Publications by authors named "Anna Catania"

The increasing use of marginal lungs for transplantation encourages novel approaches to improve graft quality. Melanocortins and their receptors (MCRs) exert multiple beneficial effects in pulmonary inflammation. We tested the idea that treatment with the synthetic α-melanocyte-stimulating hormone analogue [Nle4,D-Phe7]-α-MSH (NDP-MSH) during ex vivo lung perfusion (EVLP) could exert positive influences in lungs exposed to different injuries.

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The clinical hallmarks of infections caused by critical respiratory viruses consist of pneumonia, which can progress to acute lung injury (ALI), and systemic manifestations including hypercoagulopathy, vascular dysfunction, and endotheliitis. The disease outcome largely depends on the immune response produced by the host. The bio-molecular mechanisms underlying certain dire consequences of the infection partly arise from an aberrant production of inflammatory molecules, an event denoted as "cytokine storm".

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Lignocellulosic fibers and microcellulose have been obtained by simple alkaline treatment from softwood almond shells. In particular, the Prunus dulcis Miller (D.A.

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Cellulosic fibres have been obtained by green procedures from the cladodes of (L.) Mill., constituting a large agro industrial waste in our territory.

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Aims And Objectives: To investigate the experiences of male partners of female breast cancer patients who had undergone surgery and oncological treatment and who were still raising children.

Background: Research on the psychological effects of breast cancer has focused primarily on the patients undergoing treatment, neglecting the effect of such a condition on their closest family members. This study addresses this gap by focusing on understanding the effects of this disease on male partners of these patients.

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Melanocortin peptides induce neuroprotection in acute and chronic experimental neurodegenerative conditions. Melanocortins likewise counteract systemic responses to brain injuries. Furthermore, they promote neurogenesis by activating critical signaling pathways.

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Background: Alpha-melanocyte-stimulating-hormone (α-MSH) has marked anti-inflammatory potential. Proinflammatory cytokines are critical mediators of the disturbed cartilage homeostasis in osteoarthritis, inhibiting anabolic activities and increasing catabolic activities in chondrocytes. Since human chondrocytes express α-MSH receptors, we evaluated the role of the peptide in modulating chondrocyte production of pro-inflammatory cytokines, matrix metalloproteinases (MMPs), tissue inhibitors of MMPs (TIMPs), inducible nitric oxide synthase (iNOS) and nitric oxide (NO) in response to interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α).

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Melanocortins are endogenous peptides that exert protective actions on the host physiology. The broad modulatory effects of these molecules suggest that they might influence the mediator network induced during liver regeneration. The research aim was to determine if melanocortin treatment alters liver molecular changes induced by partial hepatectomy (PH).

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Previous investigations indicate that α-melanocyte-stimulating hormone (α-MSH) and certain synthetic analogues of it exert antimicrobial effects against bacteria and yeasts. However, these molecules have weak activity in standard microbiology conditions and this hampers a realistic clinical use. The aim in the present study was to identify novel peptides with broad-spectrum antimicrobial activity in growth medium.

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The therapeutic benefits of adrenocorticotropic hormone in multiple sclerosis are usually ascribed to its corticotropic actions. Evidence is presented that adrenocorticotropic hormone, approved for multiple sclerosis relapses, acts via corticosteroid-independent melanocortin pathways to engender down-modulating actions on immune-system cells and the cytokines they synthesize. Immune response-dampening effects are also brought about by agent-induced neurotransmitters that inhibit immunocytes.

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Background: Melanocortin peptides improve hemodynamic parameters and prevent death during severe hemorrhagic shock. In the present research we determined influences of a synthetic melanocortin 1/4 receptor agonist on the molecular changes that occur in rat liver during hemorrhage.

Methods: Controlled-volume hemorrhage was performed in adult rats under general anesthesia by a stepwise blood withdrawal until mean arterial pressure fell to 40 mmHg.

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We evaluated the erythrocyte deformability in a group of subjects with polycythemia vera (PV) using a Rheodyn-SSD Laser Diffractometer, at the shear stresses of 6, 12, 30 and 60 Pa. Our data showed a significant decrease of red cell deformability, expressed as elongation index (EI), in PV subjects compared with normal controls. These results suggest that the hyperviscosity syndrome accompanying this myeloproliferative disease may be considered a mixed form, resulting from the association of a polycythemic condition with a sclerocythemic disorder.

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Subarachnoid hemorrhage (SAH) is still a major cause of morbidity and mortality. α-Melanocyte stimulating hormone (α-MSH) and other melanocortin peptides exert potent neuroprotective action and they might modulate key molecules involved in SAH-induced vasospasm. The aim of this research was to determine whether treatment with the α-MSH analog Nle4,DPhe7-α-MSH (NDP-MSH) exerts protective effects in experimental SAH in the rat.

