The perception of the illness and the self-efficacy in the management of emotions in cardiac patients

Cardiac rehabilitation is the sum of psychological, physical and social treatments that are offered to cardiac patients to maintain or regain an active position in society. This study wants to evaluate changes in the perception of the illness and in the self-efficacy of the management of positive and negative emotions in patients who went through cardiac rehabilitation. Sixty-seven patients (20 females, 47 males) were selected within the cardiac rehabilitation unit in the Hospital of Cittadella (Italy). Illness Perception Questionnaire - revised version and the Scale for the self-efficacy of the management of positive and negative emotions were submitted at the beginning and at the end of the rehabilitation program. One-way analyses-of-variance were performed to evaluate different answers in questionnaires between pre- and post-evaluation, and to explore gender differences. A significant change was found in the perception of duration of illness, perceived as permanent and longer after the cardiac rehabilitation program. Furthermore, at the end of the cardiac rehabilitation program men perceived the illness more chronic than women, even if they are less worried and anxious. Intensive cardiac rehabilitation has a great emotional impact on cardiac patients, influencing their perception and management of the illness. Working on emotions, through psychological groups, helps patients change their beliefs by offering them a different perspective to approach the illness

Mitochondrial Ca2+-dependent NLRP3 activation exacerbates the Pseudomonas aeruginosa-driven inflammatory response in cystic fibrosis

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Physiological and RNA sequencing data of white lupin plants grown under Fe and P deficiency

This DIB article provides details about transcriptional and physiological response of Fe- and P-deficient white lupin roots, an extensive and complete description of plant response is shown in the research article \u201cPhysiological and transcriptomic data highlight common features between iron and phosphorus acquisition mechanisms in white lupin roots\u201d Venuti et al. [1]. White lupin plants were grown under hydroponic system and three different nutritional regimes: Fe deficiency (-Fe), P deficiency (-P), or Fe and P sufficiency (+P + Fe). Depending on nutritional treatment, white lupin plants showed changes in the fresh weights, in root external acidification and FeIII-reductase activity. Moreover, the transcriptomic changes occurring in apices and clusters of Fe-deficient lupin roots were investigated and compared with differences of gene expression occurring in P-deficient plants (-P) and in Fe- and P-sufficient plants (+P + Fe). Transcriptomic data are available in the public repository Gene Expression Omnibus (http://www.ncbi.nlm.nih.gov/geo) under the series entry (GSE112220). The annotation, mapping and enrichment analyses of differentially modulated transcripts were assessed

The versatility of mitochondrial calcium signals: From stimulation of cell metabolism to induction of cell death

AbstractBoth the contribution of mitochondria to intracellular calcium (Ca2+) signalling and the role of mitochondrial Ca2+ uptake in shaping the cytoplasmic response and controlling mitochondrial function are areas of intense investigation. These studies rely on the appropriate use of emerging techniques coupled with judicious data interpretation to a large extent. The development of targeted probes based on the molecular engineering of luminescent proteins has allowed the specific measurement of Ca2+ concentration ([Ca2+]) and adenosine trisphosphate concentration ([ATP]) in intracellular organelles or cytoplasmic subdomains. This approach has given novel information on different aspects of mitochondrial homeostasis

Human aquaporin-11 guarantees efficient transport of H2O2 across the endoplasmic reticulum membrane

Hydrogen peroxide (H2O2) is an essential second intracellular messenger. To reach its targets in the cytosol, H2O2 must cross a membrane, a feat that requires aquaporins (AQP) endowed with 'peroxiporin' activity (AQP3, AQP8, AQP9). Here, we exploit different organelle-targeted H2O2-sensitive probes to show that also AQP11 efficiently conduits H2O2. Unlike other peroxiporins, AQP11 is localized in the endoplasmic reticulum (ER), accumulating partly in mitochondrial-associated ER membranes (MAM). Its downregulation severely perturbs the flux of H2O2 through the ER, but not through the mitochondrial or plasma membranes. These properties make AQP11 a potential regulator of ER redox homeostasis and signaling.This work was supported in part through grants from the Associazione Italiana Ricerca sul Cancro (IG 2016-18824 to R.S.), the Fondazione Cariplo (2015-0591 to R.S.), and the Telethon (GGP15059 to R.S.). A.R. was supported by local funds from the University of Ferrara and the Italian Ministry of Health (GR-2016-02364602). Italian Association for Cancer Research (AIRC, IG-18624), Telethon (GGP11139B), and local funds from the University of Ferrara to P.P

