Publications by authors named "Chiara Meregalli"

Article Synopsis
  • The study investigates how body fat distribution, particularly abdominal obesity (AO), affects the immune response to a SARS-CoV-2 vaccine booster in individuals with a history of infection.
  • Researchers measured specific antibody levels in 511 subjects over several months after receiving the booster dose, looking at differences between those with and without AO.
  • Results suggest that people with AO who were previously infected show a stronger immune response after the booster, indicating that this group may benefit from the additional dose of the vaccine.
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Summary: Psoriasis is often associated with abdominal obesity and type-2 diabetes (T2D). The inflammatory process in psoriasis can target adipose tissue depots, especially those surrounding the heart and coronary arteries, exposing to an increased risk of cardiovascular diseases. A 50-year-old female patient referred to us for abdominal obesity and T2D, which were not controlled with lifestyle modifications.

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Tubulointerstitial fibrosis is observed in diabetic nephropathy. It is still debated whether tubular cells, undergoing epithelial-mesenchymal transition (EMT) in high glucose (HG) conditions, may contribute to interstitial fibrosis development. In this study, we investigated the phenotypic and molecular EMT-like changes and the alteration of inflammatory and fibrogenic secretome induced by HG in human primary tubular cell cultures.

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Article Synopsis
  • Human epicardial adipose tissue (EAT) is linked to various heart diseases and consists of a mix of adipocytes and immune cells, allowing interaction with the heart muscle.
  • The study aimed to evaluate EAT's expression of receptors for GIP, GCG, and GLP-1, with findings indicating that GIPR and GCGR mRNAs are present in EAT, primarily in macrophages.
  • EAT samples were collected from 33 patients with cardiovascular diseases, and both microarray and immunohistochemistry analyses confirmed the presence of these receptors, contributing to the understanding of potential therapeutic targets.
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The mechanism upon which human kidneys undergo regeneration is debated, though different lineage-tracing mouse models have tried to explain the cellular types and the mechanisms involved. Different sources of human renal progenitors have been proposed, but it is difficult to argue whether these populations have the same capacities that have been described in mice. Using the nephrosphere (NS) model, we isolated the quiescent population of adult human renal stem-like PKH/CD133+/CD24- cells (RSC).

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Clear cell renal cell carcinoma (ccRCC) has a poor prognosis despite novel biological targeted therapies. Tumor aggressiveness and poor survival may correlate with tumor grade at diagnosis and with complex metabolic alterations, also involving glucose and lipid metabolism. However, currently no grade-specific metabolic therapy addresses these alterations.

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In end-stage chronic kidney disease, the option of organ transplantation is limited because of the scarce availability of kidneys. The combination of stem cell research, regenerative medicine, and tissue engineering seems a promising approach to produce new transplantable kidneys. Currently, the possibility to repopulate naturally obtained scaffolds with cells of different sources is advancing.

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Human clear cell renal cell carcinoma (ccRCC) is therapy resistant; therefore, it is worthwhile studying in depth the molecular aspects of its progression. In ccRCC the biallelic inactivation of the VHL gene leads to stabilization of hypoxia-inducible factors (HIFs). Among the targets of HIF-1α transcriptional activity is the LOX gene, which codes for the inactive proenzyme (Pro-Lox) from which, after extracellular secretion and proteolysis, derives the active enzyme (Lox) and the propeptide (Lox-PP).

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Renal tubular cells are involved in the tubular interstitial fibrosis observed in diabetic nephropathy. It is debated whether epithelial-mesenchymal transition (EMT) affects tubular cells, which under high-glucose conditions overproduce transforming growth factor-β (TGF-β), a fibrogenic cytokine involved in interstitial fibrosis development. Our study investigated the involvement of non-receptor tyrosine kinase Arg (also called Abl2) in TGF-β production.

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