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Infantile spasms is an epileptic encephalopathy of early infancy with specific clinical and electroencephalographic (EEG) features, limited treatment options, and a poor prognosis. Efforts to develop improved treatment options have been hindered by the lack of experimental models in which to test prospective therapies. The neuropeptide adrenocorticotropic hormone (ACTH) is effective in many cases of infantile spasms, although its mechanism(s) of action is unknown.

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Systemic inflammatory reactions are pivotal in many disorders and have important secondary influences in many more. Although inflammation is initially useful to limit infection, it can also be detrimental and cause organ failure. Modulation of systemic reactions is important to restrict mediator release and limit cell activation that could cause harmful consequences.

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Melanocortin peptides, the collective term for alpha-, beta-, and gamma-melanocyte-stimulating hormone (alpha-, beta-, gamma-MSH) and adrenocorticotropic hormone (ACTH), are elements of an ancient modulatory system. Natural melanocortins derive from the common precursor pro-opiomelanocortin (POMC). Five receptor subtypes for melanocortins (MC1-MC5) are widely distributed in brain regions and in peripheral cells.

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Introduction: The melanocortin peptides have marked anti-inflammatory potential, primarily through inhibition of proinflammatory cytokine production and action on phagocytic cell functions. Gout is an acute form of arthritis caused by the deposition of urate crystals, in which phagocytic cells and cytokines play a major pathogenic role. We examined whether alpha-melanocyte-stimulating hormone (alpha-MSH) and its synthetic derivative (CKPV)2 influence urate crystal-induced monocyte (Mo) activation and neutrophil responses in vitro.

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alpha-Melanocyte-stimulating hormone (alpha-MSH) is a pro-opiomelanocortin (POMC)-derived peptide that exerts multiple protective effects on host cells. Previous investigations showed that treatment with alpha-MSH or synthetic melanocortin agonists reduces heart damage in reperfusion injury and transplantation. The aim of this preclinical research was to determine whether melanocortin treatment induces preconditioning-like cardioprotection.

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Acute brain injury and brain death exert detrimental effects on peripheral host cells. Brain-induced impairment of immune function makes patients more vulnerable to infections that are a major cause of morbidity and mortality after stroke, trauma, or subarachnoid hemorrhage (SAH). Systemic inflammation and organ dysfunction are other harmful consequences of CNS injury.

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In their report, Rauch et al. did not find candidacidal activity of α-melanocyte-stimulating hormone (α-MSH) in Sabouraud dextrose broth. The lack of killing activity by the natural α-MSH in broth medium may occur because of accelerated Candida replication or peptide degradation by fungal enzymes.

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Cell-cycle defects are responsible for cancer onset and growth. We studied the expression profile of 60 genes involved in cell cycle in a series of malignant mesotheliomas (MMs), normal pleural tissues, and MM cell cultures using a quantitative polymerase chain reaction-based, low-density array. Nine genes were significantly deregulated in MMs compared with normal controls.

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Background: Alpha-melanocyte stimulating hormone (alpha-MSH) is a neuropeptide which modulates inflammation. Prior studies have documented decreased alpha-MSH concentrations in patients with acute traumatic brain injury and subarachnoid hemorrhage. We hypothesized that alpha-MSH levels would be decreased in critically injured patients and that this would correlate with poor outcome.

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Nitric oxide (NO) has a role in the pathophysiology of acute and chronic cardiovascular events. We studied the plasma concentration of NO stable end products (nitrite and nitrate--NOx) in 43 patients aged<46 years, with recent acute myocardial infarction (AMI). The evaluation was effected at the initial stage, after 3 and 12 months.

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In a group of young subjects with acute myocardial infarction (AMI) (68 men and 7 women; mean age 39.6+/-5.7 years) we examined the plasma concentration of elastase, the thiobarbituric acid-reactive substances (TBARS) and the total antioxidant status (TAS) at the initial stage of AMI.

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Alpha-melanocyte stimulating hormone (alpha-MSH) and other melanocortins make up a family of endogenous peptides derived from pro-opiomelanocortin. Through binding to five melanocortin receptors (MCR), these peptides exert multiple influences on the host, including anti-inflammatory and immunomodulatory effects. The wide distribution of at least three melanocortin receptor subtypes (MC1R, MC3R and MC4R) in neural, glial and endothelial cells suggests that these receptors could be pharmacological targets for neuroprotective therapies.

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