The Multifaceted Roles of Autophagy in Infectious, Obstructive, and Malignant Airway Diseases

Autophagy is a highly conserved dynamic process by which cells deliver their contents to lysosomes for degradation, thus ensuring cell homeostasis. In response to environmental stress, the induction of autophagy is crucial for cell survival. The dysregulation of this degradative process has been implicated in a wide range of pathologies, including lung diseases, representing a relevant potential target with significant clinical outcomes. During lung disease progression and infections, autophagy may exert both protective and harmful effects on cells. In this review, we will explore the implications of autophagy and its selective forms in several lung infections, such as SARS-CoV-2, Respiratory Syncytial Virus (RSV) and Mycobacterium tuberculosis (Mtb) infections, and different lung diseases such as Cystic Fibrosis (CF), Chronic Obstructive Pulmonary Disease (COPD), and Malignant Mesothelioma (MM)

Functional and structural alterations in the endoplasmic reticulum and mitochondria during apoptosis triggered by C2-ceramide and??CD95/APO-1/FAS receptor stimulation

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Molecular Mechanisms of Autophagy in Cancer Development, Progression, and Therapy

Autophagy is an evolutionarily conserved and tightly regulated process that plays an important role in maintaining cellular homeostasis. It involves regulation of various genes that function to degrade unnecessary or dysfunctional cellular components, and to recycle metabolic substrates. Autophagy is modulated by many factors, such as nutritional status, energy level, hypoxic conditions, endoplasmic reticulum stress, hormonal stimulation and drugs, and these factors can regulate autophagy both upstream and downstream of the pathway. In cancer, autophagy acts as a double-edged sword depending on the tissue type and stage of tumorigenesis. On the one hand, autophagy promotes tumor progression in advanced stages by stimulating tumor growth. On the other hand, autophagy inhibits tumor development in the early stages by enhancing its tumor suppressor activity. Moreover, autophagy drives resistance to anticancer therapy, even though in some tumor types, its activation induces lethal effects on cancer cells. In this review, we summarize the biological mechanisms of autophagy and its dual role in cancer. In addition, we report the current understanding of autophagy in some cancer types with markedly high incidence and/or lethality, and the existing therapeutic strategies targeting autophagy for the treatment of cancer

Immunosuppressive activity of tumor-infiltrating myeloid cells in patients with meningioma

Meningiomas WHO grade I and II are common intracranial tumors in adults that normally display a benign outcome, but are characterized by a great clinical heterogeneity and frequent recurrence of the disease. Although the presence of an immune cell infiltrate has been documented in these tumors, a clear phenotypical and functional characterization of the immune web is missing. Here, we performed an extensive immunophenotyping of peripheral blood and fresh tumor tissue at surgery by multiparametric flow cytometry in 34 meningioma patients, along with immunosuppressive activity of sorted cells of myeloid origin. Four subsets of myeloid cells, phenotypically corresponding to myeloid-derived suppressor cells (MDSCs) are detectable in the blood and in the tumor tissue of patients and three of them are significantly expanded in the blood of patients, but show no evidence of suppressive activity. At the tumor site, a large leukocyte infiltrate is present, predominantly constituted by CD33 myeloid cells, largely composed of macrophages endowed with suppressive activity and significantly expanded in grade II meningioma patients as compared to grade I

A chemogenomic screening identifies CK2 as a target for pro-senescence therapy in PTEN-deficient tumours

Enhancement of cellular senescence in tumours triggers a stable cell growth arrest and activation of an antitumour immune response that can be exploited for cancer therapy. Currently, there are only a limited number of targeted therapies that act by increasing senescence in cancers, but the majority of them are not selective and also target healthy cells. Here we developed a chemogenomic screening to identify compounds that enhance senescence in PTEN-deficient cells without affecting normal cells. By using this approach, we identified casein kinase 2 (CK2) as a pro-senescent target. Mechanistically, we show that Pten loss increases CK2 levels by activating STAT3. CK2 upregulation in Pten null tumours affects the stability of Pml, an essential regulator of senescence. However, CK2 inhibition stabilizes Pml levels enhancing senescence in Pten null tumours. Taken together, our screening strategy has identified a novel STAT3-CK2-PML network that can be targeted for pro-senescence therapy for cancer