Sensitive fluorescent chemosensor for Hg(II) in aqueous solution using 4'-dimethylaminochalcone.

Mercury (Hg) is an element with high toxicity, especially to the nervous system, and fluorescent pigments are used to visualize dynamic processes in living cells. A little explored fluorescent core is chalcone. Herein, we synthesized chalcone (2E)-3-(4-(dimethylamino)phenyl)-1-phenylprop-2-en-1-one (8) and assessed its photophysical properties. Moreover, the application of this chemosensor in aqueous media shows a selective fluorescence quenching effect with Hg(II). The figures of merit for the chemosensor were calculated to be LOD = 136 nM and LOQ = 454 nM, as well as a stoichiometry of 1:1. Furthermore, the association constant (Ka) and fluorescence quenching constant (KSV) were calculated using the Benesi-Hildebrand and Stern-Volmer equations to be Ka= 9.08 × 104 and KSV= 1.60 × 105, respectively. Finally, by using a computational approach, we explain the interaction between chalcone (8) and Hg(II) and propose a potential quenching mechanism based on the blocking of photoinduced electron transfer.

Tongue Flap for Management of Large Palatal Fistulas.

ABSTRACT: One of the worst complications after a primary palatoplasty is the lesion of the neurovascular bundle, results into a type of flap necrosis, having as a final consequence a residual palatine fistula.In our institution the authors usually use tongue flap to repair large fistulas.The authors retrospectively reviewed all patients with large palatal fistulas that were repaired with tongue flap at Fundacion Gantz between January 2002 and December 2020.Fundacion Gantz has 1.067 patients with palatal surgeries, with an incidence of 5,8% for palatal fistulas and 3,2% (n = 2) were considered large.Surgery was done on 24 patients with large residual palatal fistula, all of them with tongue flaps as outpatient surgery. Fifteen were girls and 9 were boys, between 13 and 40 years.The average size of the fistula was 2,5 cm and 100% are localized in the anterior palate.The incidence of complications with tongue flap was 12, 5%: 2 dehiscences and 1 persistent residual fistula. The authors had no complications in phonation due to the lingual donor area.The authors consider that this outpatient surgery, is a reprodutible and safe technique, with a low rate of complications, which allows us to recommend it for the treatment of large palatal fistulas.

(Pro)renin receptor activation increases profibrotic markers and fibroblast-like phenotype through MAPK-dependent ROS formation in mouse renal collecting duct cells.

Recent studies suggested that activation of the PRR upregulates profibrotic markers through reactive oxygen species (ROS) formation; however, the exact mechanisms have not been investigated in CD cells. We hypothesized that activation of the PRR increases the expression of profibrotic markers through MAPK-dependent ROS formation in CD cells. Mouse renal CD cell line (M-1) was treated with recombinant prorenin plus ROS or MAPK inhibitors and PRR-shRNA to evaluate their effect on the expression of profibrotic markers. PRR immunostaining revealed plasma membrane and intracellular localization. Recombinant prorenin increases ROS formation (6.0 ± 0.5 vs 3.9 ± 0.1 nmol/L DCF/µg total protein, P < .05) and expression of profibrotic markers CTGF (149 ± 12%, P < .05), α-SMA (160 ± 20%, P < .05), and PAI-I (153 ± 13%, P < .05) at 10-8  mol/L. Recombinant prorenin-induced phospho ERK 1/2 (p44 and p42) at 10-8 and 10-6  mol/L after 20 minutes. Prorenin-dependent ROS formation and augmentation of profibrotic factors were blunted by ROS scavengers (trolox, p-coumaric acid, ascorbic acid), the MEK inhibitor PD98059 and PRR transfections with PRR-shRNA. No effects were observed in the presence of antioxidants alone. Prorenin-induced upregulation of collagen I and fibronectin was blunted by ROS scavenging or MEK inhibition independently. PRR-shRNA partially prevented this induction. After 24 hours prorenin treatment M-1 cells undergo to epithelial-mesenchymal transition phenotype, however MEK inhibitor PD98059 and PRR knockdown prevented this effect. These results suggest that PRR might have a significant role in tubular damage during conditions of high prorenin-renin secretion in the CD.

Distribution, metabolism, and toxicity of antimony species in wistar rats. A bio-analytical approach.

This work studied the distribution, reactivity, and biological effects of pentavalent or trivalent antimony (Sb(V), Sb(III)) and N-methylglucamine antimonate (NMG-Sb(V)) in Wistar Rats. The expression of fibrosis genes such as α - SMA, PAI-1, and CTGF were determined in Liver, and Kidney tissues. Wistar rats were treated with different concentrations of Sb(V), Sb(III), As(V) and As(III), and MA via intra-peritoneal injections. The results indicated a noteworthy elevation in mRNA levels of plasminogen activator 1 (PAI-1) in the kidneys of rats that were injected. The main accumulation site for Sb(V) was observed to be the liver, from which it is primarily excreted in its reduced form (Sb(III)) through the urine. The generation of Sb(III) in the kidneys has been found to induce damage through the expression of α-SMA and CTGF, and also lead to a higher creatinine clearance compared to As(III).

Augmented transcripts of kidney injury markers and renin angiotensin system in urine samples of overweight young adults.

Obesity has been firmly established as a major risk factor for common disease states including hypertension, type 2 diabetes mellitus, and chronic kidney disease. Increased body mass index (BMI) contributes to the activation of both the systemic and intra-tubular renin angiotensin systems (RAS), which are in turn associated with increased blood pressure (BP) and kidney damage. In this cross-sectional study, 43 subjects of normal or increased body weight were examined in order to determine the correlation of BMI or body fat mass (BFM) with blood pressure, fasting blood glucose (FBG), and urinary kidney injury markers such as interleukin-18 (IL-18), connective tissue growth factor (CTGF), neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 (KIM-1). Our results showed that: (1) subjects with increased body weight showed significantly higher BP, BFM, total body water and metabolic age; (2) BMI was positively correlated to both systolic (R2 = 0.1384, P = 0.01) and diastolic BP (R2 = 0.2437, P = 0.0008); (3) BFM was positively correlated to DBP (R2 = 0.1232, P = 0.02) and partially correlated to urine protein (R2 = 0.047, P = 0.12) and FBG (R2 = 0.07, P = 0.06); (4) overweight young adults had higher urinary mRNA levels of renin, angiotensinogen, IL-18 and CTGF. These suggest that BMI directly affects BP, kidney injury markers, and the activation of the intra-tubular RAS even in normotensive young adults. Given that BMI measurements and urine analyses are non-invasive, our findings may pave the way to developing a new and simple method of screening for the risk of chronic kidney disease in adults.