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Introduction:ob/ob mice are a leptin-deficient type 2 diabetes mellitus model, which, on a BTBR background, mimics the glomerular pathophysiology of diabetic nephropathy (DN). Since leptin deficiency reduces blood pressure (BP) and endothelial nitric oxide synthase (eNOS) lowers BP and is kidney protective, we attempted to develop a more robust DN model by introducing eNOS deficiency in BTBR ob/ob mice. Methods:Six experimental groups included littermate male and female BTBR ob/ob or wild-type for ob (control) as well as wild-type (WT), heterozygote (HET), or knockout (KO) for eNOS. Systolic BP (by automated tail-cuff) and GFR (by FITC-sinistrin plasma kinetics) were determined in awake mice at 27–30 weeks of age, followed by molecular and histological kidney analyses. Results:Male and female ob/ob WT presented hyperglycemia and larger body and kidney weight, GFR, glomerular injury, and urine albumin to creatinine ratio (UACR) despite modestly lower BP versus control WT. These effects were associated with a higher tubular injury score and renal mRNA expression of NGAL only in males, whereas female ob/ob WT unexpectedly had lower KIM-1 and COL1A1 expression versus control WT, indicating sex differences. HET for eNOS did not consistently alter BP or renal outcome in control or ob/ob. In comparison, eNOS KO increased BP (15–25 mm Hg) and worsened renal markers of injury, inflammation and fibrosis, GFR, UACR, and survival rates, as observed in control and, more pronouncedly, in ob/ob mice and independent of sex. Conclusions:Deletion, but not heterozygosity, of eNOS raises blood pressure and aggravates nephropathy in BTBR ob/ob mice.

Titanium-oxo cluster (TOC)-based metal–organic frameworks (MOFs) have received considerable attention in recent years due to their ability to expand the application of TOCs to fields that require highly stable frameworks. Herein, a new cyclic TOC formulated as [Ti6O6(OiPr)8(TTFTC)(phen)2]2(1, where TTFTC = tetrathiafulvalene tetracarboxylate and phen = phenanthroline) was crystallographically characterized. TOC 1takes a rectangular ring structure with two phen-modified Ti6clusters as the width and two TTFTC ligands as the length. An intracluster ligand-to-ligand (TTF-to-phen) charge transfer in 1was found for TOCs for the first time. Compound 1undergoes topotactic conversion to generate stable TOC-MOF P1, in which the rectangular framework in 1formed by a TOC core and ligands is retained, as verified by comprehensive characterization. P1shows an efficient and rapid selective adsorption capacity for cationic dyes. The experimental adsorption capacity (qex) of P1reaches a value of up to 789.2 mg/g at 298 K for the crystal violet dye, which is the highest among those of various adsorbents. The calculated models are first used to reveal the structure–property relationship of the cyclic host to different guest dyes. The results further confirmed the host MOF structure of P1.

The development of new polymer-based room-temperature phosphorescence materials is of great significance. By a special molecule design and a set of feasible property-enhancing strategies, coumarin derivatives (CMDs, Ma–Mf) were doped into polyvinyl alcohol (PVA), polyacrylamide (PAM), corn starch, and polyacrylonitrile (PAN) as information anti-counterfeiting. CMDs-doped PVA and CMDs-doped corn starch films showed long-lived phosphorescence emissions up to 1246 ms (Ma-PVA) and 697 ms (Ma-corn starch), reaching over 10 s afterglow under naked eye observation under ambient conditions. Significantly, CMDs-doped PAM films can display long-lived phosphorescence emissions in a wide temperature range (100–430 K). For example, the Me-PAM film has a phosphorescence lifetime of 16 ms at 430 K. The use of PAM with the strong polarity and rigidity has expanded the temperature range of long-life polymer-based phosphorescent materials. The present long-lived phosphorescent systems provide the possibility for developing new polymer-based organic afterglow materials with robust phosphorescence.

