Two Decades of Developmentalism: Bottlenecks and Plans of State Intervention in Brazil in the Second Half of the Twentieth Century

This work takes as its theme public policies on development. It aims an overall analysis of the most urgent issues of political and economic plans launched in Brazil in the second half of the twentieth century. Specifically, the intention is to discuss the establishment of government policies in combating bottlenecks in the national economy through the Plans. This is an article based on concepts of development and the major general lines of the development plans in this country. Kon’s works (1999) are the fundamental theoretical basis. We notice that Brazil experienced two very different decades, the 1970s and 1980s: the first focused investment for economic growth; the second, turned to fighting inflation. Because of discourses and appointed limits, developmentalism occurred, but no development in the strict sense. Between public debt and inflation addiction, which were parallel in the two mentioned decades, (still) rests the same issue in the country: What is development? What is the country’s development

Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage

The aberrant activation of complement system in several kidney diseases suggests that this pillar of innate immunity has a critical role in the pathophysiology of renal damage of different etiologies. A growing body of experimental evidence indicates that complement activation contributes to the pathogenesis of acute kidney injury (AKI) such as delayed graft function (DGF) in transplant patients. AKI is characterized by the rapid loss of the kidney’s excretory function and is a complex syndrome currently lacking a specific medical treatment to arrest or attenuate progression in chronic kidney disease (CKD). Recent evidence suggests that independently from the initial trigger (i.e., sepsis or ischemia/reperfusions injury), an episode of AKI is strongly associated with an increased risk of subsequent CKD. The AKI-to-CKD transition may involve a wide range of mechanisms including scar-forming myofibroblasts generated from different sources, microvascular rarefaction, mitochondrial dysfunction, or cell cycle arrest by the involvement of epigenetic, gene, and protein alterations leading to common final signaling pathways [i.e., transforming growth factor beta (TGF-β), p16ink4a, Wnt/β-catenin pathway] involved in renal aging. Research in recent years has revealed that several stressors or complications such as rejection after renal transplantation can lead to accelerated renal aging with detrimental effects with the establishment of chronic proinflammatory cellular phenotypes within the kidney. Despite a greater understanding of these mechanisms, the role of complement system in the context of the AKI-to-CKD transition and renal inflammaging is still poorly explored. The purpose of this review is to summarize recent findings describing the role of complement in AKI-to-CKD transition. We will also address how and when complement inhibitors might be used to prevent AKI and CKD progression, therefore improving graft function

Isolation and Expansion of Muscle Precursor Cells from Human Skeletal Muscle Biopsies

One of the major issues concerning human skeletal muscle progenitor cells is represented by the efficient isolation and in vitro expansion of cells retaining the ability to proliferate, migrate and differentiate once transplanted. Here we describe a method (1) effective in obtaining human muscle precursor cells both from fresh and frozen biopsies coming from different muscles, (2) selective to yield cells uniformly positive for CD56 and negative for CD34 without FACS sorting, (3) reliable in maintaining proliferative and in vitro differentiative capacity up to passage 10

Isolation and Expansion of Muscle Precursor Cells from Human Skeletal Muscle Biopsies

One of the major issues concerning human skeletal muscle progenitor cells is represented by the efficient isolation and in vitro expansion of cells retaining the ability to proliferate, migrate and differentiate once transplanted. Here we describe a method (1) effective in obtaining human muscle precursor cells both from fresh and frozen biopsies coming from different muscles, (2) selective to yield cells uniformly positive for CD56 and negative for CD34 without FACS sorting, (3) reliable in maintaining proliferative and in vitro differentiative capacity up to passage 10

