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The aim of this work was to verify the beneficial potential of Silicon on the growth of potato genotypes in order to select potato genotypes that best respond to Si application. Four potato genotypes were used: SMIJ319-7, Dakota Rose, SMIF212-3 and SMINIA793101, grown in hydroponic system. The plants were transferred to nutrient solutions with four Si concentrations: 0; 0.5; 2.5; and 5.0 mM as NaSiO3. After seven days of exposure to treatments, leaf area, leaf number, shoot length, and fresh and dry weight of roots, stem and leaves were determined. The application of 0.5 mM Si promoted an increase in growth parameters of plants used in this work, mainly in leaf area, leaf number, and leaf and stem dry weight. However, the application of higher concentrations of Si (2.5 mM) promoted reduction in the growth parameters, mainly in leaf area. It was also possible to observe a genotypic variation with respect to Si, SMIJ319-7 and SMIF212-3 genotypes being the most responsive to Si. Therefore, the concentration of 0.5 mM Si is considered optimal for potentiating the growth of potato plants, and SMIJ319-7 and SMIF212-3 genotypes are the most responsive to Si. [ABSTRACT FROM AUTHOR]

The pathogenic mechanisms that underlie the progression of remote degeneration after spinal cord injury (SCI) are not fully understood. In this study, we examined the relationship between endoplasmic reticulum (ER) stress and macroautophagy, hereafter autophagy, and its contribution to the secondary damage and outcomes that are associated with remote degeneration after SCI. Using a rat model of spinal cord hemisection at the cervical level, we measured ER stress and autophagy markers in the axotomized neurons of the red nucleus (RN). In SCI animals, mRNA and protein levels of markers of ER stress, such as GRP78, CHOP, and GADD34, increased 1 day after the injury, peaking on Day 5. Notably, in SCI animals, the increase of ER stress markers correlated with a blockade in autophagic flux, as evidenced by the increase in microtubule-associated protein 2 light chain 3 (LC3-II) and p62/SQSTM1 (p62) and the decline in LAMP1 and LAMP2 levels. After injury, treatment with guanabenz protected neurons from UPR failure and increased lysosomes biogenesis, unblocking autophagic flux. These effects correlated with greater activation of TFEB and improved neuronal survival and functional recovery-effects that persisted after suspension of the treatment. Collectively, our results demonstrate that in remote secondary damage, impairments in autophagic flux are intertwined with ER stress, an association that contributes to the apoptotic cell death and functional damage that are observed after SCI., (© 2022. The Author(s).)

Purpose: The UMass Chan Medical School/New England AIDS Education and Training Center Community-Based HIV and Viral Hepatitis Fellowship was launched in 2014 to train physicians and nurse practitioners to become experts in outpatient management of HIV, hepatitis B and C, and latent tuberculosis. The purpose of this study was to identify areas of strength and improvement and understand fellows' perceptions of the program and its impact on their current positions and career trajectories., Methods: Qualitative study utilizing a semi-structured interview guide with (11) fellowship graduates (8 MDs; 3 NPs). 45 to 60 min interviews were conducted in April and May 2021, recorded and transcribed. Transcripts were analyzed for representative themes and general patterns in the data., Results: Results indicate high satisfaction with the fellowship, which left a positive and indelible impact on their careers and patient care. Fellows highlighted the program's commitment to health equity, its role in transforming them into leaders and advocates for HIV in primary care, and their ability to balance their work and training demands with their personal lives and needs. The fellowship motivated them to become more involved in public health initiatives, serve marginalized communities and reduce their health disparities. They expressed confidence in their ability to independently manage outpatient HIV, viral hepatitis B and C, and latent tuberculosis, and found areas of overlap with their work in primary care., Conclusion: As the care of people with HIV becomes more commonplace in primary care clinics, it is imperative that primary care providers receive the necessary training and education to meet this need. Our study of 11 former fellows shows that the Community-Based HIV and Viral Hepatitis Fellowship offers such training, spreads it to other institutions, and can be a model for other programs nationwide.

