese women in Gansu. A total of 7236 women aged 40 to 55 years met study eligibility criteria. The modified Kupperman Menopausal Index scale was used to assess the severity of menopausal syndrome. Cox regression was applied to estimate hazard ratio and 95% confidence interval, and logistic regression was performed to calculate odds ratio and confidence interval. The mean age at menopause was 47.91 ± 3.31 years. There is no relationship between parity and age at menopause. Women with nulliparity or multiparity seemed to have higher risks of moderate and severe menopausal syndrome. The potential beneficial effects of one or two births on menopausal syndrome were also observed by applying the multivariable logistic regression analysis, particularly in urogenital symptoms. Women with nulliparity and multiparity appeared to be at the higher risks of menopause syndrome.
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Menopausia , Paridad , Adulto , Factores de Edad , China , Estudios Transversales , Femenino , Humanos , Persona de Mediana Edad , Medición de Riesgo , Índice de Severidad de la EnfermedadRESUMEN
Primulina ophiopogoides is a perennial herb of Gesneriaceae distributed on the limestone rocks. Here, the complete chloroplast (cp) genome of P. ophiopogoides was assembled and characterized. The cp genome is in a total length of 152,718 bp with the typical quadripartite structure, containing 2 inverted repeats (IRs) of 25,472 bp separated by a large single-copy (LSC) region of 83,615 bp and a small single-copy (SSC) region of 18,159 bp. The whole cp genome of P. ophiopogoides contains 131 genes, including 86 protein-coding genes, 37 tRNAs genes, and 8 rRNAs. The phylogenetic analysis indicated that P. ophiopogoides displayed a closer kinship to Primulina linearifolia.
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BACKGROUND: Triple-negative breast cancer (TNBC) is one of the leading causes of death among females around the world. However, the molecular mechanism of the disease among TNBC patients remains to be further studied. METHODS: In our study, four microarray data and two high throughput sequencing data were acquired from the GEO database, and the differentially expressed genes (DEGs) between TNBC and normal tissues had been analyzed. Analysis of functional enrichment and pathway enrichment of DEGs was conducted by the Funrich software, and protein-protein interaction (PPI) network gained from the STRING, and hub genes were confirmed by the Cytoscape. Kaplan-Meier plotter (KM plotter) online dataset had been used to analyze DEGs of overall survival (OS), and progression-free survival (PFS). RESULTS: In total, 1638 DEGs were gained in our study covering 984 upregulated and 654 downregulated genes. Moreover, a PPI network was constructed, and cyclin-dependent kinase 1 (CDK1), cyclin B1 (CCNB1), and cyclin A2 (CCNA2) were found as top genes with higher node degrees. CDK1, CCNA2, and CCNB1were obviously enriched in the cell cycle. The top upregulated genes including CDK1, CCNB1, CCNA2, and PLK1 were overexpressed in TNBC, and correlated with worse OS in breast cancer. High expression of CCNB1 was correlated with worse PFS in TNBC (HR = 1.42, 95% CI: 1.04-1.94, P = 0.028). Besides, there was a correlation between CCNB1 and CDK1 in TNBC, as well as between CCNA2 and CDK1 (r = 0.804, P < 0.001; r = 0.577, P < 0.001, respectively). CONCLUSION: Our results suggest that cyclin CDK1, CCNB1, and CCNA2 are overexpressed in TNBC and they could act as novel biomarkers for the diagnosis and treatment of TNBC.
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Biomarcadores de Tumor/genética , Proteína Quinasa CDC2/genética , Ciclina A2/genética , Ciclina B1/genética , Neoplasias de la Mama Triple Negativas/diagnóstico , Mama/patología , Conjuntos de Datos como Asunto , Femenino , Perfilación de la Expresión Génica , Regulación Neoplásica de la Expresión Génica , Humanos , Estimación de Kaplan-Meier , Pronóstico , Supervivencia sin Progresión , Neoplasias de la Mama Triple Negativas/genética , Neoplasias de la Mama Triple Negativas/mortalidad , Neoplasias de la Mama Triple Negativas/patología , Regulación hacia ArribaRESUMEN
The complete chloroplast genome sequence of Semiaquilegia guangxiensis was assembled and the phylogenetic relationship with other species in Trib. Isopyreae was inferred in this study. The chloroplast genome is 164,047 bp in length. A typical quadripartite structure was detected, including two inverted repeats (IRs) of 29,581 bp, which are separated by a large single-copy (LSC) and a small single-copy (SSC) of 87,490 bp and 17,395 bp, respectively. Moreover, The genome comprises 132 genes, including 88 protein-coding genes, 36 tRNA genes, and 8 rRNA genes. The overall GC content of the chloroplast genome is 38.9%. The phylogenetic analysis indicated that S. guangxiensis is most closely related to its congener S. adoxoides, and Semiaquilegia is most closely related to Aquilegia in Ranunculaceae.
