Significant reduction of renal mass triggers a chain of events that result in glomerular hypertension/hyperfiltration, proteinuria, glomerulosclerosis, tubulointerstitial injury, and end-stage renal disease. These events are mediated by a constellation of hemodynamic, oxidative, and inflammatory reactions that are, in part, driven by local AT 1 receptor (AT 1 r) activation by angiotensin II (Ang II). Here we explored the effects of 5/6 nephrectomy with and without AT 1 r blockade (losartan for 8 weeks) on AT 1 r and AT 2 r and Ang II-positive cell count, pathways involved in oxidative stress and inflammation [NAD(P)H oxidase, nuclear factor B (NFB), 12-lipooxygenase, cyclooxygenase (COX)-1, COX-2, monocyte chemoattractant protein (MCP)-1, plasminogen activator inhibitor (PAI)-1, renal T cell, and macrophage infiltration] as well as renal function and structure. The untreated group exhibited hypertension, deterioration of renal function and structure, reduced or unchanged plasma renin activity, aldosterone concentration, marked up-regulations of AT 1 r (250%), Ang II-expressing cell count (Ͼ20-fold), NAD(P)H oxidase subunits (gp91 phox, p22 phox , and P47 phox ; 20 -40%), COX-2 (250%), 12-lipooxygenase (100%), MCP-1 (400%), and PAI-1 (Ͼ20-fold), activation of NFB, and interstitial infiltrations of T cells and macrophages in the remnant kidneys. AT 1 r blockade attenuated the biochemical and histological abnormalities, prevented hypertension, and decelerated deterioration of renal function and structure. Thus, the study demonstrated a link between up-regulation of Ang II/AT 1 r system and oxidative stress, inflammation, hypertension, and progression of renal disease in rats with renal mass reduction.Significant reduction in renal mass by subtotal nephrectomy or by various disease processes triggers a chain of events that culminates in progressive glomerulosclerosis, tubulointerstitial injury, proteinuria, and end-stage renal disease (Remuzzi et al., 2006). Progressive deterioration of the remnant/diseased kidney function and structure is associated with and largely mediated by profound alteration of renal hemodynamics, inflammation, and oxidative stress (Mackenzie et al., 2000). In this context, renal mass reduction results in glomerular capillary hypertension and glomerular hyperfiltration, which play a major role in the pathogenesis of proteinuria and glomerulosclerosis (Hostetter et al., 2001). This assertion is supported by the observations that prevention/alleviation of the maladaptive hemodynamic alterations by lowering dietary protein or blocking renin-angiotensin system (RAS) decelerates progression of renal disease (Nickenig and Harrison, 1994;Mackenzie et al., 2000). In addition to the hemodynamic factors, accumulation of the inflammatory cells plays a major part in progression of renal disease (Chow et al., 2004;Rodríguez-Iturbe et al., 2004b). This supposition is consistent with the demonstration that inhibition of leukocyte recruitment by chemokine receptor antagonists and treatment with immun...

Background: Chronic consumption of a high-salt diet causes hypertension (HTN) and renal injury in Dahl salt-sensitive (SSR) but not salt-resistant rats (SRR). These events are, in part, mediated by oxidative stress and inflammation in the kidney and vascular tissues. Activation of the angiotensin II type 1 (AT₁) receptor plays an important role in the pathogenesis of oxidative stress and inflammation in many hypertensive disorders. However, the systemic renin-angiotensin system (RAS) is typically suppressed in salt-sensitive HTN. This study was designed to test the hypothesis that differential response to a high-salt diet in SSR versus SRR may be related to upregulation of tissue RAS and pathways involved in inflammation and reactive oxygen species (ROS) production. Methods and Results: SSR and SRR were studied 3 weeks after consumption of high- (8%) or low-salt (0.07%) diets. The SSR consuming a low-salt diet exhibited significant increases in AT₁ receptor, cyclooxygenase (COX) 2, plasminogen activator inhibitor (PAI) and phospho-IĸB in the kidney as compared to those found in SRR. The high-salt diet resulted in severe HTN and proteinuria (in SSR but not SRR) and marked elevations of renal tissue monocyte chemoattractant protein 1, p22^phox, NADPH oxidase subunit 4, angiotensin-II-positive cell count, infiltrating T cells and macrophages and further increases in AT₁ receptor, COX-2, PAI-1 and phospho-IĸB in the SSR group. The high-salt diet significantly lowered plasma renin activity (PRA) in SRR but not in the SSR. COX-1 abundance was similar on the low-salt diet and rose equally with the high-salt diet in both groups. Among subgroups of animals fed the low-salt diet, kidney glutathione peroxidase (GPX) abundance was significantly lower in the SSR than SRR. The high-salt diet raised GPX and mitochondrial superoxide dismutase (SOD) abundance in the SRR kidneys but failed to do so in SSR. Cu/Zn-SOD abundance was similar in the subgroups of SSR and SRR fed the low-salt diet. The high-salt diet resulted in downregulation of Cu/Zn-SOD in SSR but not SRR. Conclusions: Salt sensitivity in the SSR is associated with upregulations of the intrarenal angiotensin system, ROS-generating and proinflammatory/profibrotic proteins and an inability to raise antioxidant enzymes and maximally suppress PRA in response to high salt intake. These events can contribute to renal injury with high salt intake in SSR.