The arrival of Spaniards in the Caribbean islands introduced to the region the practice of applying pigments onto buildings. The pigments that remain on these buildings may provide data on their historical evolution and essential information for tackling restoration tasks. In this study, a 17th-century mural painting located in the Cathedral of Santo Domingo on the Hispaniola island of the Caribbean is characterised via UV-VIS-NIR, Raman and FTIR spectroscopy, XRD and SEM/EDX. The pigments are found in the older Chapel of Our Lady of Candelaria, currently Chapel of Our Lady of Mercy. The chapel was built in the 17th century by black slave brotherhood and extended by Spaniards. During a recent restoration process of the chapel, remains of mural painting appeared, which were covered by several layers of lime. Five colours were identified: ochre, green, red, blue and white. Moreover, it was determined that this mural painting was made before the end of the 18th century, because many of the materials used were no longer used after the industrialisation of painting. However, since both rutile and anatase appear as a white pigment, a restoration may have been carried out in the 20th century, and it has been painted white.

Docosahexaenoic acid (DHA) is a ω-3 fatty acid typically obtained from the diet or endogenously synthesized through the action of elongases (ELOVLs) and desaturases. DHA is a key central nervous system constituent and the precursor of several molecules that regulate the resolution of inflammation. In the present study, we questioned whether the impaired synthesis of DHA affected neural plasticity and inflammatory status in the adult brain. To address this question, we investigated neural and inflammatory markers from mice deficient for ELOVL2 (Elovl2 -/- ), the key enzyme in DHA synthesis. From our findings, Elovl2 -/- mice showed an altered expression of markers involved in synaptic plasticity, learning, and memory formation such as Egr-1, Arc1, and BDNF specifically in the cerebral cortex, impacting behavioral functions only marginally. In parallel, we also found that DHA-deficient mice were characterized by an increased expression of pro-inflammatory molecules, namely TNF, IL-1β, iNOS, caspase-1 as well as the activation and morphologic changes of microglia in the absence of any brain injury or disease. Reintroducing DHA in the diet of Elovl2 -/- mice reversed such alterations in brain plasticity and inflammation. Hence, impairment of systemic DHA synthesis can modify the brain inflammatory and neural plasticity status, supporting the view that DHA is an essential fatty acid with an important role in keeping inflammation within its physiologic boundary and in shaping neuronal functions in the central nervous system., (© 2019 The Authors. The FASEB Journal published by Wiley Periodicals, Inc. on behalf of Federation of American Societies for Experimental Biology.)

The CNS is endowed with an intrinsic ability to recover from and adapt secondary compensatory mechanisms to injury. The basis of recovery stems from brain plasticity, defined as the brain's ability to make adaptive changes on structural and functional levels, ranging from molecular, synaptic, and cellular changes in response to alterations in their environment. In this multitude of responses, microglia have an active role and contribute to brain plasticity through their dynamic responses. This review will provide an overview of microglial responses in the context of acute CNS injury and their function in post-traumatic repair and assess the changes that are induced by damage in remote areas from, but functionally connected to, the primary site of injury. In the second section, we highlight the effects of several therapeutic approaches, with particular interest paid to specialized pro-resolving lipid mediators, in modulating microglial responses in remote regions and enhancing long-term functional recovery via suppression of neurodegenerative cascades that are induced by damage, which may contribute to a translational bridge from bench to bedside., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Remote damage is a secondary phenomenon that usually occurs after a primary brain damage in regions that are distant, yet functionally connected, and that is critical for determining the outcomes of several CNS pathologies, including traumatic brain and spinal cord injuries. The understanding of remote damage-associated mechanisms has been mostly achieved in several models of focal brain injury such as the hemicerebellectomy (HCb) experimental paradigm, which helped to identify the involvement of many key players, such as inflammation, oxidative stress, apoptosis and autophagy. Currently, few interventions have been shown to successfully limit the progression of secondary damage events and there is still an unmet need for new therapeutic options. Given the emergence of the novel concept of resolution of inflammation, mediated by the newly identified ω3-derived specialized pro-resolving lipid mediators, such as resolvins, we reported a reduced ability of HCb-injured animals to produce resolvin D1 (RvD1) and an increased expression of its target receptor ALX/FPR2 in remote brain regions. The in vivo administration of RvD1 promoted functional recovery and neuroprotection by reducing the activation of Iba-1+ microglia and GFAP+ astrocytes as well as by impairing inflammatory-induced neuronal cell death in remote regions. These effects were counteracted by intracerebroventricular neutralization of ALX/FPR2, whose activation by RvD1 also down-regulated miR-146b- and miR-219a-1-dependent inflammatory markers. In conclusion, we propose that innovative therapies based on RvD1-ALX/FPR2 axis could be exploited to curtail remote damage and enable neuroprotective effects after acute focal brain damage.

