Retraction Note: Correlation between COVID-19 and air pollution: the effects of PM2.5 and PM10 on COVID-19 outcomes.

The article "Correlation between COVID-19 and air pollution: the effects of PM2.5 and PM10 on COVID-19 outcomes", by E. Kalluçi, E. Noka, K. Bani, X. Dhamo, I. Alimehmeti, K. Dhuli, G. Madeo, C. Micheletti, G. Bonetti, C. Zuccato, E. Borghetti, G. Marceddu, M. Bertelli, published in Eur Rev Med Pharmacol Sci 2023; 27 (6 Suppl): 39-47-DOI: 10.26355/eurrev_202312_34688-PMID: 38112947 has been retracted by the Editor in Chief. Following concerns raised on PubPeer, the Editor in Chief has initiated an investigation to evaluate the validity of the results. Despite the authors' prompt responses to the identified issues, the Editor in Chief has decided to withdraw the article due to significant errors in the text and final statements, as well as undisclosed conflicts of interest. The Publisher apologizes if these concerns have not been detected during the review process. The authors have been informed about the retraction. This article has been retracted. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/34688.

Author Correction: Achievement of sustainable development goals through the Mediterranean diet.

Correction to: Eur Rev Med Pharmacol Sci 2023; 27 (6 Suppl): 89-99-DOI: 10.26355/eurrev_202312_34693 After publication and following some post-publication concerns, the authors have applied the following corrections to the galley proof. -       The conflict of interest section has been amended as follows: M.C. Medori and D. Malacarne are employees at MAGI'S LAB. K. Donato is employee at MAGI EUREGIO and MAGISNAT. M. Bertelli is president of MAGI EUREGIO, MAGISNAT, and MAGI's LAB. E. Borghetti is president at AERSAFE srl. C. Zuccato is researcher at AERSAFE srl. E. Borghetti is patent inventor (IT202100021344A1, IT202100020330A1, WO2021260537A1, WO2022259165A1). M. Bertelli is patent inventor (US20220362260A1, US20230173003A1, WO2022079498A1). D. Malacarne is patent inventor (WO2022079498A1; US20230173003A1). S. Michelini is patent inventor (US20220362260A1). M. Bertelli, S. Michelini, and K. Donato are patent applicants (Application Number: 18/516,241). M. Bertelli and K. Donato are patent applicants (Application Number: 18/466.879). M. Bertelli, K. Donato, and S. Michelini are patent applicants (Application Number: 63/495,155). The remaining authors have no conflict of interest to disclose. There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/34693.

Achievement of sustainable development goals through the Mediterranean diet.

The prosperity of our planet relies on the cardinal concept of sustainable development. The dietary choices of humans play a pivotal role in creating a peaceful and contented world. In this context, the Mediterranean diet (MD) has emerged as a valuable approach to accomplishing such progress, wherein the rights of all living beings are equally honored. This review aims to analyze the significance of a plant-based diet, particularly the Mediterranean diet, in attaining sustainable development goals. A comprehensive search of the literature was conducted to gather the most reliable and published scientific evidence from books and papers. Within this research endeavor, specific Sustainable Development Goals (SDGs) are individually addressed in relation to the adoption of the Mediterranean diet as a foundational nutritional paradigm. Our research findings underscore the immense importance of the MD and advocate for its worldwide implementation to accomplish sustainable development objectives. The MD emerges as the most suitable dietary option for fostering sustainability and tranquility in our world. It is crucial to prioritize the global implementation of the MD to genuinely achieve sustainable development.

Unleashing the potential of biotechnology for sustainable development.

The UN Sustainable Development Goals (SDGs) strive to eliminate poverty, preserve the planet, and promote shared prosperity through sustainable and inclusive means by 2030. This requires the implementation of a diverse set of strategies to overcome challenges and foster synergies among different SDG targets, facilitating the achievement of these ambitious goals. The aim of this review is to highlight the world's progress toward SDGs with the utilization of biotechnological advancements, including targets, strategies, synergies, and challenges. We scrutinized published research articles in peer-reviewed journals, UN reports, and scientific books that were relevant to the current topic. We identified some major challenges faced by the countries, especially developing ones, in the way of sustainable progress. These include inadequate governance, fragile states, armed conflicts, rising inequality, limited economic progress, climate change, environmental degradation, and food insecurity. Biotechnological advancements contribute to sustainable resource management, environmental conservation, and ecosystem restoration. Collaboration among countries and organizations is crucial for sharing knowledge and providing technical and financial assistance to developing nations.

