RESUMO
Previous research concerning the effect of land reclamation on seawater intrusion mostly focused on the modification of the saltwater wedge and the dynamics of freshwater-saltwater interface after land reclamation, utilizing both analytical and numerical models. So far, the impact of land reclamation on the recharging and accumulation of land-based pollutants such as nitrate has been disregarded. In this work, we are the first to examine the impact of land reclamation on the discharge of nitrate together with the movement of saltwater. The influence of reclamation area and filled soil permeability on nitrate pollution and saltwater redistribution is revealed using a series of field-scale simulations based on numerical models including density flow combined with reactive transport. It was discovered that land reclamation might, on the one hand, result in a substantial redistribution based on the initial saltwater-freshwater interface and, on the other hand, significantly modify the nitrate discharge. This in total would drastically alter the distribution of nitrate in the subsurface. The reclamation area and the permeability of the reclamation material are the two elements that determine the amount of variance. For the cases with hydraulic conductivities increasing from 5 to 50 m/d, the salt mass reduction rate showed a trend of first increased (84.78 %-95.58 %) and then slowly decreased (95.58 %-74.01 %). Meanwhile, the nitrate reduction rate decreased from 80.08 % to 12.93 %, when hydraulic conductivities increased from 5 to 50 m/d. It was also found that coastal nitrate accumulation was always intensified with the enlargement of the reclamation area. Finally, we are able to assist engineers in optimizing their land reclamation strategies by taking into account both the degree of saltwater intrusion and nitrate enrichment.
RESUMO
Perioperative neurocognitive disorder (PND) is a common complication that lacks effective prevention and treatment measures. Neuroinflammation is considered to be one of the important mechanisms of PND. In this study, we investigated the effect and mechanism of anthocyanins (ANT), a natural plant ingredient, on postoperative cognition and neuroinflammation. Mice were subjected to laparotomy and treated with ANT (50-100â¯mg/kg, orally) 4â¯weeks before surgery and then once per day for 7â¯days after surgery. Morris water maze and fear conditioning tests were used to evaluate learning and memory function. Western blotting, RT-PCR and immunofluorescence were used to test the neuroprotective effects and mechanism of ANT. The results showed that ANT improved learning and memory in mice after surgery. ANT also inhibited MLK3 activation and its downstream JNK and p38 MAPK signaling cascades. Moreover, the inhibitor of MLK3 could mimic the effects of ANT. In addition, treatment with ANT significantly reduced neuroinflammation and microglia activation. In conclusion, MLK3 represents a novel target in surgery-induced neuroinflammation and cognitive dysfunction. ANT could inhibit the activation of MLK3 and be a promising agent for the prevention and treatment of PND.
Assuntos
Antocianinas/administração & dosagem , Encefalite/metabolismo , Encefalite/prevenção & controle , MAP Quinase Quinase Quinases/metabolismo , Transtornos Neurocognitivos/metabolismo , Transtornos Neurocognitivos/prevenção & controle , Fármacos Neuroprotetores/administração & dosagem , Animais , Modelos Animais de Doenças , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Aprendizagem/efeitos dos fármacos , Masculino , Memória/efeitos dos fármacos , Camundongos , Período Perioperatório , Transdução de Sinais/efeitos dos fármacos , MAP Quinase Quinase Quinase 11 Ativada por MitógenoRESUMO
In geotechnical engineering seepage of diaphragm walls is an important issue which may cause engineering disasters. It is therefore of great significance to develop reliable monitoring technology to monitor the leakage. The purpose of this study is to explore the application of a distributed optical fiber temperature measurement system in leakage monitoring of underground diaphragm walls using 1 g model tests. The principles of seepage monitoring based on distributed optical fiber temperature measurement technology are introduced. Fiber with heating cable was laid along the wall to control seepage flow at different speeds. The temperature rise of the fiber during seepage was also recorded under different heating power conditions. In particular the effect of single variables (seepage velocity and heating power) on the temperature rise of optical fibers was discussed. Test results indicated that the temperature difference between the seepage and non-seepage parts of diaphragm wall can be monitored well using fiber-optic external heating cable. Higher heating power also can improve the resolution of fiber-optic seepage. The seepage velocity had a linear relationship with the final stable temperature after heating, and the linear correlation coefficient increases with the increase of heating power. The stable temperature decreased with the increase of flow velocity. The findings provide a basis for quantitative measurement and precise location of seepage velocity of diaphragm walls.
RESUMO
Diabetic peripheral neuropathy (DPN) is one of the most common complications of diabetes, but currently no protein biomarkers have been introduced into clinical diagnosis, especially among early-stage diabetic patients. Our previous study in animal model showed Toll-like receptor (TLR) 4 and its downstream signaling molecules were associated with DPN. To assess the diagnostic values of TLR4, TNF-α, and IL-6 as biomarkers, here we detected their expressions in peripheral blood from normal controls, type 2 diabetic and DPN subjects. Both TLR4 mRNA and protein expressions increased significantly in DPN compare with both diabetic and control subjects. The protein levels of TNF-α and IL-6 were also raised significantly and correlated with TLR4 expression. Receiver operating characteristics (ROC) analysis suggested TLR4 and TNF-α had great potential advantages to predict the progression of neuropathy, the risks of DPN were increased in subjects with higher TLR4 (odds ratio: 5.27; 95% CI: 1.02-26.40) and TNF-α (odds ratio: 12.67; 95% CI: 2.35-68.22). These findings demonstrated TLR4 and TNF-α could be potential sensitive diagnostic biomarkers for DPN in both general population and type 2 diabetic subjects.
Assuntos
Diabetes Mellitus Tipo 2/sangue , Neuropatias Diabéticas/diagnóstico , Receptor 4 Toll-Like/sangue , Fator de Necrose Tumoral alfa/sangue , Biomarcadores/sangue , Estudos de Casos e Controles , Neuropatias Diabéticas/sangue , Feminino , Humanos , Interleucina-6/sangue , Masculino , Pessoa de Meia-IdadeRESUMO
SMND-309, a novel compound named (2E)-2-{6-[(E)-2-carboxylvinyl]-2,3-dihydroxyphenyl}-3-(3,4-dihydroxyphenyl) propenoic acid, is a new derivate of salvianolic acid B. The present study was conducted to investigate whether SMND-309 has a protective effect on brain injury after focal cerebral ischemia, and if it did so, to investigate its effects on brain mitochondria. Adult male SD rats were subjected to middle cerebral artery occlusion (MCAO) by bipolar electro-coagulation. Behavioral tests and brain patho-physiological tests were used to evaluate the damage to central nervous system. Origin targets including mitochondria production of reactive oxygen species, antioxidant potentia, membrane potential, energy metabolism, mitochondrial respiratory enzymes activities and mitochondria swelling degree were evaluated. The results showed that SMND-309 decreased neurological deficit scores, reduced the number of dead hippocampal neuronal cells in accordance with its depression on mitochondria swelling degree, reactive oxygen species production, improvements on mitochondria swelling, energy metabolism, membrane potential level and mitochondrial respiratory chain complex activities. All of these findings indicate that SMND-309 exerted potent neuroprotective effects in the model of permanent cerebral ischemia, contributed to its protections on brain mitochondrial structure and function.