13 research outputs found

    Diagnosis and Treatment of Pulmonary Disease in Sea Turtles (Caretta caretta)

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    The aim of this study was to describe the clinical signs, radiographic, endoscopic and CT findings, cytological and microbiological findings and treatments of pulmonary diseases in sea turtles, in order to obtain an accurate diagnosis that avoids unnecessary therapy and antibiotic-resistance phenomena. In total, 14 loggerheads (Caretta caretta), with clinical and/or radiographic findings of pulmonary pathology, were assessed through various combinations of clinical, radiological, CT, endoscopic examination and bronchoalveolar lavage, which recovered fluid for cytologic and microbiologic analysis. In all cases, radiographic examination led to a diagnosis of pulmonary disorders—4 unilateral and 10 bilateral. All bacteria cultured were identified as Gram-negative. Antibiotic resistance was greater than 70% for all beta-lactams tested. In addition, all bacterial strains were 100% resistant to colistin sulfate and tetracycline. Specific antibiotic therapies were formulated for seven sea turtles using Enrofloxacin, and for four sea turtles using ceftazidime. In two turtles, antibiotic therapy was not included due to the presence of antibiotic resistance against all the antibiotics evaluated. In both cases, the coupage technique and environmental management allowed the resolution of the lung disease without antibiotics. All 14 sea turtles were released back into the sea. Radiographic examination must be considered the gold standard for screening sea turtles that show respiratory signs or abnormal buoyancy. Susceptibility testing with antimicrobials allowed appropriate therapy, including the reduction of antibiotic-resistance

    Loss of CDKL5 Causes Synaptic GABAergic Defects That Can Be Restored with the Neuroactive Steroid Pregnenolone-Methyl-Ether

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    : CDKL5 deficiency disorder (CDD) is an X-linked neurodevelopmental disorder characterised by early-onset drug-resistant epilepsy and impaired cognitive and motor skills. CDD is caused by mutations in cyclin-dependent kinase-like 5 (CDKL5), which plays a well-known role in regulating excitatory neurotransmission, while its effect on neuronal inhibition has been poorly investigated. We explored the potential role of CDKL5 in the inhibitory compartment in Cdkl5-KO male mice and primary hippocampal neurons and found that CDKL5 interacts with gephyrin and collybistin, two crucial organisers of the inhibitory postsynaptic sites. Through molecular and electrophysiological approaches, we demonstrated that CDKL5 loss causes a reduced number of gephyrin puncta and surface exposed γ2 subunit-containing GABAA receptors, impacting the frequency of miniature inhibitory postsynaptic currents, which we ascribe to a postsynaptic function of CDKL5. In line with previous data showing that CDKL5 loss impacts microtubule (MT) dynamics, we showed that treatment with pregnenolone-methyl-ether (PME), which promotes MT dynamics, rescues the above defects. The impact of CDKL5 deficiency on inhibitory neurotransmission might explain the presence of drug-resistant epilepsy and cognitive defects in CDD patients. Moreover, our results may pave the way for drug-based therapies that could bypass the need for CDKL5 and provide effective therapeutic strategies for CDD patients

    Narrazioni e migrazioni

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    La migrazione, da oggetto di ricerca marginale nell'ambito delle scienze umane e sociali, come rimarcava Abdelmalek Sayad, assurge nell'epoca attuale ad oggetto di ricerca fondamentale per interrogarsi sul legame sociale e sulla relazione con l'alterità dove l'altro, portatore di una differenza oggettiva con il suo arrivo e la sua permanenza, porta con sé storie sociali che vanno ri-conosciute, ri-elaborate e approfondite, insieme alle strutture che ne caratterizzano la persona: le strutture sociali, le tradizioni e le religioni, le strutture politiche e mentali. L'erranza dei migranti, la transmigrazione di persone e storie sociali tra mondi e culture, comporta dei cambiamenti ed à al tempo stesso fecondazione reciproca di diversità che si arricchiscono reciprocamente. L'erranza richiede tuttavia uno spazio d'incontro tra sensibilità e patrimoni culturali differenti, in parte negato da una società che ha paura dell'alterità, dove l'incontro diventa narrazione di due o più alterità. Il tema e l'esperienza della narrazione, divenuta elemento significativo della cultura contemporanea e pratica sociale dove più persone mettono in comune una storia, si costituisce come approccio fondamentale al rapporto con culture diverse. Se la ricerca sociale non può pertanto trascurare ed ignorare la storia sociale delle persone, non vi è osservazione e comprensione delle relazioni umane che possa al tempo stesso sottovalutare gli spazi attraverso i quali transitano e vivono le persone, considerando il rapporto con noi stessi e l'altro nell'ambito del rapporto con lo spazio di vita. Nei due contributi presentati in questa sezione le narrazioni vengono infatti utilizzate come strumenti per aprire un punto d'osservazione su alcuni aspetti del fenomeno migratorio a partire dai vissuti individuali dei migranti. La raccolta delle narrazioni - integrata con percorsi etnografici - fa emergere spunti molto interessanti non solo sui percorsi di vita dei singoli migranti o sulle categorie di significato da loro utilizzate per dare senso all'esperienza migratoria, ma anche sulla migrazione in generale. Viene inoltre problematizzato l'utilizzo delle narrazioni, interrogandosi sul reale contributo conoscitivo di questa fonte e sulla sua capacità di comunicare le caratteristiche del contesto in cui agisce l'intervistato e le interazioni che in esso hanno luogo