Correlation between COVID-19 and air pollution: the effects of PM2.5 and PM10 on COVID-19 outcomes.

OBJECTIVE: Given its effects on long-term illnesses, like heart problems and diabetes, air pollution may be among the reasons that led COVID-19 to get worse and kill a larger number of people. Experiments have shown that breathing in polluted air weakens the immune system, making it easier for viruses to enter the body and grow. Viruses may be able to survive in the air by interacting in complex ways with particles and gases. These interactions depend on the air's chemical makeup, the particles' electric charges, and environmental conditions like humidity, UV light, and temperature. Moreover, exposure to UV rays and air pollution may reduce the organism's production of antimicrobial molecules, thus supporting viral infections. More epidemiological studies are needed to determine what effects air pollution has on COVID-19. In this review, we will discuss how air pollutants such as PM2.5 and PM10 contribute to the transmission of COVID-19. MATERIALS AND METHODS: We have used nine target cities in the Tuscany region to verify this certainty, and in all these cases, the air pollution factors were found to be strongly correlated with COVID-19 cases. For each city, we applied a multivariate analysis and found an appropriate model that better fits the data. RESULTS: This review underlines that both short-term and long-term exposure to air pollution may be crucial exasperating factors for SARS-CoV-2 transmission and COVID-19 severity and lethality. The statistical analysis concludes that air pollution should be accounted for as a possible risk factor in future COVID-19 investigations, and it should be avoided as much as possible by the general population. CONCLUSIONS: Our research highlighted the correlation between COVID-19 and air pollution. Reducing air pollution exposure should be one of the first measures against COVID-19 spread.

Disruption of astrocyte-neuron cholesterol cross talk affects neuronal function in Huntington's disease.

In the adult brain, neurons require local cholesterol production, which is supplied by astrocytes through apoE-containing lipoproteins. In Huntington's disease (HD), such cholesterol biosynthesis in the brain is severely reduced. Here we show that this defect, occurring in astrocytes, is detrimental for HD neurons. Astrocytes bearing the huntingtin protein containing increasing CAG repeats secreted less apoE-lipoprotein-bound cholesterol in the medium. Conditioned media from HD astrocytes and lipoprotein-depleted conditioned media from wild-type (wt) astrocytes were equally detrimental in a neurite outgrowth assay and did not support synaptic activity in HD neurons, compared with conditions of cholesterol supplementation or conditioned media from wt astrocytes. Molecular perturbation of cholesterol biosynthesis and efflux in astrocytes caused similarly altered astrocyte-neuron cross talk, whereas enhancement of glial SREBP2 and ABCA1 function reversed the aspects of neuronal dysfunction in HD. These findings indicate that astrocyte-mediated cholesterol homeostasis could be a potential therapeutic target to ameliorate neuronal dysfunction in HD.

In vivo delivery of DN:REST improves transcriptional changes of REST-regulated genes in HD mice.

Current therapeutic strategies for Huntington's disease (HD) are focused on symptom management of disease progression. Transcriptional dysregulation is one of the major characteristics in HD. REST is a transcriptional repressor that silences gene expression through binding to RE1/NRSE sites found in the regulatory regions of numerous neuronal genes. Dysregulation of REST and its targeted genes has been reported in different cell and mouse HD models, as well as in biopsies from human patients. In this work, we characterized transcriptional dysregulation associated with REST in two different HD mouse models and assessed the therapeutic effect of interfering with REST function by overexpressing a dominant-negative form (DN:REST). We show that delivery of DN:REST in the motor cortex restores brain-derived neurotrophic factor (BDNF) mRNA and protein levels by reducing endogenous REST occupancy at the Bdnf locus. Similarly, expression of other REST-regulated genes such as Synapsin I (Syn1), Proenkephalin (Penk1) and Cholinergic receptor muscarinic 4 (Chrm4) were restored to normal levels while non-REST-regulated genes were unaffected. This is the first study conducted to investigate REST's role in vivo in a neurodegenerative disease. Our data show that DN:REST in motor cortex reversed RESTs repressive effects on target genes. However, the lack of therapeutic effect on motor function suggests that a more widespread rescue of REST-regulated sites in the affected brain regions may be necessary.

Cortical expression of brain derived neurotrophic factor and type-1 cannabinoid receptor after striatal excitotoxic lesions.

