Image2_The buffering of a riverine carbonate system under the input of acid mine drainage: Example from a small karst watershed, southwest China.JPEG

In a karstic area affected by acid mine drainage (AMD), hydrochemical conditions, such as temperature, salinity, alkalinity, DIC, dissolved oxygen, and nutrients, may affect the buffering capacity of carbonate systems in freshwater systems. The resulting pH fluctuation is larger than that of a marine system. Therefore, this study focuses on the buffering of a riverine carbonate system under the input of AMD and discusses the variations in a series of buffering factors, including the Revelle factor, γDIC, γAlk βDIC, βAlk, ωDIC, and ωAlk. The results revealed that the Revelle factor could reflect the buffering process effectively; in addition, the maximum value of the Revelle factor appeared at pH = 8.5. The data points for pH greater than this value indicated that the Huatan River had the ability to absorb atmospheric CO2 in spring. Conversely, the data for pH less than this value reflected the buffering of H+ during CO2 degassing in summer and autumn. In winter, the data were around the maximum value, indicating the weakest buffering capacity. As a result, the dynamics of the carbonate system caused the most sensitive response to pH. In addition, the maximum Revelle factor value did not always indicate the carbonate system had reached equilibrium; the presence of strong CO2 degassing was still a possibility. Under acidic conditions, as CO2(aq) increased, the absolute values of γDIC, βDIC, ωDIC, and γAlk increased correspondingly, indicating the enhanced buffering capacity of H+ during CO2 degassing. Under the four Representative Concentration Pathways scenarios (RCPs) included in the IPCC’s fifth assessment report, the degassing rate of the Huatan River would decrease by 5%, 15%, 26%, or 48%, depending on the scenario. Even though the Huatan River revealed CO2 degassing characteristics in winter and spring under current conditions, it will eventually become a sink for atmospheric CO2 as atmospheric CO2 concentration increases. In this light, the carbon sink effect in karst areas will become increasingly important.</p

Table1_The buffering of a riverine carbonate system under the input of acid mine drainage: Example from a small karst watershed, southwest China.DOCX

In a karstic area affected by acid mine drainage (AMD), hydrochemical conditions, such as temperature, salinity, alkalinity, DIC, dissolved oxygen, and nutrients, may affect the buffering capacity of carbonate systems in freshwater systems. The resulting pH fluctuation is larger than that of a marine system. Therefore, this study focuses on the buffering of a riverine carbonate system under the input of AMD and discusses the variations in a series of buffering factors, including the Revelle factor, γDIC, γAlk βDIC, βAlk, ωDIC, and ωAlk. The results revealed that the Revelle factor could reflect the buffering process effectively; in addition, the maximum value of the Revelle factor appeared at pH = 8.5. The data points for pH greater than this value indicated that the Huatan River had the ability to absorb atmospheric CO2 in spring. Conversely, the data for pH less than this value reflected the buffering of H+ during CO2 degassing in summer and autumn. In winter, the data were around the maximum value, indicating the weakest buffering capacity. As a result, the dynamics of the carbonate system caused the most sensitive response to pH. In addition, the maximum Revelle factor value did not always indicate the carbonate system had reached equilibrium; the presence of strong CO2 degassing was still a possibility. Under acidic conditions, as CO2(aq) increased, the absolute values of γDIC, βDIC, ωDIC, and γAlk increased correspondingly, indicating the enhanced buffering capacity of H+ during CO2 degassing. Under the four Representative Concentration Pathways scenarios (RCPs) included in the IPCC’s fifth assessment report, the degassing rate of the Huatan River would decrease by 5%, 15%, 26%, or 48%, depending on the scenario. Even though the Huatan River revealed CO2 degassing characteristics in winter and spring under current conditions, it will eventually become a sink for atmospheric CO2 as atmospheric CO2 concentration increases. In this light, the carbon sink effect in karst areas will become increasingly important.</p

Additional file 1: of PD-1 deficiency promotes TFH cells expansion in ITV-immunized mice by upregulating cytokines secretion

Figure S1. The parasitemia in ITV-immunized mice after the final injection of CQ. After the last CQ injection, the parasitemia was recorded in four groups. The data are presented as the mean Âą SD. Data were compared with the nonparametric Mann-Whitney test. (TIF 4538 kb

Comparative Proteome Analysis of Brown Adipose Tissue in Obese C57BL/6J Mice Using iTRAQ-Coupled 2D LC-MS/MS