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PURPOSE: In this study, we investigated the expression and function of Epidermal growth factor receptor kinase substrate 8 (EPS8) in glioblastoma (GBM), and further explored the underlying mechanisms that regulate it. PATIENTS AND METHODS: The expression and potential mechanisms of EPS8 in GBM were evaluated through multiple online public databases. The expression level EPS8 in GBM tissues and cell lines were detected by immunohistochemical staining and Western blot. Then, the prognosis of EPS8 and GBM patients were analyzed. Loss-of-function experiments were conducted to determine the role of EPS8 for the biological behavior of GBM cells. In addition, the tumorigenic ability of nude mice was tested in vivo. RESULTS: EPS8 is highly expressed in GBM tissues and indicates poor patient prognosis. In cell experiments, EPS8 can promote the proliferation, migration and invasion of GBM cells. In vivo, EPS8 promotes tumor formation in nude mice. EPS8 can activate the PI3K/Akt signaling pathway to function. CONCLUSION: EP8S plays a role in the development of GBM and may be a potential therapeutic target for GBM.
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OBJECTIVES: To evaluate the effectiveness of long-term treatment of statins for chronic obstructive pulmonary disease (COPD), and to answer which one is better. METHODS: General meta-analysis was performed to produce polled estimates of the effect of mortality, inflammatory factors, and lung function index in COPD patients by the search of PubMed, Web of Science, Embase, and China National Knowledge Infrastructure for eligible studies. A network meta-analysis was performed to synthetically compare the effectiveness of using different statins in COPD patients. RESULTS: General meta-analysis showed that using statins reduced the risk of all-cause mortality, heart disease-related mortality and COPD acute exacerbation (AECOPD) in COPD patients, the RR (95% CI) were 0.72 (0.63,0.84), 0.72 (0.53,0.98) and 0.84 (0.79,0.89), respectively. And using statins reduced C-reactive protein (CRP) and pulmonary hypertension (PH) in COPD patients, the SMD (95% CI) were - 0.62 (- 0.52,-0.72) and - 0.71 (- 0.85,-0.57), respectively. Network meta-analysis showed that Fluvastatin (97.7%), Atorvastatin (68.0%) and Rosuvastatin (49.3%) had higher cumulative probability than other statins in reducing CRP in COPD patients. Fluvastatin (76.0%) and Atorvastatin (75.4%) had higher cumulative probability than other satins in reducing PH in COPD patients. CONCLUSIONS: Using statins can reduce the risk of mortality, the level of CRP and PH in COPD patients. In addition, Fluvastatin and Atorvastatin are more effective in reducing CRP and PH in COPD patients.
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Inhibidores de Hidroximetilglutaril-CoA Reductasas/administración & dosificación , Mediadores de Inflamación/metabolismo , Metaanálisis en Red , Enfermedad Pulmonar Obstructiva Crónica/tratamiento farmacológico , Enfermedad Pulmonar Obstructiva Crónica/metabolismo , Atorvastatina/administración & dosificación , Esquema de Medicación , Fluvastatina/administración & dosificación , Humanos , Mediadores de Inflamación/antagonistas & inhibidores , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Simvastatina/administración & dosificación , Factores de Tiempo , Resultado del TratamientoRESUMEN
The aim of the study was to evaluate on the effectiveness of screening modalities in the prevention of colorectal cancer (CRC) occurrence and deaths. General meta-analysis was performed to produce pooled estimates of the effect of CRC incidence and mortality using a search of PubMed, Web of Science, and the Cochrane Library for eligible studies from January 1992 to March 2016. A network meta-analysis was performed to synthetically compare the effectiveness of 5 frequently used screening modalities. A total of 44 studies with a focus on mortality from CRC using different screening methods were included. General meta-analysis showed that fecal immunohistochemical testing (FIT), flexible sigmoidoscopy (FS), colonoscopy, combination of fecal occult blood testing and FS screening respectively reduced CRC mortality by 59% (relative risk [RR], 0.41; 95% confidence interval [CI], 0.29-0.59), 33% (RR, 0.67; 95% CI, 0.58-0.78), 61% (RR, 0.39; 95% CI, 0.31-0.50), 38% (RR, 0.62; 95% CI, 0.42-0.91) compared with no screening, whereas guaiac fecal occult blood testing (gFOBT) reduced CRC-related mortality by 14% (RR, 0.86; 95% CI, 0.82-0.90). Subgroup analysis showed that summary estimates of reduction in distal CRC mortality and proximal CRC mortality were 26% (95% CI, 62%-89%) and 10% (95% CI, 83%-98%). A network meta-analysis revealed rank probability analysis in which the colonoscopy had a 94.6% probability of being the most effective examination to reduce CRC mortality. In addition, the network meta-analysis estimated odds ratio, which was a 79% reduction (95% CI, 0.09-0.60) in CRC mortality when screening with FIT was compared with annual or biennial gFOBT and colonoscopy was approximately 80% more effective than gFOBT for reducing CRC mortality (RR, 0.25; 95% CI, 0.13-0.54). Analysis of the effects of different screening methods showed that there was a significant reduction in the incidence of colon cancer, excluding gFOBT. This meta-analysis confirmed that gFOBT, FIT, FS, and colonoscopy were all effective in preventing CRC deaths and a major reduction in distal but not proximal CRC mortality was found. In addition, they were more effective in preventing CRC incidence in addition to gFOBT. The network meta-analysis suggests that colonoscopy is the most effective screening for preventing CRC deaths.
