The traditional, the innovative, the ephemeral: conception, realization, intervention in contemporary art

The traditional, the innovative, the ephemeral: conception, realization, intervention in contemporary art. One must consider the traditional, the innovative and also the ephemeral related to the artistic intentions and thus to the interventions on works of contemporary art, for which the concepts of originality and authenticity do not always correspond. The Brandian vision and point of view do not completely resolve the problematics relative to restoration and conservation: artists realize their artifacts with the intention of undermining tradition or, however, of interpreting it in an unusual way. There are, therefore, cases when a diagnostic-analytical and conservative intervention is possible correspondently to the different and numerous typologies of the materials (poor, plastic, industrial) and techniques (collage, enamel on rubber foam, paint on textile or plastic, neon). A vocation for the ephemeral can be transformed into the adoption of deteriorated materials or into the realization of works of conceptual art and net-art. Some case studies are treated in the comparison of art works of different age. The solutions to the aforementioned problematics are offered and the importance of the involvement of the historical-technical experts, authors and manufacturers of the materials used in the artifacts is highlighted. Finally the procedure of intervention cannot be the same for all works of contemporary art. One must employ a methodology based on the critical study, not only of the materials used but also of the philosophy and creative conceptual intentions of the artist

PINK1 homozygous W437X mutation in a patient with apparent dominant transmission of parkinsonism.

We analyzed the PINK1 gene in 58 patients with early-onset Parkinsonism and detected the homozygous mutation W437X in 1 patient. The clinical phenotype was characterized by early onset (22 years of age), good re- sponse to levodopa, early fluctuations and dyskinesias, and psychiatric symptoms. The mother, heterozygote for W437X mutation, was affected by Parkinson’s disease and 3 further relatives were reported affected, according to an autosomal dominant transmission

Chronic heart failure is characterized by altered mitochondrial function and structure in circulating leucocytes

Oxidative stress is currently viewed as a key factor in the genesis and progression of Heart Failure (HF). The aim of this study was to characterize the mitochondrial changes linked to oxidative stress generation in circulating peripheral blood mononuclear cells isolated from chronic HF patients (HF_PBMCs) in order to highlight the involvement of mitochondrial dysfunction in the pathophysiology of HF. To assess the production of reactive oxygen species (ROS), mitochondrial function and ultrastructure and the mitophagic flux in circulating PBMCs we enrolled 15 patients with HF and a control group of ten healthy subjects. The HF_PBMCs showed a mitochondrial population consisting of damaged and less functional organelles responsible of higher superoxide anion production both at baseline and under in vitro stress conditions, with evidence of cellular apoptosis. Although the mitophagic flux at baseline was enhanced in HF_PBMCs at level similar to those that could be achieved in control PBMCs only under inflammatory stress conditions, the activation of mitophagy was unable to preserve a proper mitochondrial dynamics upon stress stimuli in HF. In summary, circulating HF_PBMCs show structural and functional derangements of mitochondria with overproduction of reactive oxidant species. This mitochondrial failure sustains a leucocyte dysfunctional status in the blood that may contribute to development and persistence of stress conditions within the cardiovascular system in HF

Life Monza: project description and actions’ updating

The introduction of Low Emission Zones, urban areas subject to road traffic restrictions in order to ensure compliance with the air pollutants limit values set by the European Directive on ambient air quality (2008/50/EC), is a common and well-established action in the administrative government of cities. The impacts on air quality improvement are widely analysed, whereas the effects and benefits concerning the noise have not been addressed in a comprehensive manner. As a consequence, the definition, the criteria for the analysis and the management methods of a Noise Low Emission Zone are not clearly expressed and shared yet. The LIFE MONZA project (Methodologies fOr Noise low emission Zones introduction And management - LIFE15 ENV/IT/000586) addresses these issues. The first objective of the project, co-funded by the European Commission, is to introduce an easy-replicable method for the identification and the management of the Noise Low Emission Zone, an urban area subject to traffic restrictions, whose impacts and benefits regarding noise issues will be analyzed and tested in the pilot area of the city of Monza, located in Northern Italy. Background conditions, structure, objectives of the project and actions’ progress will be discussed in this article

Reduced brain UCP2 expression mediated by microRNA-503 contributes to increased stroke susceptibility in the high-salt fed stroke-prone spontaneously hypertensive rat