<div><p>High-fat diet (HFD) leads to the development of obesity accompanied by insulin resistance, which increases the risk of type 2 diabetes mellitus and cardiovascular disease. Brown adipose tissue (BAT) plays an essential role in energy metabolism, thus it will give us promising treatment targets through elucidating underlying mechanisms of BAT in obesity. In this study, female C57BL/6J mice were fed HFD or normal diet (ND) for 22 weeks. Hyperinsulinemic-euglycemic clamp was performed to evaluate insulin sensitivity, which was independently correlated with obesity. Using isobaric tag for relative and absolute quantification (iTRAQ) coupled with 2D LC-MS/MS, we quantitated 3048 proteins in BAT. As compared HFD with ND, we obtained 727 differentially expressed proteins. Functional analysis found that those proteins were mainly assigned to the pathway of mitochondrial function. In this pathway, carnitine O-palmitoyltransferase 2 (CPT2), uncoupling protein 1 (UCP1) and apoptosis-inducing factor 1 (AIF1) were up-regulated significantly by HFD, and they were confirmed by western blotting. The results indicated that HFD might induce the apoptosis of brown adipocytes via the up-regulated AIF1. Meanwhile, HFD also stimulated fatty acid β-oxidation and raised compensatory energy consuming through the increases of CPT2 and UCP1, respectively. However, the apoptosis of brown adipocytes might weaken the compensatory energy expenditure, and finally contribute to overweight/obesity. So, preventing the apoptosis of brown adipocytes may be the key target to treat obesity.</p></div

Reactive Oxygen Species are Essential for Placental Angiogenesis During Early Gestation

Background. Preeclampsia (PE) is associated with insufficient placental perfusion attributed to maldevelopment of the placental vasculature. Reactive oxygen species (ROS) are implicated in angiogenesis, but their regulatory effects and mechanisms in placental vascular development remain unclear. Methods. Placental oxidative stress was determined throughout gestation by measuring 4-hydroxynonenal (4HNE) and malondialdehyde (MDA). The antioxidant MitoQ was administered to pregnant mice from GDs 7.5 to 11.5; placental morphology and angiogenesis pathways were examined on GDs 11.5 and 18.5. Moreover, we established a mouse mFlt-1-induced PE model and assessed blood pressure, urine protein levels, and placental vascular development on GDs 11.5 and 18.5. Human umbilical vein endothelial cells (HUVECs) were treated with various H2O2 concentrations to evaluate cell viability, intracellular ROS levels, and tube formation capability. MitoQ, an AKT inhibitor and an ERK1/2 inhibitor were applied to validate the ROS-mediated mechanism regulating placental angiogenesis. Results. First-trimester placentas presented significantly higher MDA and 4HNE levels. MitoQ significantly reduced the blood vessel density and angiogenesis pathway activity in the placenta on GDs 11.5 and 18.5. Serum sFlt-1 levels were elevated, and we observed poor placental angiogenesis and PE-like symptoms in cases with mFlt-1 overexpression. Moderate H2O2 treatment promoted HUVEC proliferation and angiogenesis, whereas these improvements were abolished by MitoQ, AKT inhibitor, or ERK1/2 inhibitor treatment. Conclusions. Moderate ROS levels are essential for placental angiogenesis; diminishing ROS with potent antioxidants during placentation decreases placental angiogenesis and increases PE risk. Therefore, antioxidant therapy should be considered carefully for normal pregnant women during early gestation

Body weight and metabolic status of mice were affected by HFD.

<p>HFD significantly altered the body weight (A), and induced glucose intolerance (B) in C57BL/6J mice. Black circle = Normal diet group, black squares = High-fat diet group. Data are mean ± SEM (n = 6), *p<0.05, **p<0.01, ***p<0.001.</p

Fold change of BAT proteins between HFD and ND group (mean ± SEM) measured by iTRAQ coupled with LC-MS/MS and western blotting (normalized to β-actin).

<p>CPT2, Carnitine O-palmitoyltransferase 2; UCP1, uncoupling protein 1</p><p>AIF1, apoptosis-inducing factor 1.</p><p>Fold change of BAT proteins between HFD and ND group (mean ± SEM) measured by iTRAQ coupled with LC-MS/MS and western blotting (normalized to β-actin).</p

Differential proteins between HFD and ND group in BAT were analyzed through the PANTHER classification system.

<p>(A) Cell Component of whole genome, BAT protein profile and the differentially expressed proteins in BAT. (B) Molecular Function assigned to whole genome, BAT protein profile and the differentially expressed proteins in BAT. (C) Biological processes assigned to whole genome, BAT protein profile and the differentially expressed proteins in BAT.</p

Body weight, adipose tissue weight and metabolic profile of female C57BL/6J mice fed ND or HFD for 22 weeks (mean ± SEM).

<p>Body weight, adipose tissue weight and metabolic profile of female C57BL/6J mice fed ND or HFD for 22 weeks (mean ± SEM).</p

Proposed schematic diagram of BAT in obesity and impaired insulin sensitivity induced by HFD.

<p>It is likely that HFD activates the catabolism of fatty acid and the compensatory energy expenditure for anti-obesity through the up regulation of CPT2 and UCP1 in BAT, respectively. In addition, HFD also induces the apoptosis of brown adipocytes via the up regulation of AIF1, to weaken its anti-obesity effect. Attenuating compensatory action of BAT might cause imbalance of energy metabolism in BAT and WAT, and contribute to the development of obesity and impaired insulin resistance.</p