Why stem/progenitor cells lose their regenerative potential

Nowadays, it is clear that adult stem cells, also called as tissue stem cells, play a central role to repair and maintain the tissue in which they reside by their selfrenewal ability and capacity of differentiating into distinct and specialized cells. As stem cells age, their renewal ability declines and their capacity to maintain organ homeostasis and regeneration is impaired. From a molecular perspective, these changes in stem cells properties can be due to several types of cell intrinsic injury and DNA aberrant alteration (i.e epigenomic profile) as well as changes in the tissue microenviroment, both into the niche and by systemic circulating factors. Strikingly, it has been suggested that aging-induced deterioration of stem cell functions may play a key role in the pathophysiology of the various agingassociated disorders. Therefore, understanding how resident stem cell age and affects near and distant tissues is fundamental. Here, we examine the current knowledge about aging mechanisms in several kinds of adult stem cells under physiological and pathological conditions and the principal aging-related changes in number, function and phenotype that determine the loss of tissue renewal properties. Furthermore, we examine the possible cell rejuvenation strategies. Stem cell rejuvenation may reverse the aging phenotype and the discovery of effective methods for inducing and differentiating pluripotent stem cells for cell replacement therapies could open up new possibilities for treating age-related diseases

PREVALENZA DI ANTICORPI ANTI- YERSINIA IN DONATORI DI SANGUE.

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LEPTOSPIROSI CON ISOLAMENTO COLTURALE POSITIVO

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Predictor Analysis in Radiofrequency Ablation of Benign Thyroid Nodules: A Single Center Experience

PURPOSE: To confirm the efficacy of ultrasound (US) guided radiofrequency ablation (RFA) in the treatment of benign thyroid nodules, we evaluated as primary outcome the technical efficacy and clinical success in a single center dataset. The secondary outcome was to find a correlation between nodules’ pre-treatment features and volume reduction rate (VRR) ≥75% at 12 months after RFA and during follow-up period. METHODS: This retrospective study included 119 consecutive patients (99 females, 20 males, 51.5 ± 14.4 years) with benign thyroid nodules treated in our hospital between October 2014 and December 2018 with a mean follow-up of 26.8 months (range 3–48). Clinical and US features before and after RFA were evaluated by a US examination at 1, 3, 6, 12 months and annually thereafter up to 48 months. RESULTS: The median pre-treatment volume was 22.4 ml; after RFA we observed a statistically significant volume reduction from the first month (11.7 ml) to the last follow-up (p 22.4 ml (HR 0.54, p 0.036) were found to be independent positive and negative predictors of VRR ≥75% respectively. One-month post RFA VRR ≥50% represented the best positive predictor of technical success. CONCLUSIONS: This study confirmed the efficacy of RFA in the treatment of benign thyroid nodules. In particular we show that by selecting macrocystic nodules smaller than 22.4 ml better long-term response can be achieved, which is predicted by an early shrinkage of the nodule

Emerging role of Lipopolysaccharide binding protein in sepsis-induced acute kidney injury

Sepsis remains a serious cause of morbidity and mortality in critically ill patients, with limited therapeutic options available. Of the several disorders connected with sepsis, acute kidney injury (AKI) is one of the major complications. The pathophysiology of sepsis-induced AKI is characterized by severe inflammation in renal parenchyma with endothelial dysfunction, intra-glomerular thrombosis and tubular injury. Endothelial dysfunction is regulated by several mechanisms implicated in cellular de-differentiation, such as endothelial-to-mesenchymal transition (EndMT). Gram-negative bacteria and their cell wall component lipopolysaccharides (LPSs) are frequently involved in the pathogenesis of AKI. The host recognition of LPS requires a specific receptor, which belongs to the Toll-like receptor (TLR) family of proteins, called TLR4, and two carrier proteins, namely the LPS-binding protein (LBP) and cluster of differentiation 14 (CD14). In particular, LBP is released as a consequence of Gram-negative infection and maximizes the activation of TLR4 signalling. Recent findings regarding the emerging role of LBP in mediating sepsis-induced AKI, and the possible beneficial effects resulting from the removal of this endogenous adaptor protein, will be discussed in this review