Metal–organic frameworks (MOFs) have attracted noticeable attention as promising candidates for electrochemical energy storage. However, the lack of electrical conductivity and the weak stability of most MOFs result in poor electrochemical performances. Here, a tetrathiafulvalene (TTF)-based complex, formulated as [(CuCN)2(TTF(py)4)] (1) (TTF-(py)4= tetra(4-pyridyl)-TTF), is assembled by in situ generation of coordinated CN–from a nontoxic source. Single-crystal X-ray diffraction analysis reveals that compound 1possesses a two-dimensional layered planar structure, which is further stacked in parallel to form a three-dimensional supramolecular framework. The planar coordination environment of 1is the first example of a TTF-based MOF. Attributed to the unique structure and redox TTF ligand, the electrical conductivity of 1is significantly increased by 5 orders of magnitude upon iodine treatment. The iodine-treated 1(1-ox) electrode displays typical battery-type behavior through electrochemical characterizations. The supercapattery based on the 1-oxpositrode and AC negatrode presents a high specific capacity of 266.5 C g–1at a specific current of 1 A g–1with a remarkable specific energy of 62.9 Wh kg–1at a specific power of 1.1 kW kg–1. The excellent electrochemical performance of 1-oxis one of the best among those reported supercapatteries, demonstrating a new strategy for developing MOF-based electrode materials.

Poor electrical conductivity and instability of metal–organic frameworks (MOFs) have limited their energy storage and conversion efficiency. In this work, we report the application of oxidatively doped tetrathiafulvalene (TTF)-based MOFs for high-performance electrodes in supercapatteries. Two isostructural MOFs, formulated as [M(py-TTF-py)(BPDC)]·2H2O (M = NiII(1), ZnII(2); py-TTF-py = 2,6-bis(4′-pyridyl)TTF; H2BPDC = biphenyl-4,4′-dicarboxylic acid), are crystallographically characterized. The structural analyses show that the two MOFs possess a three-dimensional 8-fold interpenetrating diamond-like topology, which is the first example for TTF-based dual-ligand MOFs. Upon iodine treatment, MOFs 1and 2are converted into oxidatively doped 1-oxand 2-oxwith high crystallinity. The electrical conductivity of 1-oxand 2-oxis significantly increased by six∼seven orders of magnitude. Benefiting from the unique structure and the pronounced development of electrical conductivity, the specific capacities reach 833.2 and 828.3 C g–1at a specific current of 1 A g–1for 1-oxand 2-ox, respectively. When used as a battery-type positrode to assemble a supercapattery, the AC∥1-oxand AC∥2-ox(AC = activated carbon) present an energy density of 90.3 and 83.0 Wh kg–1at a power density of 1.18 kW kg–1and great cycling stability with 82% of original capacity and 92% columbic efficiency retention after 10,000 cycles. Ex situ characterization illustrates the ligand-dominated mechanism in the charge/discharge processes. The excellent electrochemical performances of 1-oxand 2-oxare rarely reported for supercapatteries, illustrating that the construction of unique highly dense and robust structures of MOFs followed by postsynthetic oxidative doping is an effective approach to fabricate MOF-based electrode materials.

The tobacco whitefly, Bemisia tabaci, is a notorious pest affecting various crops globally, and it exhibits high levels of resistance to various insecticides. Afidopyropen is a recently commercialized pyropene insecticide for B. tabacicontrol with high selectivity and a novel mode of action. We previously identified a high level of afidopyropen resistance in a field-collected population after selection in the lab, and named it the HD-Afi strain. In the present study, minimal cross-resistance in the HD-Afi strain was found between afidopyropen and other common chemical agents. However, the P450 enzyme activity in HD-Afi was 2.18 times the level in susceptible strain HD-S. Expression analysis revealed that two of 12 candidate P450 genes, namely CYP6DW3and CYP4C64, were significantly up-regulated in HD-Afi. Silencing CYP6DW3and CYP4C64by RNA interference (RNAi) substantially increased the susceptibility of whitefly adults, confirming their involvement in afidopyropen resistance. Homology modeling and molecular docking analyses demonstrated stable binding of afidopyropen to CYP6DW3and CYP4C64, with binding free energies of -6.87 and -6.11 kcal mol-1, respectively. The findings of this study suggest that the induction of CYP6DW3and CYP4C64facilitates afidopyropen detoxification, contributing to the development of resistance in B. tabaci.