An involvement of one particular neurotrophin, namely, the brain-derived neurotrophic factor (BDNF), has been demonstrated in the pathophysiology Huntington's disease. Type-1 cannabinoid (CB1) receptor has been postulated to upregulate BDNF gene transcription. To better understand the relationship between CB1 and BDNF levels in a situation where the striatum is degenerating, we studied, by dual label immunofluorescence, the distribution of CB1 and BDNF in cortical neurons projecting to the striatum in our rat quinolinic acid model of striatal excitotoxicity. We completed our study with quantitative analyses of BDNF protein levels and CB1 binding activity in the cortex. We show that, 2 weeks post lesion, cortical neurons contain more BDNF compared with controls and to earlier time points. Such BDNF up-regulation coincides with a higher binding activity and an increased protein expression of CB1. We suggest that after excitotoxic lesions, CB1 might, at least transiently, upregulate BDNF in the attempt to rescue striatal neurons from degeneration.

Comparative expression profiles of ShcB and ShcC phosphotyrosine adapter molecules in the adult brain.

Shc family of adaptor molecules has been demonstrated to play an important role during the transition from proliferating neural stem cells to postmitotic neurons. Previous studies from our group demonstrated a progressive decrease of ShcA levels occurring in coincidence with the end of embryonic neurogenesis and neuronal maturation, being ShcB and ShcC the major Shc molecules expressed in the mature brain. A growing body of evidence indicates that ShcB and ShcC are neuronal specific molecules exerting important roles in neuronal survival and phenotypic stability thus becoming potential attracting target molecules for development of drugs for interfering with brain demises. Here, we examine the expression pattern of ShcB and ShcC in neuronal populations composing the adult central and peripheral nervous system, in order to better elucidate their roles in vivo. We found a heterogeneous and peculiar presence and subcellular localization of ShcB and ShcC in specific neuronal populations, enlightening a potential specific requirement of these two molecules in the survival/maintenance of defined neuronal subtypes.

Loss of huntingtin-mediated BDNF gene transcription in Huntington's disease.

Huntingtin is a 350-kilodalton protein of unknown function that is mutated in Huntington's disease (HD), a neurodegenerative disorder. The mutant protein is presumed to acquire a toxic gain of function that is detrimental to striatal neurons in the brain. However, loss of a beneficial activity of wild-type huntingtin may also cause the death of striatal neurons. Here we demonstrate that wild-type huntingtin up-regulates transcription of brain-derived neurotrophic factor (BDNF), a pro-survival factor produced by cortical neurons that is necessary for survival of striatal neurons in the brain. We show that this beneficial activity of huntingtin is lost when the protein becomes mutated, resulting in decreased production of cortical BDNF. This leads to insufficient neurotrophic support for striatal neurons, which then die. Restoring wild-type huntingtin activity and increasing BDNF production may be therapeutic approaches for treating HD.

Huntingtin's neuroprotective activity occurs via inhibition of procaspase-9 processing.

Huntington's Disease is an inherited neurodegenerative disease that affects the medium spiny neurons in the striatum. The disease is caused by the expansion of a polyglutamine sequence in the N terminus of Huntingtin (Htt), a widely expressed protein. Recently, we have found that Htt is an antiapoptotic protein in striatal cells and acts by preventing caspase-3 activity. Here we report that Htt overexpression in other CNS-derived cells can protect them from more than 20 days exposure to fatal stimuli. In particular, we found that cytochrome c continues to be released from mitochondria into the cytosol of cells that overexpress normal Htt. However, procaspase-9 is not processed, indicating that wild-type Htt (wtHtt) acts downstream of cytochrome c release. These data show that Htt inhibits neuronal cell death by interfering with the activity of the apoptosome complex.

Loss of normal huntingtin function: new developments in Huntington's disease research.

Huntington's disease is characterized by a loss of brain striatal neurons that occurs as a consequence of an expansion of a CAG repeat in the huntingtin protein. The resulting extended polyglutamine stretch confers a deleterious gain-of-function to the protein. Analysis of the mutant protein has attracted most of the research activity in the field, however re-examination of earlier data and new results on the beneficial functions of normal huntingtin indicate that loss of the normal protein function might actually equally contribute to the pathology. Thus, complete elucidation of the physiological role(s) of huntingtin and its mode of action are essential and could lead to new therapeutic approaches.