Publications by authors named "Federica Wolf"

Endothelial dysfunction is a crucial event in the early pathogenesis of cardiovascular diseases and is linked to magnesium (Mg) deficiency. Indeed, in endothelial cells, low Mg levels promote the acquisition of a pro-inflammatory and pro-atherogenic phenotype. This paper investigates the mechanisms by which Mg deficiency promotes oxidative stress and affects endothelial behavior in human umbilical vascular endothelial cells (HUVECs).

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Since the start of the COVID-19 pandemic, it has become increasingly clear that the disease can have relevant multisystemic and long-term effects, and several studies have attempted to identify key determinants of the disease course. Here we discuss recent evidence suggesting that, in long COVID patients, combined magnesium and vitamin D deficiencies associate with a higher number of clinical manifestations, as compared to patients with normal levels of both nutrients. We highlight the potential synergistic effects of these deficiencies and propose that future studies should explore a causal link with the risk of developing long COVID.

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Purpose: Serum magnesium is the most frequently used laboratory test for evaluating clinical magnesium status. Hypomagnesemia (low magnesium status), which is associated with many chronic diseases, is diagnosed using the serum magnesium reference range. Currently, no international consensus for a magnesemia normal range exists.

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Article Synopsis
  • Nutritional deficiencies, particularly magnesium (Mg), are prevalent in inflammatory bowel diseases (IBD) and are linked to disease severity in patients.
  • Research using a murine model of colitis showed that Mg supplementation improves gut microbiota by increasing beneficial bacteria and reducing harmful ones, enhancing overall intestinal health.
  • The study suggests that dietary Mg could be an effective and affordable way to alleviate symptoms of IBD and support a healthier gut microbiome.
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Purpose: In less than one and a half year, the COVID-19 pandemic has nearly brought to a collapse our health care and economic systems. The scientific research community has concentrated all possible efforts to understand the pathogenesis of this complex disease, and several groups have recently emphasized recommendations for nutritional support in COVID-19 patients. In this scoping review, we aim at encouraging a deeper appreciation of magnesium in clinical nutrition, in view of the vital role of magnesium and the numerous links between the pathophysiology of SARS-CoV-2 infection and magnesium-dependent functions.

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  • Hypomagnesemia is a common issue in cancer patients treated with cetuximab (CTX), often due to magnesium loss through the kidneys.
  • The study explores whether CTX also affects magnesium absorption in the intestines and the potential impact of magnesium supplementation on CTX's effectiveness.
  • Findings reveal that CTX decreases magnesium absorption by disrupting EGF signaling, but magnesium supplementation does not reduce CTX's anti-cancer activity, suggesting it could help manage magnesium levels safely in patients.
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More and more studies are accumulating about COVID-19. Some aspects of the pathogenesis of the disease recall events occurring in Mg deficiency, such as a drop of T cells, increased plasma concentration of inflammatory cytokines, and endothelial dysfunction. We hypothesize that a low Mg status, which is rather common, might foment the transition from mild to critical clinical manifestations of the disease.

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Background: Inflammatory bowel disease (IBD) predisposes to colorectal cancer (CRC) with some specific features that distinguish it from sporadic CRC. Magnesium (Mg) homeostasis is severely compromised in IBD patients, which may affect both inflammation and tumor development. Efficient transcellular Mg transport in intestinal cells depends on the transient receptor potential melastatin (TRPM) channels type 6 and 7, but their expression has never been investigated in the context of IBD-related CRC.

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Derangement of magnesium homeostasis underlies the pathophysiology of many diseases, including cancer. Recent advances support the view that aberrant expression of Mg channels and other Mg homeostatic factors may affect many hallmarks of cancer. The seminal idea of magnesium as a key regulator of cell proliferation has been enriched by novel intriguing findings that link magnesium and Mg transporters to distinctive and complementary capabilities that enable tumour growth and metastatic dissemination.

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Article Synopsis
  • Intestinal magnesium uptake is crucial for overall magnesium balance in the body, and the colon cells express two key magnesium channels, TRPM6 and TRPM7, whose exact roles are not well understood.* -
  • Researchers studied the effects of reducing the expression of TRPM6 or TRPM7 in human colon cell lines, finding that silencing TRPM7 increased magnesium absorption and promoted cell growth, while reducing TRPM6 had little impact.* -
  • The study suggests that TRPM7 and TRPM6 work together, forming complexes essential for magnesium influx, and highlights that TRPM6 cannot be functionally substituted by TRPM7 in colon cells.*
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  • Magnesium is crucial for health and is often low in patients with inflammatory bowel disease (IBD), potentially affecting inflammation and disease progression.* -
  • A study showed that IBD patients had low magnesium levels, and in a mouse model, a magnesium-deficient diet worsened colitis by damaging the intestines and reducing magnesium absorption.* -
  • Supplementing magnesium improved intestinal health and inflammation in the mice, suggesting that addressing magnesium levels could be a simple and effective way to help IBD patients.*
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Context: The emerging global-health paradigm requires medical teaching to be continuously redefined and updated; to this end, transnational approaches should be encouraged and medical training harmonized. Infectious diseases (ID) teaching in the current context of emerging infections, fast-increasing bacterial resistance and large-scale human migration, was chosen to develop a common international course.

Objective: We report the successful implementation of a joint European undergraduate course aiming to (i) develop a common ID core curriculum among European medical schools; (ii) promote mobility among teachers and students (iii) promote international cooperation among European teachers.

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The processes leading to anticancer drug resistance are not completely unraveled. To get insights into the underlying mechanisms, we compared colon carcinoma cells sensitive to doxorubicin with their resistant counterpart. We found that resistant cells are growth retarded, and show staminal and ultrastructural features profoundly different from sensitive cells.

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Magnesium is directly involved in the control of cell growth and survival, but its role in cancer biology and therapy is multifaceted; in particular, it is highly controversial whether magnesium levels can affect therapy outcomes. Here we investigated whether magnesium availability can modulate cellular responses to the widely used chemotherapeutic doxorubicin. We used an in vitro model consisting of mammary epithelial HC11 cells and found that high magnesium availability was correlated with diminished sensitivity both in cells chronically adapted to high magnesium concentrations and in acutely magnesium-supplemented cells.

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Neoplastic cells accumulate magnesium, an event which provides selective advantages and is frequently associated with TRPM7 overexpression. Little is known about magnesium homeostasis in drug-resistant cancer cells. Therefore, we used the colon cancer LoVo cell model and compared doxorubicin-resistant to sensitive cells.

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Antitumor drugs have long been known to introduce a measurable risk of cardiovascular events. Cardio-Oncology is the discipline that builds on collaboration between cardiologists and oncologists and aims at screening, preventing or minimizing such a risk. Overt concern about "possible" cardiovascular toxicity might expose cancer patients to the risk of tumor undertreatment and poor oncologic outcome.

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Magnesium is well established as a fundamental factor that regulates cell proliferation. However, the molecular mechanisms linking mitogenic signals, extracellular magnesium availability and intracellular effectors are still largely unknown. In the present study we sought to determine whether EGF regulates magnesium homeostasis in normal HC11 mammary epithelial cells.

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