Exogenous erythropoietin (EPO) is used to treat anemia in patients with chronic kidney disease (CKD). Concerns about the possible adverse effect of EPO on the progression of CKD have been raised owing to nonerythroid cell effects. We investigated the effects of low-dose EPO, independent of correcting anemia, on existing glomerulosclerosis. Adult mice underwent 5/6 nephrectomy and were randomized into the following 4 groups at week 8 after surgery: vehicle (VEH), losartan (angiotensin II type 1 receptor blocker [ARB]), darbepoetin-α (DA), or combination (DA+ARB). Four weeks later, mice were euthanized, followed by evaluation of renal structure and function. Glomerular endothelial cells and podocytes were cultured to evaluate the effects of DA on cell migration, apoptosis, and Akt signaling. ARB reduced blood pressure, albuminuria, and the level of serum creatinine and increased hematocrit compared with VEH, whereas low-dose DA only reduced the level of serum creatinine. Combination treatment showed a trend to increase hematocrit and survival compared with ARB alone. Combination treatment but not ARB alone significantly reduced the progression of glomerulosclerosis compared with VEH. Low-dose DA resulted in more preserved glomerular and peritubular capillary endothelial cells with increased p-Akt and even further endothelial cell preservation in combination with ARB. In cultured glomerular endothelial cells, angiotensin II induced more apoptosis, reduced migration, and decreased p-Flk1, a receptor for the proangiogenic vascular endothelial growth factor. DA counteracted these injuries and increased p-Akt, a key factor in angiogenesis and cell survival. DA also protected cultured podocytes against transforming growth factor β–induced apoptosis and synaptopodin loss. Low-dose EPO directly protects glomerular and peritubular endothelial cells via Akt phosphorylation. Therefore, treatment using a combination of low-dose EPO and ARB results in less progression of glomerulosclerosis in an experimental CKD model.

We previously observed that high-dose angiotensin receptor blocker (ARB) can induce regression of existing glomerulosclerosis. We also found that proliferator-activated recepto-γ (PPARγ) agonist can attenuate glomerulosclerosis in a nondiabetic model of kidney disease, with specific protection of podocytes. We now assessed effects of combination therapy with ARB and pioglitazone on established glomerulosclerosis. Sprague-Dawley male rats underwent 5/6 nephrectomy (5/6 Nx) at week 0 and renal biopsy at week 8. Rats were randomized to groups with equal starting moderate glomerulosclerosis, and treated with ARB, PPARγ agonist (pioglitazone), combination or vehicle from weeks 8 to 12. Body weight, systolic blood pressure (SBP), and urinary protein (UP) were measured at intervals. In rats with established sclerosis, SBP, UP, and GS were equal in all groups at week 8 before treatment by study design. Untreated control rats had hypertension, decreased GFR, and progressive proteinuria and glomerulosclerosis at week 12. Only combination therapy significantly ameliorated hypertension and proteinuria. ARB alone or pioglitazone alone had only numerically lower SBP and UP than vehicle at week 12. Both pioglitazone alone and combination had significantly less decline in GFR than vehicle. Combination-induced regression of glomerulosclerosis in more rats from weeks 8 to 12 than ARB or pioglitazone alone. In parallel, combination treatment reduced plasminogen activator inhibitor-1 expression and macrophage infiltration, and preserved podocytes compared with vehicle. These results were linked to increased AT2receptor and Mas1 mRNA in the combination group. PPARγ agonists in combination with ARB augment regression of glomerulosclerosis, with downregulation of injurious RAAS components vs PPARγ alone, with increased anti-fibrotic/healing RAAS components, enhanced podocyte preservation, and decreased inflammation and profibrotic mechanisms.

We previously observed that high-dose angiotensin receptor blocker (ARB) can induce regression of existing glomerulosclerosis. We also found that proliferator-activated recepto-γ(PPARγ) agonist can attenuate glomerulosclerosis in a nondiabetic model of kidney disease, with specific protection of podocytes. We now assessed effects of combination therapy with ARB and pioglitazone on established glomerulosclerosis. Sprague-Dawley male rats underwent 5/6 nephrectomy (5/6 Nx) at week 0 and renal biopsy at week 8. Rats were randomized to groups with equal starting moderate glomerulosclerosis, and treated with ARB, PPARγagonist (pioglitazone), combination or vehicle from weeks 8 to 12. Body weight, systolic blood pressure (SBP), and urinary protein (UP) were measured at intervals. In rats with established sclerosis, SBP, UP, and GS were equal in all groups at week 8 before treatment by study design. Untreated control rats had hypertension, decreased GFR, and progressive proteinuria and glomerulosclerosis at week 12. Only combination therapy significantly ameliorated hypertension and proteinuria. ARB alone or pioglitazone alone had only numerically lower SBP and UP than vehicle at week 12. Both pioglitazone alone and combination had significantly less decline in GFR than vehicle. Combination-induced regression of glomerulosclerosis in more rats from weeks 8 to 12 than ARB or pioglitazone alone. In parallel, combination treatment reduced plasminogen activator inhibitor-1 expression and macrophage infiltration, and preserved podocytes compared with vehicle. These results were linked to increased AT2receptor and Mas1 mRNA in the combination group. PPARγagonists in combination with ARB augment regression of glomerulosclerosis, with downregulation of injurious RAAS components vsPPARγalone, with increased anti-fibrotic/healing RAAS components, enhanced podocyte preservation, and decreased inflammation and profibrotic mechanisms.