UCP2 maps nearby the lod score peak of STR1-stroke QTL in the SHRSP rat strain. We explored the potential contribution of UCP2 to the high-salt diet (JD)-dependent increased stroke susceptibility of SHRSP. Male SHRSP, SHRSR, two reciprocal SHRSR/SHRSP-STR1/QTL stroke congenic lines received JD for 4 weeks to detect brain UCP2 gene/protein modulation as compared with regular diet (RD). Brains were also analyzed for NF-κB protein expression, oxidative stress level and UCP2-targeted microRNAs expression level. Next, based on knowledge that fenofibrate and Brassica Oleracea (BO) stimulate UCP2 expression through PPARα activation, we monitored stroke occurrence in SHRSP receiving JD plus fenofibrate versus vehicle, JD plus BO juice versus BO juice plus PPARα inhibitor. Brain UCP2 expression was markedly reduced by JD in SHRSP and in the (SHRsr.SHRsp-(D1Rat134-Mt1pa)) congenic line, whereas NF-κB expression and oxidative stress level increased. The opposite phenomenon was observed in the SHRSR and in the (SHRsp.SHRsr-(D1Rat134-Mt1pa)) reciprocal congenic line. Interestingly, the UCP2-targeted rno-microRNA-503 was significantly upregulated in SHRSP and decreased in SHRSR upon JD, with consistent changes in the two reciprocal congenic lines. Both fenofibrate and BO significantly decreased brain microRNA-503 level, upregulated UCP2 expression and protected SHRSP from stroke occurrence. In vitro overexpression of microRNA-503 in endothelial cells suppressed UCP2 expression and led to a significant increase of cell mortality with decreased cell viability. Brain UCP2 downregulation is a determinant of increased stroke predisposition in high-salt-fed SHRSP. In this context, UCP2 can be modulated by both pharmacological and nutraceutical agents. The microRNA-503 significantly contributes to mediate brain UCP2 downregulation in JD-fed SHRSP

Reducing Sepsis Hospitalisations through a Standardized Quality Improvement Program in Skilled Nursing Facilities

Context: Sepsis hospitalisations with subsequent skilled nursing facility (SNF) admissions have had an annual cost of $41 billion in the United States. There has been a limited amount of literature on early interventions for sepsis in long-term care. Objective: To assess the impact of a pilot sepsis quality improvement program (SQIP) aimed at early identification and intervention in 10 partnering SNFs in New York City. Methods: Obtained baseline data of sepsis hospitalisations in 2017 among 10 SNFs. A SQIP was implemented utilizing the systemic inflammatory response syndrome criteria with a modified threshold temperature of 37.2°C (99.0°F). Sepsis hospitalisations were reported and validated for the intervention period in 2018 and compared to the baseline. A cost savings analysis was completed by utilizing local hospital billing records. Findings: Overall, there was a reduction of 54 sepsis hospitalisations when comparing the intervention period (183 sepsis hospitalisations) to the baseline (237 sepsis hospitalisations), a 22.8$45,000 USD. The SQIP had an estimated cost savings between $1,039,662–$3,188,430 USD. Limitations: Implementation at each facility was voluntary, so there may have been varying degrees of SQIP implementation. However, the hospital primary diagnosis of sepsis and cost were accurately reported. Implications: A SQIP in a long-term care setting could reduce avoidable hospitalisations and offer cost savings. The SQIP reported is a complex intervention and needs to be methodologically understood as such. The intervention shows promise and important insights into its implementation and evaluation have been developed which would be helpful in further evaluation

Herpes zoster ophthalmicus in two women after Pfizer-BioNTech (BNT162b2) vaccine

Varicella‐zostervirus(VZV) isresponsibleforaprimaryinfection (i.e., chickenpox); subsequently, thevirus remains dormant at the level of thespinal dorsal root andcranial ganglia. Inconditionsof stressor immunosuppression, itcanreactivateandcausesecondary herpes zoster (HZ) infection. HZOaccounts for 10%–20%ofHZ casesandischaracterizedbyinvolvementoftheophthalmicbranch ofthefifthcranialnerve. It isconsideredadangerousconditionthat couldleadtosevereconsequencessuchasblindnessin20%–70%of thecases.3Themainriskfactors for thereactivationofVZVarea compromiseofthecell‐mediatedimmunity(CMI)thatpresentsitself inoldage, insomechronicdiseasessuchasdiabetes, autoimmune disease,HIV,andduringimmunosuppressivetherapies.4 Several casesofHZhavebeendescribed inPfizervaccinerecipients,however,onlyoneofthemwithophthalmiclocalization, ina 56‐year‐oldwomanwithrheumatoidarthritis.5 Wereport twocasesofpostvaccineHZOalthoughararelyreportedadverseeventwithpotentiallyseriousconsequences. HZOwasalsodiagnosedinfourpatientssufferingfromamoderateformofCOVID‐19infection6thatwereeffectivelytreatedwith antiviralswithoutanyvisual sequelae. Inthesecases, thetriggering factorforviralreactivationisprobablyduetolymphopeniasecondary to SARS‐CoV‐2