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Neoplasias Colorrectales/diagnóstico , Detección Precoz del Cáncer/métodos , Tamizaje Masivo/métodos , Colonoscopía/métodos , Neoplasias Colorrectales/epidemiología , Neoplasias Colorrectales/patología , Humanos , Incidencia , Metaanálisis en Red , Sangre Oculta , Sigmoidoscopía/métodosRESUMEN
Camellia flavida is an endangered species of yellow camellia growing in limestone mountains in southwest China. The current classification of C. flavida into two varieties, var. flavida and var. patens, is controversial. We conducted a genetic analysis of C. flavida to determine its taxonomic structure. A total of 188 individual plants from 20 populations across the entire distribution range in southwest China were analyzed using two DNA fragments: a chloroplast DNA fragment from the small single copy region and a single-copy nuclear gene called phenylalanine ammonia-lyase (PAL). Sequences from both chloroplast and nuclear DNA were highly diverse; with high levels of genetic differentiation and restricted gene flow. This result can be attributed to the high habitat heterogeneity in limestone karst, which isolates C. flavida populations from each other. Our nuclear DNA results demonstrate that there are three differentiated groups within C. flavida: var. flavida 1, var. flavida 2, and var. patens. These genetic groupings are consistent with the morphological characteristics of the plants. We suggest that the samples included in this study constitute three taxa and the var. flavida 2 group is the genuine C. flavida. The three groups should be recognized as three management units for conservation concerns.
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BACKGROUND AND AIMS: Our study aims to evaluate the efficacy and safety of long-term treatment of statins for coronary heart disease (CHD). METHODS: Efficacy outcomes included changes in blood lipids, risk of CHD mortality and all-cause mortality. Safety outcomes were evaluated by the risk of adverse events (AE). Bayesian network meta-analysis was used to compare the direct and indirect effects between different statins. RESULTS: The systematic review showed that levels of blood lipids decreased during statin treatment. High dose of atorvastatin was the most obvious treatment for the reduction of blood lipids. Network meta-analysis showed that statins were significantly more effective than the control in reducing the risk of CHD mortality (Odds Ratio (OR) 0.69, 95% CI 0.61-0.77) and all-cause mortality (OR 0.84, 95% CI 0.80-0.87). In terms of reducing the risk of CHD morality, fluvastatin (77.3%), atorvastatin (72.3%) and lovastatin (68.4%) had higher cumulative probability than other statins, which were more effective treatments for the reduction of CHD morality. In terms of reducing all-cause mortality, atorvastatin (78.6%), fluvastatin (77.1%) and pitavastatin (74.1%) had higher cumulative probability than other statins, which were more effective treatment for reducing the all-cause mortality. Compared with placebo, statins increased the incidence risk of muscle disease (OR 1.05, 95% CI 1.00-1.10) and kidney disease (OR 1.11, 95% CI 1.05-1.72). CONCLUSIONS: Statins significantly reduced levels of blood lipids, with a high dose of atorvastatin being the most effective in blood-lipid level modification. Statins reduced the risk of CHD mortality and all-cause mortality, with atorvastatin and fluvastatin being the most effective in reducing the risk of CHD mortality and all-cause mortality. Statins increased the risk of muscle disease and kidney damage.
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Enfermedad Coronaria/tratamiento farmacológico , Inhibidores de Hidroximetilglutaril-CoA Reductasas/farmacología , Anticolesterolemiantes/farmacología , Atorvastatina/farmacología , Teorema de Bayes , Enfermedad Coronaria/patología , Ácidos Grasos Monoinsaturados/farmacología , Fluvastatina , Humanos , Indoles/farmacología , Enfermedades Renales/tratamiento farmacológico , Lípidos/sangre , Lovastatina/análogos & derivados , Lovastatina/farmacología , Músculos/efectos de los fármacos , Metaanálisis en Red , Seguridad del Paciente , Pravastatina/farmacología , Quinolinas/farmacología , Ensayos Clínicos Controlados Aleatorios como Asunto , Simvastatina/farmacología , Resultado del TratamientoRESUMEN
PREMISE OF THE STUDY: Microsatellite markers were developed in the invasive species Bidens alba (Asteraceae) to assess its population structure and to facilitate tracking its expansion in China. ⢠METHODS AND RESULTS: Using 454 pyrosequencing, 20 microsatellite primer sets were developed for B. alba. The markers were tested on one population of B. alba (30 individuals) and one population of the closely related B. pilosa (30 individuals) in China. For B. alba, all of the markers were polymorphic, and the number of alleles per locus ranged from three to 32. The expected heterozygosity values were from 0.3787 to 0.9284, and the Shannon-Wiener index was from 0.6796 to 2.8401. ⢠CONCLUSIONS: These markers will be useful for investigating the genetic structure, genetic diversity, and invasion dynamics of B. alba and will also be useful in studies of B. pilosa.