Earthquakes are human recognized natural disasters, causing tremendous loss of life and property to human society, so how to strengthen the seismic capacity of the building more effectively is one of the challenges faced by scientists.While the use of a damping device is an effective method. With the rapid economic and social development, the urban transport problem is an extremely serious livelihood problem faced by all countries. To solve urban traffic congestion, in many cities setting up viaducts is a widely used way to ease urban traffic pressure, and elevated expressways are the main bridges among continuous bridges. In order to ensure the safe operation of the urban elevated road system, we must make the correct evaluation of their seismic capacity. This paper focuses on the continuous beam bridge seismic response history analysis of installing viscous dampers and lock-up devices,compared with the general scheme of continuous bridge.

Increased oxidative stress and inflammation has a role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Drugs with antioxidant and anti-inflammatory properties, such as N-acetylcysteine, might provide a useful therapeutic approach for COPD. We aimed to assess whether N-acetylcysteine could reduce the rate of exacerbations in patients with COPD.

In recent years, more attention is given to solar blind ultraviolet (SBUV) detection in corona discharge detection and defect diagnosis of partial discharge has been widely used. However, there are still such key techniques should be further studied such as electro-optic characteristics and the quantitative relationship between corona current and UV emission intensity in the process of corona discharge. With different AC voltage and different humidity, corona current and UV pulses are measured. It is shown that corona current and pulse number rise with the voltage mounting up, and decline very weakly with humidity increasingly. In addition, further discusses about the quantitative relationship between electro-optic parameters is implemented by using transfer function. The experiment results, under the conditions of different AC voltage and different humidity, indicate that transfer function maintained between 2.00 to 4.25 changes little, varied no more than 52.9%. UV pulse number, therefore, can be used to characterize corona current intensity. The conclusions above are significant for characterizing the level of corona discharge directly by UV emission intensity, and they are helpful for improving the accuracy of defect diagnosis.

The mechanisms for increased risk of chronic kidney disease (CKD) in obesity remain unclear. The renin-angiotensin system is implicated in the pathogenesis of both adiposity and CKD. We investigated whether the angiotensin type 1 (AT1) receptor, composed of dominant AT1aand less expressed AT1bin wild-type (WT) mice, modulates development and progression of kidney injury in a high-fat diet (HFD)-induced obesity model. WT mice had increased body weight, body fat, and insulin levels and decreased adiponectin levels after 24 wk of a high-fat diet. Identically fed AT1aknockout (AT1aKO) mice gained weight similarly to WT mice, but had lower body fat and higher plasma cholesterol. Both obese AT1aKO and obese WT mice had increased visceral fat and kidney macrophage infiltration, with more proinflammatory M1 macrophage markers as well as increased mesangial expansion and tubular vacuolization, compared with lean mice. These abnormalities were heightened in the obese AT1aKO mice, with downregulated M2 macrophage markers and increased macrophage AT1breceptor. Treatment with an AT1receptor blocker, which affects both AT1aand AT1b, abolished renal macrophage infiltration with inhibition of renal M1 and upregulation of M2 macrophage markers in obese WT mice. Our data suggest obesity accelerates kidney injury, linked to augmented inflammation in adipose and kidney tissues and a proinflammatory shift in macrophage and M1/M2 balance.

Obesity is established as an important contributor of increased diabetes mellitus, hypertension, and cardiovascular disease, all of which can promote chronic kidney disease (CKD). Recently, there is a growing appreciation that, even in the absence of these risks, obesity itself significantly increases CKD and accelerates its progression.

