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Abstract Background Scoliosis is defined as a three-dimensional deformity of the spine characterized by lateral tilt and axial rotation of the vertebrae. Its magnitude in the frontal plane is identified by a Cobb angle greater than 10o. The aim of the study was to systematically examine the clinimetric properties of the Spinal Appearance Questionnaire (SAQ) in its cross-cultural adaptations in different languages. Methods Medline (PubMed), CINAHL, EMBASE, Science Direct, PsycINFO and WorldWideScience.org databases were used for screening studies until July 16, 2022. In this study, records on the development, evaluation and translation of the SAQ instrument in adolescents with idiopathic scoliosis were included. In addition, two independent reviewers defined whether the studies were eligible and analyzed their psychometric properties of internal consistency, reliability, content validity, cross-cultural validity, construct validity and structural validity, according to the COnsensus-based Standards for the selection of health Measurement INstruments (COSMIN). The modified GRADE was applied for evidence synthesis. Results A total of 95 articles were selected by title and abstract. After removing duplicates and reading and searching the references, a total of 13 studies were included in this review. The original version of the SAQ was described in English, and the instrument was translated into Polish, Canadian French, Simplified Chinese, Spanish (Europe), Danish, Traditional Chinese, Portuguese (Brazil), Korean, German, Turkish and Persian. The evidence was moderate for construct validity, low for internal consistency, and very low for reliability and cross-cultural validity; the content and structural validity properties did not present minimum data for classification. Conclusion The quality of the evidence regarding the clinimetric properties of the SAQ instrument in adolescents with idiopathic scoliosis was low due to the absence of clinimetric properties or dubious methodological quality. However, for clinical practice and research, we recommend the use of the instrument to assess the self-perception of the spine in adolescents. For future translations and adaptations, we recommend the use of the COSMIN guidelines.

RESUMO O objetivo deste estudo é analisar o perfil clínico-hospitalar de neonatos com o diagnóstico de hérnia diafragmática congênita (HDC), no período de 2008 a 2018 em um hospital de referência materno-infantil. Trata-se de um estudo transversal e analítico descritivo, que incluiu principalmente dados de prontuários com os códigos Q79.0, Q79.1, J986, K44 e K44.0 da Classificação Internacional de Doenças (CID-10). Os critérios de exclusão de prontuários foram o diagnóstico de outros tipos de hérnia diafragmática, sem o aspecto congênito; a internação em unidades que não fossem UTI Neonatal; e a idade no ato de internação igual ou superior a 29 dias. Analisou-se um total de 25.602 prontuários, dos quais 14 corresponderam a HDC. O acometimento por gênero foi de 71,43% masculino (10 casos) e 28,57% feminino (4), com 21,34% das localizações de HDC tipo Bochdalek à direita (3) e 78,57% à esquerda (11). Todos os neonatos deste estudo passaram por ventilação mecânica invasiva (VMI) 9,21 ± 5,55 dias. A cirurgia foi indicada em 11 casos (78,57%), com vias de acesso por toracotomia em 4 (36,36%) e por laparotomia subcostal em 7 (63,64%), todos com uso de dreno torácico homolateral ao hemitórax. O tempo total de internação foi de 19,42 ± 15,36 dias. Observou-se a evolução de alta melhorada em oito pacientes (57,14%) e o óbito de seis (42,86%), com idade de 6,19 ± 4,79 dias, sem referência de acompanhamento do desenvolvimento neuropsicomotor posteriormente. Ocorreram baixas incidências de casos por ano, e o gênero de acometimento, as malformações associadas e o tempo de VMI foram semelhantes a outras populações no mundo.

