UNIVERSITY VALUE FOR SUSTAINABILITY. REFLECTIONS FROM A CASE STUDY

Numa fase caracterizada por mudanças políticas internacionais e nacionais, crises socioeconómicas, emergências ambientais, mudanças estruturais do sistema de instrução superior, os papéis das universidades na sociedade assumem novo significado e conteúdos adicionais. O documento examina o papel no qual as universidades podem atuar, para favorecer e acompanhar os processos locais de desenvolvimento sustentável, segundo os resultados de uma sondagem realizada numa pequena universidade italiana, a Universidade da região Molise. A investigação examinou o parecer do pessoal interno, e das partes externas envolvidas, sobre a identidade, os papéis e os valores que a Universidade da região Molise desenvolve no território, na sociedade, no desenvolvimento local sustentável. O caso de estudo evidencia a importância do envolvimento das partes num processo contínuo de identificação e de concriação de valores para a sustentabilidade.In a phase characterized by international and domestic political changes, socio-economic crises, environmental emergencies, structural changes of the higher education system, the universities’ roles in the society takes on a new significance and additional contents. The paper discusses the role that universities may play in encouraging and accompanying local sustainable development processes based on the results of a survey implemented in a small Italian university, the University of Molise. The survey investigated the opinion of internal staff and external stakeholders about the identity, the roles and values that University of Molise plays for the territory, the society, the local sustainable development. The case study highlights the importance of stakeholder involvement along a continuous process of identification and co-creation of values for sustainability

Hyperprolactinemia induced by hCG leads to metabolic disturbances in female mice

The metabolic syndrome is a growing epidemic; it increases the risk for diabetes, cardiovascular disease, fatty liver, and several cancers. Several reports have indicated a link between hormonal imbalances and insulin resistance or obesity. Transgenic (TG) female mice overexpressing the human chorionic gonadotropin β-subunit (hCGβ+ mice) exhibit constitutively elevated levels of hCG, increased production of testosterone, progesterone and prolactin, and obesity. The objective of this study was to investigate the influence of hCG hypersecretion on possible alterations in the glucose and lipid metabolism of adult TG females. We evaluated fasting serum insulin, glucose, and triglyceride levels in adult hCGβ+ females and conducted intraperitoneal glucose and insulin tolerance tests at different ages. TG female mice showed hyperinsulinemia, hypertriglyceridemia, and dyslipidemia, as well as glucose intolerance and insulin resistance at 6 months of age. A 1-week treatment with the dopamine agonist cabergoline applied on 5-week-old hCGβ+ mice, which corrected hyperprolactinemia, hyperandrogenism, and hyperprogesteronemia, effectively prevented the metabolic alterations. These data indicate a key role of the hyperprolactinemia-induced gonadal dysfunction in the metabolic disturbances of hCGβ+ female mice. The findings prompt further studies on the involvement of gonadotropins and prolactin on metabolic disorders and might pave the way for the development of new therapeutic strategies.Fil: Ratner, Laura Daniela. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Stevens, Guillermina. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Ramos Mejía"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Bonaventura, Maria Marta. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Lux, Victoria Adela R.. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Poutanen, Matti. University of Turku; FinlandiaFil: Calandra, Ricardo Saul. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Huhtaniemi, Ilpo T.. University of Turku; FinlandiaFil: Rulli, Susana Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentin

Improvement of phonemic fluency following leftward prism adaptation

Anatomo functional studies of prism adaptation (PA) have been shown to modulate a brain frontal-parieto-temporal network, increasing activation of this network in the hemisphere ipsilateral to the side of prism deviation. This effect raises the hypothesis that left prism adaptation, modulating frontal areas of the left hemisphere, could modify subjects' performance on linguistic tasks that map on those areas. To test this hypothesis, 51 healthy subjects participated in experiments in which leftward or rightward prism adaptation were applied before the execution of a phonemic fluency task, i.e., a task with strict left hemispheric lateralization onto frontal areas. Results showed that leftward PA significantly increased the number of words produced whereas rightward PA did not significantly modulate phonemic fluency. The present findings document modulation of a language ability following prism adaptation. The results could have a huge clinical impact in neurological populations, opening new strategies of intervention for language and executive dysfunctions

Boosting Phonological Fluency Following Leftward Prismatic Adaptation: A New Neuromodulation Protocol for Neurological Deficits?

