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91.
Lourdes M G García Ana Paula T de Godoi Osvaldo A Serra Juliana F de Lima Leonardo de P A Almeida Tatiane C Dotta Silmara A M Corona Andra C dos Reis Alma B C E B Catirse 《Journal of esthetic and restorative dentistry : official publication of the American Academy of Esthetic Dentistry ... [et al.]》2020,32(1):51-56
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Lívia L. Corrêa Leonardo Vieira Neto Giovanna A. Balarini Lima Rafael Gabrich Luiz Carlos D. de Miranda M?nica R. Gadelha 《International braz j urol : official journal of the Brazilian Society of Urology》2015,41(1):110-115
Introduction
Non-androgenic growth factors are involved in the growth regulation of prostate cancer (PCa).Objective
This is the first Brazilian study to correlate, in a population of patients operated for PCa, PSA, total testosterone, insulin-like growth factor-I (IGF-I) and insulin-like growth factor-binding protein-3 (IGFBP-3) with Gleason score and to compare with a control group with benign prostate hyperplasia (BPH).Materials and Methods
This retrospective single-center study included 49 men with previously diagnosed PCa and 45 with previously diagnosed BPH. PSA, testosterone, IGF-I, IGFBP-3 were determined in both groups.Results
PSA and IGFBP-3 levels were significantly higher in the PCa group as compared to the BPH group (p<0.001 and p=0.004, respectively). There was a significant difference when we compared the PSA before surgery (p<0.001) and at the inclusion in the study (p<0.001) and IGFBP3 (0.016) among patients with Gleason <7, ≥7 and BPH. In the PCa group, PSA, testosterone, IGF-I and IGFBP-3 levels were comparable between Gleason <7 and ≥7.Conclusions
Our data suggest that in localized PCa, the quantification of PSA and, not of IGF-1, may provide independent significant information in the aggressiveness. IGFBP-3 could be a biochemical marker of disease control in PCa patients. 相似文献95.
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The indium-mediated allylation of novel 3-(2-Boc-hydrazono)indolin-2-one derivatives, followed by a palladium-catalysed carboamination reaction, is described to afford unprecedented spirocyclic oxindoles in good yields. The method provides an efficient access to both cis and trans diastereoisomers of highly functionalized compounds, bearing an N-Boc, 5-substituted pyrazolidine ring at the C3-oxindole spiro junction. The versatility of the method is fully demonstrated starting from a series of substituted isatins and employing a variety of aryl halides in the key cyclization step.The indium-mediated allylation of novel 3-(2-Boc-hydrazono)indolin-2-one derivatives, followed by a palladium-catalysed carboamination reaction, is described to afford unprecedented spirocyclic oxindoles in good yields. 相似文献
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Tatiani Botelho Vinícius B. Marques Maylla R. Simes Patricia R. do Val Lima Fabiana V. Simes Dalton V. Vassallo Leonardo dos Santos 《Basic & clinical pharmacology & toxicology》2019,124(2):190-198
Mercury intoxication is a public health risk factor due to its hazardous effect to several organs, including the cardiovascular system. There is evidence of endothelial dysfunction after exposure to mercury, but the effects on endothelium‐dependent vasodilatation are still unknown. In the present study, we aimed to evaluate the chronic effects of high HgCl2 doses on the mechanisms of vasodilatation. Wistar rats were injected with HgCl2 (1st dose 10.86 μg/kg, and daily doses 0.014 μg/kg for 30 days i.m.), and saline was used as control. Mercury exposure reduced the acetylcholine‐induced vasodilatation in aortic rings, which was restored by incubation with antioxidant tiron. Inhibition of the NO synthase, Na+/K+‐ATPase and K+ channels indicates reduced participation of these factors. In the mercury group, there were an increased local anion superoxide and a reduced NO. The vasodilatation to exogenous NO was partially inhibited by co‐incubation with TEA plus tiron, suggesting that reduced NO bioavailability is the responsible to that decreased the participation of K+ channels. Moreover, there was an increased participation of the Na+/K+‐ATPase associated with an up‐regulation of its alpha‐1 subunit. In conclusion, reduced NO bioavailability plays a major role in the impaired participation of K+ channels and Na+/K+‐ATPase in the acetylcholine‐mediated relaxation, although sodium pump is up‐regulated probably as a compensatory mechanism. 相似文献
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