    Clinical Findings, Management, Imaging, and Outcomes in Sea Turtles with Traumatic Head Injuries: A Retrospective Study of 29 <i>Caretta caretta</i>

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    Sea turtles are considered endangered species, largely due to anthropogenic activities. Much of the trauma in these species involves the carapace and skull, resulting in several degrees of damage to the pulmonary and nervous systems. Among traumatic injuries, those involving the skull can be complicated by brain exposure, and turtles with severe skull injuries that have nervous system impairment, emaciation, and dehydration can often die. Between July 2014 and February 2022, a total of 1877 loggerhead sea turtles (Caretta caretta) were referred for clinical evaluation at the Sea Turtle Clinic (STC) of the Department of Veterinary Medicine of the University of Bari. A retrospective study of 29 consecutive cases of loggerhead sea turtles (Caretta caretta) with skull lesions of different degrees of severity is reported. On admission, physical and neurological evaluations were performed to assess and grade the lesions and neurological deficits. In 20 of the 29 sea turtles with more serious head trauma, computed tomography (CT) findings in combination with physical and neurological assessment enabled the evaluation of the potential correlation between deficits and the extent of head injuries. All sea turtles underwent curettage of the skull wounds, and the treatment protocol included the use of the plant-derived dressing 1 Primary Wound Dressing® (Phytoceutical AG, Endospin Italia) applied on the wound surface as a primary dressing. Out of 29 sea turtles, 21 were released after a time ranging from a few days to 8 months. To the best of our knowledge, the literature lacks specific data on the incidence, correlations with neurological deficits, complications, and survival rate of loggerhead sea turtles with traumatic head injuries

    Chondroblastic Osteosarcoma Associated with Previous Chronic Osteomyelitis Caused by Serratia liquefaciens in a German Shepherd Dog

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    Development of bone tumors as a result of chronic osteomyelitis represents a relatively rare and late complication in humans and animals. We described a malignant transformation (chondroblastic osteosarcoma) in a 7-year-old German shepherd with a history of polyostotic osteomyelitis caused by Serratia liquefaciens when the dog was 15 months old. The tumor developed in the right humeral diaphysis, one of the sites of polyostotic osteomyelitis. To the best of our knowledge this is the first report of polyostotic osteomyelitis caused by Serratia liquefaciens in dogs

    The functional role of CDKL5 at the inhibitory synapse and its interaction with the cytoplasmatic collybistin-gephyrin complex

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    Mutations in the cyclin-dependent kinase-like 5 gene (CDKL5) are responsible for a severe neurodevelopmental disorder, namely CDKL5 deficiency disorder (CDD), characterised by early-onset epileptic encephalopathy, severe intellectual disability and intractable seizures. So far, the role of CDKL5 in excitatory synapses has been widely explored; on the contrary, more has still to be investigated regarding its influence on the inhibitory compartment. Our recent data showed that CDKL5 loss impacts the number of synaptic GABAARs, which may be explained by its interaction with the postsynaptic scaffolding complex containing gephyrin (GPHN) and collybistin (CB). GPHN is the core scaffolding protein of the inhibitory synapse, while CB is a brain specific GEF, involved in GPHN recruiting to postsynaptic sites. CB is retained in a folded-inactive conformation by its auto-inhibitory SH3 domain; when this domain interacts with other proteins, CB switches in the open-active conformation. Interestingly, through various biochemical and immunofluorescence approaches based on different derivatives of both proteins, we have demonstrated that CDKL5 can release CB from its inactive conformation allowing the distribution of GPHN to sub-membranous sites in expressing cells

    The functional role of CDKL5 at the inhibitory synapse and its interaction with the cytoplasmatic collybistin-gephyrin complex

    No full text
    Mutations in the cyclin-dependent kinase-like 5 gene (CDKL5) are responsible for a severe neurodevelopmental disorder, namely CDKL5 deficiency disorder (CDD), characterized by earlyonset epileptic encephalopathy, severe intellectual disability and intractable seizures. So far, the role of CDKL5 in excitatory synapses has been widely explored; on the contrary, more has still to be investigated regarding its influence on the inhibitory compartment. Our recent data showed that CDKL5 loss impacts the number of synaptic GABAARs, which may be explained by its interaction with the postsynaptic scaffolding complex containing gephyrin and collybistin. Gephyrin is the core scaffolding protein of the inhibitory synapse, while CB is a brain specific GEF, involved in recruiting gephyrin to postsynaptic sites. CB is retained in a folded-inactive conformation by its auto-inhibitory SH3 domain; when this domain interacts with other proteins, CB switches in the open-active conformation. Interestingly, through various biochemical and immunofluorescence approaches based on different derivatives of both proteins, we have demonstrated that CDKL5 can release CB from its inactive conformation allowing the distribution of gephyrin to sub-membranous sites in expressing cells. The interaction of CDKL5 with CB requires the SH3 domain of the latter as well as the catalytic activity of CDKL5. We are currently investigating whether CB is phosphorylated in CDKL5 dependent manner through the PhosTagTM approach. In conclusion, our results seem to place CDKL5 as a novel key regulator of the postsynaptic scaffolding complex of inhibitory synapses. Furthermore, elucidating the synaptic networks regulated by CDKL5 from a molecular point of view are likely to pave the way to understand the molecular mechanisms underlying CDD and, possibly, to develop target-based therapeutic approaches
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