Prism adaptation (PA) has been recently shown to modulate a brain frontal-parieto-temporal network, with an increase of excitation of this network in the hemisphere ipsilateral to the side of prismatic deviation. This effect raises the hypothesis that left prismatic adaptation, modulating the excitability of frontal areas of the left hemisphere could modulate subjects’ performance on linguistic tasks that map on those areas. To test this hypothesis, sixty-one healthy subjects participated in experiments in which leftward, rightward or no-PA were applied before the execution of a phonological fluency task, i.e. a task with the strict left hemispheric lateralization and mapping onto frontal areas. Leftward-PA significantly increased the number of words produced compared with the pre-PA (p = .0017), R-PA (p=.00013) and no-PA (p=.0005) sessions. In contrast, rightward-PA did not significantly modulate phonological fluency compared with the pre-PA (p = .92) and no-PA (p = .99) sessions. The effect of leftward PA on phonological fluency correlated with the magnitude of spatial aftereffect, i.e. the spatial bias towards the side of space opposite to prismatic deviation following prisms removal (r = .51; p = .04). The present findings document for the first time modulation of a language ability following prismatic adaptation. The results could have a huge clinical impact on neurological populations, opening new strategies of intervention for language and executive dysfunctions

Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice

Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, μMT[superscript −/−] mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen

A Model of DENV-3 Infection That Recapitulates Severe Disease and Highlights the Importance of IFN-γ in Host Resistance to Infection

There are few animal models of dengue infection, especially in immunocompetent mice. Here, we describe alterations found in adult immunocompetent mice inoculated with an adapted Dengue virus (DENV-3) strain. Infection of mice with the adapted DENV-3 caused inoculum-dependent lethality that was preceded by several hematological and biochemical changes and increased virus dissemination, features consistent with severe disease manifestation in humans. IFN-γ expression increased after DENV-3 infection of WT mice and this was preceded by increase in expression of IL-12 and IL-18. In DENV-3-inoculated IFN-γ−/− mice, there was enhanced lethality, which was preceded by severe disease manifestation and virus replication. Lack of IFN-γ production was associated with diminished NO-synthase 2 (NOS2) expression and higher susceptibility of NOS2−/− mice to DENV-3 infection. Therefore, mechanisms of protection to DENV-3 infection rely on IFN-γ-NOS2-NO-dependent control of viral replication and of disease severity, a pathway showed to be relevant for resistance to DENV infection in other experimental and clinical settings. Thus, the model of DENV-3 infection in immunocompetent mice described here represents a significant advance in animal models of severe dengue disease and may provide an important tool to the elucidation of immunopathogenesis of disease and of protective mechanisms associated with infection

The SARS-CoV-2 spike protein binds and modulates estrogen receptors

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) protein binds angiotensin-converting enzyme 2 as its primary infection mechanism. Interactions between S and endogenous proteins occur after infection but are not well understood. We profiled binding of S against >9000 human proteins and found an interaction between S and human estrogen receptor alpha (ER alpha). Using bioinformatics, supercomputing, and experimental assays, we identified a highly conserved and functional nuclear receptor coregulator (NRC) LXD-like motif on the S2 sub-unit. In cultured cells, S DNA transfection increased ER alpha cytoplasmic accumulation, and S treatment induced ER-dependent biological effects. Non-invasive imaging in SARS-CoV-2-infected hamsters localized lung pathology with increased ER alpha lung levels. Postmortem lung experiments from infected hamsters and humans confirmed an increase in cytoplasmic ER alpha and its colocalization with S in alveolar macrophages. These findings describe the discovery of a S-ER alpha interaction, imply a role for S as an NRC, and advance knowledge of SARS-CoV-2 biology and coronavirus disease 2019 pathology

Immunohistochemical expression and distribution of orexin, orphanin and leptin in the major salivary glands of some mammals

The aim of the study was to determine by immunochemistry the expression of leptin, orexin A andorphanin FQ in the major salivary glands (parotid, submandibular and sublingual) of rat, sheep and cow. Thesepeptides, originally synthesized in central nervous system, adipose tissue and peripheral tissues including gastrointestinaltract, play an orexigenic (orphanin and orexin) or anorexigenic (leptin) roles in the intricate neuronalnetwork appointed to the control of nutritional homeostasis. Peptide-specific immunoreactivity was presentin the studied salivary glands with various intensities in different species, in the ductal epithelium, sometimes inthe acinar epithelium, and in nervous trunks spread in connective tissue stroma. The obtained data show thatsalivary glands present an unexpected source of orexigenic and anorexigenic peptides which with their autocrine,paracrine, and endocrine mechanisms of action may participate in the control of salivary gland function

Gram-Negative Bacteria Holding Together in a Biofilm: The Acinetobacter baumannii Way

Bacterial biofilms are a serious public-health problem worldwide. In recent years, the rates of antibiotic-resistant Gram-negative bacteria associated with biofilm-forming activity have increased worrisomely, particularly among healthcare-associated pathogens. Acinetobacter baumannii is a critically opportunistic pathogen, due to the high rates of antibiotic resistant strains causing healthcare-acquired infections (HAIs). The clinical isolates of A. baumannii can form biofilms on both biotic and abiotic surfaces; hospital settings and medical devices are the ideal environments for A. baumannii biofilms, thereby representing the main source of patient infections. However, the paucity of therapeutic options poses major concerns for human health infections caused by A. baumannii strains. The increasing number of multidrug-resistant A. baumannii biofilm-forming isolates in association with the limited number of biofilm-eradicating treatments intensify the need for effective antibiofilm approaches. This review discusses the mechanisms used by this opportunistic pathogen to form biofilms, describes their clinical impact, and summarizes the current and emerging treatment options available, both to prevent their formation and to disrupt preformed A. baumannii biofilms