Untreated phenylketonuria (PKU) results in severe neurodevelopmental disorders, which can be partially prevented by an early and rigorous limitation of phenylalanine (Phe) intake. Enzyme substitution therapy with recombinant Anabaena variabilis Phe Ammonia Lyase (rAvPAL) proved to be effective in reducing blood Phe levels in preclinical and clinical studies of adults with PKU. Aims of present study were: a) to gather proofs of clinical efficacy of rAvPAL treatment in preventing neurological impairment in an early treated murine model of PKU; b) to test the advantages of an alternative delivering system for rAvPAL such as autologous erythrocytes. BTBR-Pah enu2-/- mice were treated from 15 to 64 post-natal days with weekly infusions of erythrocytes loaded with rAvPAL. Behavioral, neurochemical, and brain histological markers denoting untreated PKU were examined in early treated adult mice in comparison with untreated and wild type animals. rAvPAL therapy normalized blood and brain Phe; prevented cognitive developmental failure, brain depletion of serotonin, dendritic spine abnormalities, and myelin basic protein reduction. No adverse events or inactivating immune reaction were observed. In conclusion present study testifies the clinical efficacy of rAvPAL treatment in a preclinical model of PKU and the advantages of erythrocytes as carrier of the enzyme in term of frequency of the administrations and prevention of immunological reactions., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Spinal cord injuries (SCIs) are devastating conditions of the central nervous system (CNS) for which there are no restorative therapies. Neuronal death at the primary lesion site and in remote regions that are functionally connected to it is one of the major contributors to neurological deficits following SCI.Disruption of autophagic flux induces neuronal death in many CNS injuries, but its mechanism and relationship with remote cell death after SCI are unknown. We examined the function and effects of the modulation of autophagy on the fate of axotomized rubrospinal neurons in a rat model of spinal cord dorsal hemisection (SCH) at the cervical level. Following SCH, we observed an accumulation of LC3-positive autophagosomes (APs) in the axotomized neurons 1 and 5 days after injury. Furthermore, this accumulation was not attributed to greater initiation of autophagy but was caused by a decrease in AP clearance, as demonstrated by the build-up of p62, a widely used marker of the induction of autophagy. In axotomized rubrospinal neurons, the disruption of autophagic flux correlated strongly with remote neuronal death and worse functional recovery. Inhibition of AP biogenesis by 3-methyladenine (3-MA) significantly attenuated remote degeneration and improved spontaneous functional recovery, consistent with the detrimental effects of autophagy in remote damage after SCH. Collectively, our results demonstrate that autophagic flux is blocked in axotomized neurons on SCI and that the inhibition of AP formation improves their survival. Thus, autophagy is a promising target for the development of therapeutic interventions in the treatment of SCIs.

Background: Recent studies support the therapeutic utility of repetitive transcranial magnetic stimulation in Parkinson's disease (PD), whose progression is correlated with loss of corticostriatal long-term potentiation and long-term depression. Glial cell activation is also a feature of PD that is gaining increasing attention in the field because astrocytes play a role in chronic neuroinflammatory responses but are also able to manage dopamine (DA) levels., Methods: Intermittent theta-burst stimulation protocol was applied to study the effect of therapeutic neuromodulation on striatal DA levels measured by means of in vivo microdialysis in 6-hydroxydopamine-hemilesioned rats. Effects on corticostriatal synaptic plasticity were studied through in vitro intracellular and whole-cell patch clamp recordings while stepping test and CatWalk were used to test motor behavior. Immunohistochemical analyses were performed to analyze morphological changes in neurons and glial cells., Results: Acute theta-burst stimulation induced an increase in striatal DA levels in hemiparkinsonian rats, 80 minutes post-treatment, correlated with full recovery of plasticity and amelioration of motor performances. With the same timing, immediate early gene activation was restricted to striatal spiny neurons. Intense astrocytic and microglial responses were also significantly reduced 80 minutes following theta-burst stimulation., Conclusion: Taken together, these results provide a first glimpse on physiological adaptations that occur in the parkinsonian striatum following intermittent theta-burst stimulation and may help to disclose the real potential of this technique in treating PD and preventing DA replacement therapy-associated disturbances. © 2017 International Parkinson and Movement Disorder Society., (© 2017 International Parkinson and Movement Disorder Society.)

