RESUMO
This study identifies causes of rising arsenic (As) concentrations over 17 years in an inter-montane aquifer system located just north of the Trans-Mexican-Volcanic-Belt in the Mesa central physiographic region that is extensively developed by long-screened production wells. Arsenic concentrations increased by more than 10 µg/L in 14% (3/22) of re-sampled wells. Similarly, in a larger scale analysis wherein As concentrations measured in 137 wells in 2016 were compared to interpolated, baseline concentrations from 246 wells in 1999, As concentrations rose more than 10 µg/L in 30% of wells. Between 1999 and 2016, the percentage of all wells sampled in each basin-wide sampling campaign exceeding the World Health Organization's 10 µg/L drinking water limit increased from 38 to 64%. Principal Components Analysis (PCA), step-wise multiple regression, and Random Forest modeling (RF) revealed that high As concentrations are closely associated with high pH and temperature, and high concentrations of fluoride (F), molybdenum (Mo), lithium (Li), sodium (Na) and silica (Si), but low calcium (Ca) and nitrate (NO3) concentrations. Pumping-induced mixing with hot, geothermally impacted groundwater generates alkaline water through hydrolysis of silicate minerals. The rising pH converts oxyanion sorption sites from positive to negative releasing As (and Mo) to pore waters. The negative correlation between nitrate and As concentrations can be explained by conservative mixing of shallow, young groundwater with geothermally influenced groundwater. Therefore water carrying an anthropogenic contaminant dilutes water carrying geogenic contaminants. This process is enabled by long well screens. Over-exploitation of aquifers in geothermal regions for agriculture can drive As concentrations in water from production wells to toxic levels even as the total dissolved solids remain low.
Assuntos
Arsênio , Água Subterrânea , Poluentes Químicos da Água , Arsênio/análise , Monitoramento Ambiental , México , Poluentes Químicos da Água/análiseRESUMO
INTRODUCTION AND OBJECTIVES: Hepatocellular carcinoma (HCC) is the second most lethal cancer around the world, with poor survival rate and high metastasis rate in patients. Long noncoding RNAs (lncRNAs) have been reported to modulate the initiation and development of liver cancer. We aimed to investigate the role of lncRNA MAGI2-AS3 in HCC and underlying mechanisms. MATERIALS AND METHODS: The expression levels of MAGI2-AS3 in plasma of HCC patients and the control participants were measured by qPCR. Hep3B and MHCC97-H cells were transfected with MAGI2-AS3 and ROCK2 expression vectors. Cell migration and invasion of HCC cells transfected with the vectors were investigated by transwell assay. In addition, flow cytometry and western blot were performed for apoptosis detection. RESULTS: We found that MAGI2-AS3 was downregulated in plasma of early stage HCC patients compared to healthy controls. After surgical resection, the expression levels of MAGI2-AS3 were increased compared to pretreatment levels on the day of discharge. During the follow-up, MAGI2-AS3 was downregulated in patients developed distant recurrence, but not in other patients compared to the levels measured on the day of discharge. In HCC cells, overexpression of MAGI2-AS3 mediated the downregulation of ROCK2. Cell invasion and migration assay showed that overexpression of MAGI2-AS3 mediated the decreased cell invasion and migration rate, while ROCK2 played an opposite role and attenuated the effects of overexpression of MAGI2-AS3. CONCLUSION: Our study indicated that MAGI2-AS3 was downregulated in the distant recurrence of HCC after surgical resection and affected the invasion and migration of HCC cells via ROCK2.
Assuntos
Carcinoma Hepatocelular/cirurgia , Movimento Celular , Hepatectomia/efeitos adversos , Neoplasias Hepáticas/cirurgia , RNA Longo não Codificante/metabolismo , Quinases Associadas a rho/metabolismo , Adulto , Idoso , Carcinoma Hepatocelular/enzimologia , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/secundário , Estudos de Casos e Controles , Linhagem Celular Tumoral , Regulação para Baixo , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Hepáticas/enzimologia , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Masculino , Pessoa de Meia-Idade , Invasividade Neoplásica , RNA Longo não Codificante/genética , Transdução de Sinais , Resultado do Tratamento , Quinases Associadas a rho/genéticaRESUMO
BACKGROUND: Studies have demonstrated that transforming growth factor beta-1 (TGF-ß1) exhibits oncogenic activity in different types of cancer, including ovarian cancer (OC). However, its regulatory mechanism in OC and whether TGF-ß1 is involved in chemosensitivity regulation remains unclear. Thus, the aim of this study was to investigate the role of TGF-ß1 in OC. METHODS: The OC cell line SKOV3 was employed, and TGF-ß1 overexpression or knockdown vectors were constructed. The cell proliferation of SKOV3 was evaluated with the cell counting kit (CCK8) kit after treatment with different concentrations of cis-platinum. Western blot and protein immunoprecipitation were employed to detect changes in BRCA1 and Smad3 expression and their interactions. Tumor growth in nude mice was evaluated. RESULTS: The results showed that TGF-ß1 knockdown increased chemosensitivity by promoting BRCA1 expression and Smad3 phosphorylation. In vivo studies showed that TGF-ß1 knockdown significantly inhibited the growth of tumors, also by upregulating BRCA1 expression and Smad3 phosphorylation. CONCLUSION: Taken together, our results suggest that TGF-ß1 knockdown inhibits tumor growth and increases chemosensitivity by promotion of BRCA1/Smad3 signaling.