Is avolition in schizophrenia associated with a deficit of dorsal caudate activity? A functional magnetic resonance imaging study during reward anticipation and feedback

BACKGROUND: The neurobiological underpinnings of avolition in schizophrenia remain unclear. Most brain imaging research has focused on reward prediction deficit and on ventral striatum dysfunction, but findings are not consistent. In the light of accumulating evidence that both ventral striatum and dorsal caudate play a key role in motivation, we investigated ventral striatum and dorsal caudate activation during processing of reward or loss in patients with schizophrenia. METHOD: We used functional magnetic resonance imaging to study brain activation during a Monetary Incentive Delay task in patients with schizophrenia, treated with second-generation antipsychotics only, and in healthy controls (HC). We also assessed the relationships of ventral striatum and dorsal caudate activation with measures of hedonic experience and motivation. RESULTS: The whole patient group had lower motivation but comparable hedonic experience and striatal activation than HC. Patients with high avolition scores showed lower dorsal caudate activation than both HC and patients with low avolition scores. A lower dorsal caudate activation was also observed in patients with deficit schizophrenia compared to HC and patients with non-deficit schizophrenia. Dorsal caudate activity during reward anticipation was significantly associated with avolition, but not with anhedonia in the patient group. CONCLUSIONS: These findings suggest that avolition in schizophrenia is linked to dorsal caudate hypoactivation

Efficacy and safety of systemic isotretinoin treatment for moderate to severe acne (insights from the real-life clinical setting)

Acne is a chronic inflammatory relapsing disease that affect predominantly adolescents, with scarring as a frequent sequele. Early and appropriate therapy allows better management of the disease, longer remission, scars risk reduction, and improvement of quality of life. According to therapeutic algorithm, systemic isotretinoin can be used in severe acne and also in moderate forms resistant to other systemic treatments. The aims of this real-life observational study were to determine and compare the effectiveness of isotretinoin evaluated by Global Acne Grading System and Acne Quality of Life in moderate and in severe acne, correlation between efficacy and cumulative dose of isotretinoin, tolerability, and recurrence rate. Moreover, the differences in efficacy and tolerability between male and female patients were compared. The treatment with systemic isotretinoin led to an improvement in acne severity and quality of life in all observed subjects

In vitro characterization of mitochondrial function and structure in rat and human cells with a deficiency of the NADH:ubiquinone oxidoreductase Ndufc2 subunit

Ndufc2, a subunit of the NADH:ubiquinone oxidoreductase, plays a key role in the assembly and activity of complex I within the mitochondrial OXPHOS chain. Its deficiency has been shown to be involved in diabetes, cancer and stroke. To improve our knowledge on the mechanisms underlying the increased disease risk due to Ndufc2 reduction, we performed the present in vitro study aimed at the fine characterization of the derangements in mitochondrial structure and function consequent to Ndufc2 deficiency. We found that both fibroblasts obtained from skin of heterozygous Ndufc2 knock-out rat model showed marked mitochondrial dysfunction and PBMC obtained from subjects homozygous for the TT genotype of the rs11237379/NDUFC2 variant, previously shown to associate with reduced gene expression, demonstrated increased generation of reactive oxygen species and mitochondrial damage. The latter was associated with increased oxidative stress and significant ultrastructural impairment of mitochondrial morphology with a loss of internal cristae. In both models the exposure to stress stimuli, such as high-NaCl concentration or LPS, exacerbated the mitochondrial damage and dysfunction. Resveratrol significantly counteracted the ROS generation. These findings provide additional insights on the role of an altered pattern of mitochondrial structure-function as a cause of human diseases. In particular, they contribute to underscore a potential genetic risk factor for cardiovascular diseases, including stroke