Angiotensin type 1 (AT1) receptor blocker (ARB) ameliorates progression of chronic kidney disease. Whether this protection is due solely to blockade of AT1, or whether diversion of angiotensin II from the AT1to the available AT2receptor, thus potentially enhancing AT2receptor effects, is not known. We therefore investigated the role of AT2receptor in ARB-induced treatment effects in chronic kidney disease. Adult rats underwent 5/6 nephrectomy. Glomerulosclerosis was assessed by renal biopsy 8 wk later, and rats were divided into four groups with equivalent glomerulosclerosis: no further treatment, ARB, AT2receptor antagonist, or combination. By week 12after nephrectomy, systolic blood pressure was decreased in all treatment groups, but proteinuria was decreased only with ARB. Glomerulosclerosis increased significantly in AT2receptor antagonist vs. ARB. Kidney cortical collagen content was decreased in ARB, but increased in untreated 5/6 nephrectomy, AT2receptor antagonist, and combined groups. Glomerular cell proliferation increased in both untreated 5/6 nephrectomy and AT2receptor antagonist vs. ARB, and phospho-Erk2 was increased by AT2receptor antagonist. Plasminogen activator inhibitor-1 mRNA and protein were increased at 12 wk by AT2receptor antagonist in contrast to decrease with ARB. Podocyte injury is a key component of glomerulosclerosis. We therefore assessed effects of AT1vs. AT2blockade on podocytes and interaction with plasminogen activator inhibitor-1. Cultured wild-type podocytes, but not plasminogen activator inhibitor-1 knockout, responded to angiotensin II with increased collagen, an effect that was completely blocked by ARB with lesser effect of AT2receptor antagonist. We conclude that the benefical effects on glomerular injury achieved with ARB are contributed to not only by blockade of the AT1receptor, but also by increasing angiotensin effects transduced through the AT2receptor.

Organic–inorganic hybrid metal–polyphenols as stable structural modules have gained extensive interest due to their diverse applications. However, titanium-oxo compounds (TOCs) with large molecular polyphenols have been less explored, and they were expected to be different from small polyphenols with isolated metal ions. Herein, 4-methyl-esculetin (Mesc), a catechol derivative, was selected to construct three TOCs, namely, [Ti17O24(Mesc)4(OiPr)16] (1), [Ti12O14(OiPr)18][Ti16O14(Mesc)12(OiPr)14] (2), and [Ti3O(Mesc)2(OAc)2(OiPr)4] (3). These compounds were structurally characterized. Photocurrent responses were evaluated using the compound-sensitized TiO2electrodes. It was found that the current densities of 1–3electrodes are in the order of 1≫ 3> 2, which relates to the ligand-to-TiO core and ligand-to-ligand charge transfers (LMCT and LLCT, respectively). Density functional theory calculations showed that the lowest band gap of 1originates from its LLCT. Compound 1reacted with polyphenol tannin (TA) to form a fully transparent and robust gel (1–TA), and the gelation properties were investigated. Using the gel as a nano-TiO2fixing agent, solar cell electrodes were prepared by a low-temperature wet method. The photocurrent responsive behavior of the 1–TA/TiO2electrode was compared with that of the 1-sensitized traditional high-temperature-treated TiO2electrode. Although the current density of the former is somewhat lower than that of the traditional electrode, the low-temperature wet preparation of the 1–TA/TiO2electrode is more energy-efficient and sustainable.

A fluoroionophore sensor, N-[4-(1-pyrene)butyroyl]-L-tryptophan (PLT), has been reported. It can distinguish lead ion from other 12 metal ions viaforming a pyrene dimer and it exhibits a very high sensitivity (0.15 μM) in aqueous solution (Chem. Commun., 2006, 2702). When the indole moiety in PLT was changed to benzene, in forming a new fluoroionophore of N-[4-(1-pyrene)butyroyl]-L-phenylalanine (PLP), it could not form a pyrene dimer in response to Pb2+in water. The present study describes the spectroscopic clarification of the intrinsic differences of the binding model between PLP and PLT in binding with Pb2+. The model shows identical chelating bidentate coordination between COO-and Pb2+both in PLP-Pb and PLT-Pb; however, there is no indication of the interaction between the phenyl ring and the metal ion or the hydrogen bonding between amide groups in PLP-Pb. These differences in the binding model between PLP-Pb and PLT-Pb illustrate that the indole ring in PLT appears to play a crucial role in the high selectivity and sensitivity of PLT to lead(II) ion.