Background: After focal brain injuries occur, in addition to the effects that are attributable to the primary site of damage, the resulting functional impairments depend highly on changes that occur in regions that are remote but functionally connected to the site of injury. Such effects are associated with apoptotic and inflammatory cascades and are considered to be important predictors of outcome. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive technique that is used to treat various central nervous system (CNS) pathologies and enhance functional recovery after brain damage., Objective: This study examined the efficacy of rTMS in mitigating remote degeneration and inflammation and in improving functional recovery in a model of focal brain damage., Methods: Rats that were undergoing hemicerebellectomy (HCb) were treated with an rTMS protocol for 7 days, and neuronal death indices, glial activation, and functional recovery were assessed., Results: rTMS significantly reduced neuronal death and glial activation in remote regions and improved functional recovery., Conclusions: Our finding opens up a completely new scenario for exploiting the potential of rTMS as an anti-apoptotic and anti-inflammatory treatment.

When CNS lesions develop, neuronal degeneration occurs locally but in regions that are remote, yet functionally connected, to the primary lesion site. This process, known as "remote damage," significantly affects long-term outcomes in many CNS pathologies, such as stroke, multiple sclerosis, and traumatic brain and spinal cord injuries. Remote damage can last several days or months after the primary lesion, providing a window during which therapeutic approaches can be implemented to effect neuroprotection. The recognition of the importance of remote damage in determining disease outcomes has prompted considerable interest in examining remote damage-associated mechanisms, most of which is derived from the potential of this research to develop innovative pharmacological approaches for preserving neurons and improving functional outcomes. To this end, the hemicerebellectomy (HCb) experimental paradigm has been instrumental in highlighting the complexity and variety of the systems that are involved, identifying mechanisms of life/death decisions, and providing a testing ground for novel neuroprotective approaches. Inflammation, oxidative stress, apoptosis, autophagy, and neuronal changes in receptor mosaics are several remote damage mechanisms that have been identified and examined using the HCb model. In this review, we discuss our current understanding of remote degeneration mechanisms and their potential for exploitation with regard to neuroprotective approaches, focusing on HCb studies.

Early diagnosis of persons infected with human immunodeficiency virus (HIV) through diagnostic testing and screening is a critical priority for individual and public health. Emergency departments (EDs) have an important role in this effort. As EDs gain experience in HIV testing, it is increasingly apparent that implementing testing is conceptually and operationally complex. A wide variety of HIV testing practice and research models have emerged, each reflecting adaptations to site-specific factors and the needs of local populations. The diversity and complexity inherent in nascent ED HIV testing practice and research are associated with the risk that findings will not be described according to a common lexicon. This article presents a comprehensive set of terms and definitions that can be used to describe ED-based HIV testing programs, developed by consensus opinion from the inaugural meeting of the National ED HIV Testing Consortium. These definitions are designed to facilitate discussion, increase comparability of future reports, and potentially accelerate wider implementation of ED HIV testing.

A set of ortho-disubstituted benzene derivatives (2-X--C6H4NH--Y) designed as analgesics has been studied. Some physicochemical properties which are potentially correlated with the considered pharmacological activities are determined. Quantitative structure-activity relationships (QSAR) show that the analgesic potency (writhing test) is a function of the hydrophobic-lipophilic parameters associated with the structures under study. Since the derivatives are inactive or very poor inhibitors of prostaglandin biosynthesis, the appropriate modulation of substituents may maximize the differentiation between anti-nociceptive and analgesic activity.