Publications by authors named "Ariana Garcia-Ojalvo"

The early expectations about growth factors' (GFs') discovery as an undisputed therapeutic solution for chronic wounds progressively eclipsed when they failed to accelerate acute wound closure and restore the healing trajectory of stagnant ulcers. Critical knowledge about chronic wound biology and GF pharmacology was a conundrum at that time. Diabetes undermines keratinocytes' and fibroblasts' physiology, impairing skin healing abilities.

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Dilated cardiomyopathy (DCM) is a fatal myocardial condition with ventricular structural changes and functional deficits, leading to systolic dysfunction and heart failure (HF). DCM is a frequent complication in oncologic patients receiving Doxorubicin (Dox). Dox is a highly cardiotoxic drug, whereas its damaging spectrum affects most of the organs by multiple pathogenic cascades.

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Cancer remains a worldwide cause of morbidity and mortality. Investigational research efforts have included the administration of tumor-derived extracts to healthy animals. Having previously demonstrated that the administration of non-transmissible, human cancer-derived homogenates induced malignant tumors in mice, here, we examined the consequences of administering 50 or 100 µg of protein of crude homogenates from mammary carcinoma, pancreatic adenocarcinoma, and melanoma samples in 6 inoculations per week during 2 months.

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An impaired healing response underlies diabetic foot wound chronicity, frequently translating to amputation, disability, and mortality. Diabetics suffer from underappreciated episodes of post-epithelization ulcer recurrence. Recurrence epidemiological data are alarmingly high, so the ulcer is considered in "remission" and not healed from the time it remains epithelialized.

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Cellular memory is a controversial concept representing the ability of cells to "write and memorize" stressful experiences via epigenetic operators. The progressive course of chronic, non-communicable diseases such as type 2 diabetes mellitus, cancer, and arteriosclerosis, is likely driven through an abnormal epigenetic reprogramming, fostering the hypothesis of a cellular pathologic memory. Accordingly, cultured diabetic and cancer patient-derived cells recall behavioral traits as when in the donor's organism irrespective to culture time and conditions.

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Article Synopsis
  • Diabetic foot ulcers (DFU) have high inflammation levels due to persistent high blood sugar and local infections, making healing difficult; epidermal growth factor (EGF) treatment has shown promise in promoting healing and reducing amputation risk.
  • The study focuses on the effect of EGF on fibroblasts taken from DFU, particularly how it counters inflammation induced by lipopolysaccharides (LPS) in a simulated hyperglycaemic environment.
  • Results indicate that EGF can reduce the inflammatory response in fibroblasts challenged by LPS, suggesting it may be beneficial for DFU treatment in real-life clinical scenarios.
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  • Lower-extremity arterial disease is a growing health issue that can result in amputations and increased mortality, but the underlying causes of vascular wall changes are not well understood.* -
  • Researchers hypothesized that a "vascular tissue memory" might be passed from humans to healthy animals through signaling molecules, leading to similar vascular issues like wall thickening in the recipient animals.* -
  • In experiments, injecting arteriosclerotic tissue into rats caused significant changes in their vascular structure within days, suggesting these changes are driven by factors from the human tissue, opening up new avenues for studying atherosclerosis.*
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Background: Diabetic foot ulcers are a common diabetic complication leading to alarming figures of amputation, disability, and early mortality. The diabetic glucooxidative environment impairs the healing response, promoting the onset of a 'wound chronicity phenotype'. In 50% of ulcers, these non-healing wounds act as an open door for developing infections, a process facilitated by diabetic patients' dysimmunity.