Assuntos
Regulação para Baixo/fisiologia , Genes BRCA1/fisiologia , Neoplasias Ovarianas/metabolismo , Proteína Smad3/fisiologia , Fator de Crescimento Transformador beta1/fisiologia , Animais , Western Blotting , Linhagem Celular Tumoral , Proliferação de Células , Células Cultivadas , Resistencia a Medicamentos Antineoplásicos/fisiologia , Feminino , Técnicas de Silenciamento de Genes , Humanos , Imuno-Histoquímica , Masculino , Camundongos Endogâmicos BALB C , Neoplasias Ovarianas/tratamento farmacológico , Neoplasias Ovarianas/patologia , Reação em Cadeia da Polimerase em Tempo Real , Proteína Smad3/análise , Fator de Crescimento Transformador beta1/análise , Proteínas Supressoras de Tumor/fisiologiaRESUMO
BACKGROUND: Studies have demonstrated that transforming growth factor beta-1 (TGF-ß1) exhibits oncogenic activity in different types of cancer, including ovarian cancer (OC). However, its regulatory mechanism in OC and whether TGF-ß1 is involved in chemosensitivity regulation remains unclear. Thus, the aim of this study was to investigate the role of TGF-ß1 in OC. METHODS: The OC cell line SKOV3 was employed, and TGF-ß1 overexpression or knockdown vectors were constructed. The cell proliferation of SKOV3 was evaluated with the cell counting kit (CCK8) kit after treatment with different concentrations of cis-platinum. Western blot and protein immunoprecipitation were employed to detect changes in BRCA1 and Smad3 expression and their interactions. Tumor growth in nude mice was evaluated. RESULTS: The results showed that TGF-ß1 knockdown increased chemosensitivity by promoting BRCA1 expression and Smad3 phosphorylation. In vivo studies showed that TGF-ß1 knockdown significantly inhibited the growth of tumors, also by upregulating BRCA1 expression and Smad3 phosphorylation. CONCLUSION: Taken together, our results suggest that TGF-ß1 knockdown inhibits tumor growth and increases chemosensitivity by promotion of BRCA1/Smad3 signaling.
Assuntos
Humanos , Animais , Masculino , Feminino , Neoplasias Ovarianas/metabolismo , Regulação para Baixo/fisiologia , Genes BRCA1/fisiologia , Proteína Smad3/fisiologia , Fator de Crescimento Transformador beta1/fisiologia , Neoplasias Ovarianas/patologia , Neoplasias Ovarianas/tratamento farmacológico , Imuno-Histoquímica , Células Cultivadas , Western Blotting , Resistencia a Medicamentos Antineoplásicos/fisiologia , Proteínas Supressoras de Tumor/fisiologia , Linhagem Celular Tumoral , Proliferação de Células , Proteína Smad3/análise , Fator de Crescimento Transformador beta1/análise , Técnicas de Silenciamento de Genes , Reação em Cadeia da Polimerase em Tempo Real , Camundongos Endogâmicos BALB CRESUMO
Introgression of exotic maize (Zea mays L.) germplasm is an effective approach to broadening the genetic base of Chinese germplasm. America is the center of maize origin and germplasm diversity. By analyzing general combining ability effects and heterosis responses among maize populations from the U.S., International Maize and Wheat Improvement Center (CIMMYT), and Brazil studied by different authors, 24 elite maize populations from America region, including eight U.S. populations, eight CIMMYT populations, and eight Brazilian populations, were identified as having high potential in China. Based on adaptation improvement, we suggest to introgress BSSS(R)C10, BS10(FR)C14, BS13(S)C9, BSK(HI)C8 Syn 3, BR106, Pop44(C8), and Pop45(C3) into Chinese heterotic group A, and introgress BS11(FR)C14, BS16(S)C3 Syn 2, BS29(R)C3, BSCB1(R)C14, BR105, and Pop42(C4) into Chinese heterotic group B by forming semi-exotic populations or pools, respectively, in order to broaden the Chinese germplasm base.