Publications by authors named "Stanzione R"

Atrial natriuretic peptide (ANP), a cardiac hormone involved in the regulation of water/sodium balance and blood pressure, is also secreted by endothelial cells, where it exerts protective effects in response to stress. Autophagy is an intracellular self-renewal process involved in the degradation of dysfunctional cytoplasmic elements. ANP was recently reported to act as an extracellular regulator of cardiac autophagy.

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  • Scientists studied rats that are prone to strokes to understand how high salt diets affect their gut bacteria and stroke risk.
  • They compared two types of rats: one that is more likely to get strokes (SHRSPs) and one that is less likely (SHRSRs) while they ate a special high-salt diet for a few weeks.
  • The gut bacteria in the stroke-prone rats changed in a way that might increase their chances of having a stroke, showing that a bad diet could harm gut health and lead to serious problems.
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  • * Recent studies focus on autophagy, a cellular process, and its complex role in protecting or harming neurons during ischemic stroke, based on experiments with animal models.
  • * Properly managing autophagy could be a potential way to prevent or lessen brain injury from strokes, highlighting the need for more research in this area.
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  • - Naringenin (NRG) is shown to counteract mitochondrial dysfunction, which is important in preventing cardiovascular diseases, by selectively inhibiting the FF-ATPase enzyme involved in ATP hydrolysis.
  • - NRG interacts with FF-ATPase in a way that blocks energy transmission, particularly when calcium (Ca) ions are present, illustrating its preference for the enzyme activated by Ca over magnesium (Mg).
  • - The study indicates that NRG helps protect against cell injury in cerebral endothelial cells, restoring cell viability and function after salt-induced damage, while also improving mitochondrial activity.
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Sphingolipids exert important roles within the cardiovascular system and related diseases. Perturbed sphingolipid metabolism was previously reported in cerebral and renal tissues of spontaneously hypertensive rats (SHR). Specific defects related to the synthesis of sphingolipids and to the metabolism of Sphingosine-1-Phospahte (S1P) were exclusively identified in the stroke-prone (SHRSP) with the respect to the stroke-resistant (SHRSR) strain.

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  • Heart failure is a serious side effect of doxorubicin (DOX) in cancer patients, and this study investigates the role of the MST1 kinase in DOX-induced heart damage.
  • Researchers used mice with normal MST1 and those with a modified version that can't activate (dominant-negative) to analyze the effects of DOX treatment, finding that MST1 activation contributes to heart injury.
  • The study concludes that inhibiting MST1 can protect against DOX-induced heart damage by preventing the downregulation of SIRT3, a protective protein, which was also found altered in heart tissue from cancer patients receiving DOX.
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Background: A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele at NDUFC2/rs11237379 variant associates with reduced gene expression and impaired mitochondrial function.

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Erdheim-Chester disease (ECD), a rare form of non-Langerhans histiocytosis, is a multisystem disorder. The case reported here refers to a 49-year-old man presenting at the emergency room with respiratory symptoms. While undergoing diagnostic tests for COVID-19 infection, tomography revealed asymptomatic bilateral perirenal tumors, while renal function remained unaltered.

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  • Dkk3 (Dickkopf-3) is a protein that influences blood pressure regulation and is linked to hypertension in rats; its full role in cardiovascular health remains unclear.* -
  • Research using genetically modified mice and hypertensive rat models showed that deleting Dkk3 increased blood pressure and impaired blood vessel relaxation, but restoring Dkk3 countered these effects.* -
  • The protein functions by enhancing VEGF (vascular endothelial growth factor) expression and activating a signaling pathway that lowers blood pressure, highlighting Dkk3’s potential as a therapeutic target for hypertension.*
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Mitochondrial dysfunction, causing increased reactive oxygen species (ROS) production, is a molecular feature of heart failure (HF). A defective antioxidant response and mitophagic flux were reported in circulating leucocytes of patients with chronic HF and reduced ejection fraction (HFrEF). Atrial natriuretic peptide (ANP) exerts many cardiac beneficial effects, including the ability to protect cardiomyocytes by promoting autophagy.

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  • * Research showed that high salt significantly damages brain endothelial cells, causing oxidative stress and reduced cell viability.
  • * A bergamot polyphenolic fraction (BPF) was found to mitigate these harmful effects, improving cell function and reducing oxidative stress, suggesting it could help treat vascular disorders.
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Background: Personality's investigation has always been characterized as a central area of research for psychology, such that it was established in the 1920s as an autonomous scientific-disciplinary field. Identifying and observing the people's typical ways of "being in the world" has made possible to define the predictability of a pattern of behavioral responses related both to the possession of distinct characteristics of the agent subject and to specific environmental situations. In the actual scientific landscape, there is a strand of research that makes a description of personality through methodologies and indicators not usually used by psychology, but scientifically validated through standardized procedures.

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The compromised viability and function of cardiovascular cells are rescued by small molecules of triazole derivatives (Tzs), identified as 3a and 3b, by preventing mitochondrial dysfunction. The oxidative phosphorylation improves the respiratory control rate in the presence of Tzs independently of the substrates that energize the mitochondria. The FF-ATPase, the main candidate in mitochondrial permeability transition pore (mPTP) formation, is the biological target of Tzs and hydrophilic F domain of the enzyme is depicted as the binding region of Tzs.

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Background: The study of complex systems, such as the psychotherapeutic encounter, transcends the mechanistic and reductionist methods for describing linear processes and needs suitable approaches to describe probabilistic and scarcely predictable phenomena.

Objective: The present study undertakes a scoping review of research on the computational methods in psychotherapy to gather new developments in this field and to better understand the phenomena occurring in psychotherapeutic interactions as well as in human interaction more generally.