Intending to compare in vitro cell growth in different conditions, we established cell cultures using fin biopsies of two freshwater fishes, Astyanax bimaculatus and Geophagus proximus. Three different culture media (Leibovitz–L‐15, Dulbecco's Modified Eagle Medium [DMEM], and 199) were employed, with or without the addition of AmnioMax, maintaining a standard temperature of 29°C. Based on the results obtained, we standardized a cell growth protocol in which medium 199 was less efficient for both species. Notably, G. proximus cells exhibited superior proliferation in DMEM and L‐15 media, whereas A. bimaculatus cells demonstrated better parameters exclusively in the DMEM medium. Successful subculturing of cells with good proliferation index was observed, accompanied by preserved morphological characteristics. Therefore, the methodology outlined in this study represents an advancement in establishing fish cell cultures. [ABSTRACT FROM AUTHOR]

Morphine is a potent analgesic opioid used extensively for pain treatment. During the last decade, global consumption grew more than 4-fold. However, molecular mechanisms elicited by morphine are not totally understood. Thus, a growing literature indicates that there are additional actions to the analgesic effect. Previous studies about morphine and oxidative stress are controversial and used concentrations outside the range of clinical practice. Therefore, in this study, we hypothesized that a therapeutic concentration of morphine (1 μM) would show a protective effect in a traditional model of oxidative stress. We exposed the C6 glioma cell line to hydrogen peroxide (H2O2) and/or morphine for 24 h and evaluated cell viability, lipid peroxidation, and levels of sulfhydryl groups (an indicator of the redox state of the cell). Morphine did not prevent the decrease in cell viability provoked by H2O2 but partially prevented lipid peroxidation caused by 0.0025% H2O2 (a concentration allowing more than 90% cell viability). Interestingly, this opioid did not alter the increased levels of sulfhydryl groups produced by exposure to 0.0025% H2O2, opening the possibility that alternative molecular mechanisms (a direct scavenging activity or the inhibition of NAPDH oxidase) may explain the protective effect registered in the lipid peroxidation assay. Our results demonstrate, for the first time, that morphine in usual analgesic doses may contribute to minimizing oxidative stress in cells of glial origin. This study supports the importance of employing concentrations similar to those used in clinical practice for a better approximation between experimental models and the clinical setting.

Human exposure to relatively low levels of methylmercury is worrying, especially in terms of its genotoxicity. It is currently unknown as to whether exposure to low levels of mercury (below established limits) is safe. Genotoxicity was already shown in lymphocytes, but studies with cells of the CNS (as the main target organ) are scarce. Moreover, disturbances in the cell cycle and cellular proliferation have previously been observed in neuronal cells, but no data are presently available for glial cells. Interestingly, cells of glial origin accumulate higher concentrations of methylmercury than those of neuronal origin. Thus, the aim of this work was to analyze the possible genotoxicity and alterations in the cell cycle and cell proliferation of a glioma cell line (C6) exposed to a low, non-lethal and non-apoptotic methylmercury concentration. Biochemical (mitochondrial activity) and morphological (integrity of the membrane) assessments confirmed the absence of cell death after exposure to 3 μM methylmercury for 24 hours. Even without promoting cell death, this treatment significantly increased genotoxicity markers (DNA fragmentation, micronuclei, nucleoplasmic bridges and nuclear buds). Changes in the cell cycle profile (increased mitotic index and cell populations in the S and G2/M phases) were observed, suggesting arrest of the cycle. This delay in the cycle was followed, 24 hours after methylmercury withdrawal, by a decrease number of viable cells, reduced cellular confluence and increased doubling time of the culture. Our work demonstrates that exposure to a low sublethal concentration of MeHg considered relatively safe according to current limits promotes genotoxicity and disturbances in the proliferation of cells of glial origin with sustained consequences after methylmercury withdrawal. This fact becomes especially important, since this cellular type accumulates more methylmercury than neurons and displays a vital role protecting the CNS, especially in chronic intoxication with this heavy metal.