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  • Lower limb ulcers in type-2 diabetes (T2DM) patients can lead to amputations and decreased survival rates.
  • The study explores how T2DM tissue can transfer impaired healing traits to healthy rats, mimicking diabetic wound characteristics.
  • Findings suggest that certain factors in diabetic tissues may contribute to healing problems and could have future implications for diabetes treatment strategies.
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Insulin plays a major neuroprotective and trophic function for cerebral cell population, thus countering apoptosis, beta-amyloid toxicity, and oxidative stress; favoring neuronal survival; and enhancing memory and learning processes. Insulin resistance and impaired cerebral glucose metabolism are invariantly reported in Alzheimer's disease (AD) and other neurodegenerative processes. AD is a fatal neurodegenerative disorder in which progressive glucose hypometabolism parallels to cognitive impairment.

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Lower-extremity diabetic ulcers are responsible for 80% of annual worldwide nontraumatic amputations. Epidermal growth factor (EGF) reduction is one of the molecular pillars of diabetic ulcer chronicity, thus EGF administration may be considered a type of replacement therapy. Topical EGF ad-ministration to improve and speed wound healing began in 1989 on burn patients as part of an acute-healing therapy.

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The insulin signaling pathway plays a pivotal role in glucose metabolism and metabolic homeostasis. Disruption of this pathway is commonly seen in critical illness such as following severe burn injuries where homeostatic control is lost, leading to "insulin resistance" with poor blood glucose control. The aberrant signaling pathways involved in insulin resistance following burn injury include increases in hyperglycemic stress hormones, pro-inflammatory cytokines and free radical production.

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Diabetic foot ulcer is one of the most frightened diabetic complications leading to amputation disability and early mortality. Diabetic wounds exhibit a complex networking of inflammatory cytokines, local proteases, and reactive oxygen and nitrogen species as a pathogenic polymicrobial biofilm, overall contributing to wound chronification and host homeostasis imbalance. Intralesional infiltration of epidermal growth factor (EGF) has emerged as a therapeutic alternative to diabetic wound healing, reaching responsive cells while avoiding the deleterious effect of proteases and the biofilm on the wound's surface.

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Article Synopsis
  • * This study specifically looked at how growth hormone releasing peptide 6 (GHRP6) could prevent and potentially reverse HTS in rabbits, with treatments lasting 30 days and effects monitored through various methods.
  • * GHRP6 successfully prevented new HTS from forming without the side effects seen with the standard treatment (triamcinolone acetonide), but it didn't significantly improve existing scars; early data suggests GHRP6 works through various biological pathways related to skin cell functions and healing.
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Soon after epidermal growth factor (EGF) discovery, some models appeared demonstrating its property to enhance cutaneous wound healing. EGF was the first growth factor (GF) introduced in the clinical arena as a healing enhancer, exerting its mitogenic effects on epithelial, fibroblastoid, and endothelial cells via a tyrosine kinase membrane receptor. Compelling evidences from the 90s documented that, for EGF, locally prolonged bioavailability and hourly interaction with the receptor were necessary for a successful tissue response.

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Background: Growth hormone-releasing peptides (GHRPs) constitute a group of small synthetic peptides that stimulate the growth hormone secretion and the downstream axis activity. Mounting evidences since the early 1980s delineated unexpected pharmacological cardioprotective and cytoprotective properties for the GHRPs. However, despite intense basic pharmacological research, alternatives to prevent cell and tissue demise before lethal insults have remained as an empty niche in the clinical armamentarium.

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Article Synopsis
  • - GHRP-6 has cytoprotective effects and can reduce liver fibrosis while also showing potential in enhancing wound healing, as indicated by its impact on granulation tissue in skin wounds.
  • - In experiments with Wistar rats and rabbit models, GHRP-6 treatment facilitated faster wound closure by diminishing inflammatory responses and fibrotic cytokine expression.
  • - The research suggests that the CD36 receptor is a viable target for pharmacological approaches to improve wound healing aesthetics and reduce excessive scarring.
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  • * This study explored the effects of epidermal growth factor treatment on patients with DFUs, focusing on markers of oxidative stress and antioxidant levels.
  • * Results showed that DFU patients had high oxidative stress and low antioxidants, but treatment with epidermal growth factor improved their biochemical profiles, suggesting it helps restore redox balance.
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