Surface enhanced Raman spectroscopy based biosensor with a microneedle array for minimally invasive in vivo glucose measurements

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The influence of B2O3 on the viscosity of high Ti-bearing BF slag is studied under Ar atmosphere from 1 773 K (1 500°C) to about 1 593 K (1 320°C). The results show that the addition of B2O3 can decrease the viscosity of high Ti-bearing BF Slag containing UPC, consequently improve its fluidity. With the existence of 1.5% UPC, when the content of B2O3 increased from 0 to 4.1%, the volume fraction of perovskite decreased from 7.7% to 1.6% at 1 610 K. Meanwhile, the liquidus temperatures decreased from 1 619 K to 1 613 K. At a lower temperature, B2O3 was easy to form a eutectic and decreased the viscosity of molten slag. At a higher temperature, some tetrahedron [BO4] 5-changed into triangle [BO3] 3-which would disintegrate the chains/molecules of molten matrix and decreased its viscosity.KEY WORDS: Ti-bearing blast furnace slag; viscosity; B2O3.

Pain is a highly subjective experience. Self-report is the gold standard for pain assessment in clinical practice, but it may not be available or reliable in some populations. Neuroimaging data, such as electroencephalography (EEG) and functional magnetic resonance imaging (fMRI), have the potential to be used to provide physiology-based and quantitative nociceptive pain assessment tools that complements self-report. However, existing neuroimaging-based nociceptive pain assessments only rely on the information in pain-evoked brain activities, but neglect the fact that the perceived intensity of pain is also encoded by ongoing brain activities prior to painful stimulation. Here, we proposed to use machine learning algorithms to decode pain intensity from both pre-stimulus ongoing and post-stimulus evoked brain activities. Neural features that were correlated with intensity of laser-evoked nociceptive pain were extracted from high-dimensional pre- and post-stimulus EEG and fMRI activities using partial least-squares regression (PLSR). Further, we used support vector machine (SVM) to predict the intensity of pain from pain-related time-frequency EEG patterns and BOLD-fMRI patterns. Results showed that combining predictive information in pre- and post-stimulus brain activities can achieve significantly better performance in classifying high-pain and low-pain and in predicting the rating of perceived pain than only using post-stimulus brain activities. Therefore, the proposed pain prediction method holds great potential in basic research and clinical applications.

Microbial fuel cells (MFCs) are a promising technology that converts chemical energy into electricity. However, up to now only few MFCs have been powered by gas fuels, such as methane, and their limited performance is still challenged by the low solubility and bioavailability of gases. Here, we developed a gas diffusion cloth (GDC) anode to significantly enhance the performance of methane-powered MFCs. The GDC anode was constructed by simply coating waterproof GORE-TEX cloth with conductive carbon cloth in one step. After biofilm enrichment, the GDC anodes obtained a methane-dependent current up to 1130.2 mA m −2 , which was 165.2 times higher than conventional carbon cloth (CC) anodes. Moreover, MFCs equipped with GDC anodes generated a maximum power density of 419.5 mW m −2 . Illumina high-throughput sequencing revealed that the GDC anode biofilm was dominated mainly by Geobacter, in contrast with the most abundant Methanobacterium in planktonic cells. It is hypothesized that Methanobacterium reversed the methanogenesis process by transferring electrons to the anodes, and Geobacter generated electricity via the intermediates (e.g., acetate) of anaerobic methane oxidation. Overall, this work provides an effective route in preparing facile and cost-effective anodes for high-performance methane MFCs.

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