Transforming growth factor-β1 (TGF-β1) and the renin-angiotensin-aldosterone system are key mediators in kidney fibrosis. Integrin αvβ6, a heterodimeric matrix receptor expressed in epithelia, binds and activates latent TGF-β1. We used β6 integrin-null mice (β6−/−) to determine the role of local TGF-β1 activation in renal fibrosis in the unilateral ureteral obstruction (UUO) model. Obstructed kidneys from β6−/−mice showed less injury than obstructed kidneys from wild-type (WT) mice, associated with lower collagen I, collagen III, plasminogen activator inhibitor (PAI-1), and TGF-β1 mRNA levels and lower collagen content. Infusion with either angiotensin II (Ang II) or aldosterone (Aldo) or combination in β6−/−UUO mice significantly increased collagen contents to levels comparable to those in identically treated WT. Active TGF-β protein expression in β6−/−mice was less in UUO kidneys with or without Ang II infusion compared to matched WT mice. Activated Smad 2 levels in β6−/−obstructed kidneys were lower than in WT UUO mice, and did not increase when fibrosis was induced in β6−/−UUO mice by Ang II infusion. Anti-TGF-β antibody only partially decreased this Ang II-stimulated fibrosis in β6−/−UUO kidneys. In situhybridization and immunostaining showed low expression of PAI-1 mRNA and protein in tubular epithelium in β6−/−UUO kidneys, with increased PAI-1 expression in response to Ang II, Aldo, or both. Our results indicate that interruption of αvβ6-mediated activation of TGF-β1 can protect against tubulointerstitial fibrosis. Further, the robust induction of tubulointerstitial fibrosis without increase in activated Smad 2 levels in obstructed β6−/−mice by Ang II suggests the existence of a TGF-β1-independent pathway of induction of fibrosis through angiotensin.

AbstractGlacial ice is a unique matrix that is capable of protecting microorganisms for long-term preservation. The organisms entrapped in glacial ice can provide information on evolutionary processes and ancient biodiversity. The major objective of this study was to detect and characterize ancient fungi in glacial ice and determine their viability. We developed a protocol using rigorous decontamination procedures, conventional cultural methods, and molecular techniques (polymerase chain reaction amplification of fungal ribosomal DNA internal transcribed spacers, followed by sequence analyses) to examine the ancient fungi entrapped in glacial ice. Fifteen glacial ice subcores, ranging in age from several hundred to 140 000 yr, from two locations in Greenland were used in this study. One hundred ninety fungal isolates were obtained using conventional cultural methods. In this paper we report the morphological and molecular characteristics of eight isolates, including two Penicilliumspp., three Cladosporiumspp., one Ulocladiumsp., one basidiomycete (Pleurotussp.), and one unknown ascomycete. In addition, ten fungal sequences were amplified and sequenced directly from ice meltwater. One of them was identified as a basidiomycete. The other nine were classified as ascomycetes, of which three sequences had very low similarities with contemporary sequences in Gen-Bank. The results from this study may facilitate the future use of ancient fungi in studies of fungal ecology, distribution, epidemiology, phylogeny, and evolution.

Fibrosis, or the accumulation of extracellular matrix, is a common feature of many chronic diseases. To interrogate core molecular pathways underlying fibrosis, we cross-examine human primary cells from various tissues treated with TGF-β, as well as kidney and liver fibrosis models. Transcriptome analyses reveal that genes involved in fatty acid oxidation are significantly perturbed. Furthermore, mitochondrial dysfunction and acylcarnitine accumulation are found in fibrotic tissues. Substantial downregulation of the PGC1α gene is evident in both in vitroand in vivofibrosis models, suggesting a common node of metabolic signature for tissue fibrosis. In order to identify suppressors of fibrosis, we carry out a compound library phenotypic screen and identify AMPK and PPAR as highly enriched targets. We further show that pharmacological treatment of MK-8722 (AMPK activator) and MK-4074 (ACC inhibitor) reduce fibrosis in vivo. Altogether, our work demonstrate that metabolic defect is integral to TGF-β signaling and fibrosis.

We report herein a fluoroionophore sensor derivated from tryptophan that shows high sensitivity (detection limit up to 0.15 µM) and specific selectivity for lead ion (Pb2) over Ca2, Cd2, Co2, Cr3, Cu2, K, Mg2, Na, Fe2, Mn2, Ni2and Zn2in aqueous solution.

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