Mercury is an extremely dangerous environmental contaminant responsible for episodes of human intoxication throughout the world. Methylmercury, the most toxic compound of this metal, mainly targets the central nervous system, accumulating preferentially in cells of glial origin and causing oxidative stress. Despite studies demonstrating the current exposure of human populations, the consequences of mercury intoxication and concomitant use of drugs targeting the central nervous system (especially drugs used in long-term treatments, such as analgesics) are completely unknown. Morphine is a major option for pain management; its global consumption more than quadrupled in the last decade. Controversially, morphine has been proposed to function in oxidative stress independent of the activation of the opioid receptors. In this work, a therapeutic concentration of morphine partially protected the cellular viability of cells from a C6 glioma cell line exposed to methylmercury. Morphine treatment also reduced lipid peroxidation and totally prevented increases in nitrite levels in those cells. A mechanistic study revealed no alteration in sulfhydryl groups or direct scavenging at this opioid concentration. Interestingly, the opioid antagonist naloxone completely eliminated the protective effect of morphine against methylmercury intoxication, pointing to opioid receptors as the major contributor to this action. Taken together, the experiments in the current study provide the first demonstration that a therapeutic concentration of morphine is able to reduce methylmercury-induced oxidative damage and cell death by activating the opioid receptors. Thus, these receptors may be a promising pharmacological target for modulating the deleterious effects of mercury intoxication. Although additional studies are necessary, our results support the clinical safety of using this opioid in methylmercury-intoxicated patients, suggesting that normal analgesic doses could confer an additional degree of protection against the cytotoxicity of this xenobiotic.

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Human exposure to relatively low levels of methylmercury is worrying, especially in terms of its genotoxicity. It is currently unknown as to whether exposure to low levels of mercury (below established limits) is safe. Genotoxicity was already shown in lymphocytes, but studies with cells of the CNS (as the main target organ) are scarce. Moreover, disturbances in the cell cycle and cellular proliferation have previously been observed in neuronal cells, but no data are presently available for glial cells. Interestingly, cells of glial origin accumulate higher concentrations of methylmercury than those of neuronal origin. Thus, the aim of this work was to analyze the possible genotoxicity and alterations in the cell cycle and cell proliferation of a glioma cell line (C6) exposed to a low, non-lethal and non-apoptotic methylmercury concentration. Biochemical (mitochondrial activity) and morphological (integrity of the membrane) assessments confirmed the absence of cell death after exposure to 3 μM methylmercury for 24 hours. Even without promoting cell death, this treatment significantly increased genotoxicity markers (DNA fragmentation, micronuclei, nucleoplasmic bridges and nuclear buds). Changes in the cell cycle profile (increased mitotic index and cell populations in the S and G2/M phases) were observed, suggesting arrest of the cycle. This delay in the cycle was followed, 24 hours after methylmercury withdrawal, by a decrease number of viable cells, reduced cellular confluence and increased doubling time of the culture. Our work demonstrates that exposure to a low sublethal concentration of MeHg considered relatively safe according to current limits promotes genotoxicity and disturbances in the proliferation of cells of glial origin with sustained consequences after methylmercury withdrawal. This fact becomes especially important, since this cellular type accumulates more methylmercury than neurons and displays a vital role protecting the CNS, especially in chronic intoxication with this heavy metal. [ABSTRACT FROM AUTHOR]

Mercury is an extremely dangerous environmental contaminant responsible for episodes of human intoxication throughout the world. Methylmercury, the most toxic compound of this metal, mainly targets the central nervous system, accumulating preferentially in cells of glial origin and causing oxidative stress. Despite studies demonstrating the current exposure of human populations, the consequences of mercury intoxication and concomitant use of drugs targeting the central nervous system (especially drugs used in long-term treatments, such as analgesics) are completely unknown. Morphine is a major option for pain management; its global consumption more than quadrupled in the last decade. Controversially, morphine has been proposed to function in oxidative stress independent of the activation of the opioid receptors. In this work, a therapeutic concentration of morphine partially protected the cellular viability of cells from a C6 glioma cell line exposed to methylmercury. Morphine treatment also reduced lipid peroxidation and totally prevented increases in nitrite levels in those cells. A mechanistic study revealed no alteration in sulfhydryl groups or direct scavenging at this opioid concentration. Interestingly, the opioid antagonist naloxone completely eliminated the protective effect of morphine against methylmercury intoxication, pointing to opioid receptors as the major contributor to this action. Taken together, the experiments in the current study provide the first demonstration that a therapeutic concentration of morphine is able to reduce methylmercury-induced oxidative damage and cell death by activating the opioid receptors. Thus, these receptors may be a promising pharmacological target for modulating the deleterious effects of mercury intoxication. Although additional studies are necessary, our results support the clinical safety of using this opioid in methylmercury-intoxicated patients, suggesting that normal analgesic doses could confer an additional degree of protection against the cytotoxicity of this xenobiotic. [ABSTRACT FROM AUTHOR]