Design: Online databases were used to identify papers published 2011-2022, from which we selected 18 publications from different resources, selected according to criteria established in advance and described in the text.

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  • - NPPA (atrial natriuretic peptide) plays a significant role in protecting the heart by preventing cell damage, reducing fibrosis, and maintaining blood vessel integrity, but the exact mechanisms behind these benefits are still being studied.
  • - The study reveals that NPPA activates autophagy in cardiomyocytes (heart muscle cells) through specific receptors and signaling pathways, and this process helps cells survive stress from conditions like low glucose or lack of oxygen.
  • - Research using knockout mice demonstrates that without NPPA, there is greater cell damage during ischemia-reperfusion injury, and enhancing autophagy can reduce this damage, indicating that NPPA is a crucial factor in regulating autophagy in the heart.
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  • Mitochondrial dysfunction, particularly a deficiency in complex I, has been linked to coronary artery disease (CAD) and is implicated in various cardiovascular issues, including acute coronary syndrome (ACS).
  • A study involving 260 CAD patients found that the T allele of the /rs23117379 genetic variant is associated with an earlier onset of ACS and a higher risk of recurrence.
  • The findings suggest that this genetic variant may serve as a potential risk factor for cardiovascular diseases due to its role in mitochondrial dysfunction.
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The mitochondrial uncoupling protein 2 (UCP2) acts as an anion transporter and as an antioxidant factor able to reduce the reactive oxygen species level. Based on its effects, UCP2 prevents the membrane lipids, proteins, and DNA damage while preserving normal cellular functions. Many variants have been identified within the human .

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  • Stroke is a leading cause of death and disability globally, prompting research into biological factors that contribute to its onset, particularly mitochondrial dysfunction, autophagy, and calcium regulation in cells.
  • The study highlights the role of store-operated calcium entry (SOCE) mechanisms, specifically how mutations in the calcium sensor STIM1 affect calcium levels, potentially worsening stroke effects in certain rat strains.
  • The article emphasizes STIM1's significance in experimental stroke research, linking it to stroke vulnerability and discussing future clinical implications for human treatments.
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  • UCP2 is crucial for protecting against vascular diseases linked to high salt intake, as shown in various animal models and human studies.
  • Reducing UCP2 levels worsens vascular health and increases damage in models prone to stroke, while increasing UCP2 levels helps mitigate these harmful effects.
  • UCP2 promotes autophagy and mitophagy in response to high salt and oxidative stress, which helps maintain cell viability; when UCP2 is silenced, these protective processes are disrupted, but introducing an autophagy inducer can reverse some damage.
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  • Cerebrovascular disease is a big health problem caused by high blood pressure, and new ways to treat it are needed.
  • A sugar called trehalose (TRE) showed promise in helping prevent strokes in rats that were prone to them while eating a high-salt diet.
  • TRE helped reduce strokes and kidney damage, lowered blood pressure, and improved brain and cell functions by activating a process that clears out damaged parts of cells.
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  • Sphingolipids, key molecules in cell membranes affecting blood vessel health, are linked to various vascular disorders but their role in hypertension-related brain and kidney damage is unclear.
  • This study compared sphingolipid metabolism in hypertensive rat strains (SHRSP and SHRSR) with normotensive rats (WKY) and found significant metabolic alterations in both the brain and kidneys of hypertensive rats.
  • Specific issues, like reduced enzyme expression related to sphingosine-1-phosphate metabolism, were unique to the SHRSP strain, indicating potential pathways for future research and therapies targeting hypertension-related organ damage.
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  • Uncoupling protein 2 (UCP2) is a mitochondrial protein that regulates processes such as mitochondrial membrane potential, reactive oxygen species production, and calcium balance, with expression influenced by genetic, transcriptional, and post-translational factors.
  • Activation of UCP2 through the AMPK/PPAR-α pathway has been shown to protect against renal damage and stroke in animal studies, and UCP2 is crucial in the context of heart diseases and metabolic disorders like obesity and diabetes.
  • Genetic variants of UCP2 in humans are linked to a higher risk of type 2 diabetes and ischemic stroke, while various natural compounds and clinical drugs can modulate UCP2 levels, highlighting its potential for treating multiple health
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Background The role of microRNAs dysregulation in tobacco cigarette smoking-induced vascular damage still needs to be clarified. We assessed the acute effects of tobacco cigarette smoking on endothelial cell-related circulating microRNAs in healthy subjects. In addition, we investigated the potential role of microRNAs in smoking-dependent endothelial cell damage.

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  • Stroke is a major cause of death and disability, and its pathogenesis involves complex inflammatory and immune responses that damage brain tissue initially but can later aid in repair.
  • Damage-associated molecular patterns (DAMPs) play a crucial role in exacerbating brain injury by disrupting the blood-brain barrier and promoting inflammation, while regulatory T lymphocytes (Tregs) can have protective effects.
  • Understanding these processes is essential for developing new therapies, though translating research findings from animal models to human treatment remains challenging and requires more investigation.
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  • The study investigates the impact of the T2238C variant of the ANP gene on cardiovascular events (CVEs) in patients with atrial fibrillation (AF) who are on anticoagulation therapy.
  • It analyzed 557 patients from the ATHERO-AF cohort, classifying them into wild type, heterozygous, and homozygous variants to assess the frequency of CVEs like stroke and myocardial infarction.
  • Results showed that patients with the homozygous C2238 allele had a significantly higher risk for CVEs, confirming this variant as a potential risk factor for these cardiovascular complications in AF patients.
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