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Mild traumatic brain injuries (mTBI) are often caused by a blow to the head or a sudden jolt resulting in a wide range of physical, cognitive, and emotional temporary symptoms. Mild TBI diagnosis can be challenging and most commonly followed by post-concussion syndrome (PCS). When the symptoms are present for more than 3 months, prolonged post-concussive syndrome (PPCS) can be suspected. This review aims to identify and summarize the current status of the knowledge regarding the risk factors and predictors of the recovery from PCS and PPCS. A comprehensive search of the main scientific databases (PubMed, Web of Science, Embase, and Cochrane Library) was performed using keywords, such as: 'prolonged post-concussion syndrome', combined with 'risk factors', 'predictors', and 'outcomes'. Multiple studies reported more than one risk factor for PPCS development following mTBIs that were generally the results of sports-related concussions and car accidents. The most prevalent risk factor associated with PPCS was the female sex. Social factors/personality traits, anxiety, mental health disorders, or other health conditions from their past medical history, the occurrence of headache/migraines during TBI recovery, somatization, physical activity, and litigation were also reported to contribute to PPCS risk. An exhaustive approach is required to mitigate the risk of PPCS and to ensure optimal recovery after concussive events. However, larger prospective cohort studies evaluating patients that were examined and treated with standardized protocols could be needed to further validate these associations and mandate the highest risk factors for delayed recovery.
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The effects of exposure to environmental pollutants on neurological processes are of increasing concern due to their potential to induce oxidative stress and neurotoxicity. Considering that many industries are currently using different types of plastics as raw materials, packaging, or distribution pipes, microplastics (MPs) have become one of the biggest threats to the environment and human health. These consequences have led to the need to raise the awareness regarding MPs negative neurological effects and implication in neuropsychiatric pathologies, such as schizophrenia. The study aims to use three zebrafish models of schizophrenia obtained by exposure to ketamine (Ket), methionine (Met), and their combination to investigate the effects of MP exposure on various nervous system structures and the possible interactions with oxidative stress. The results showed that MPs can interact with ketamine and methionine, increasing the severity and frequency of optic tectum lesions, while co-exposure (MP+Met+Ket) resulted in attenuated effects. Regarding oxidative status, we found that all exposure formulations led to oxidative stress, changes in antioxidant defense mechanisms, or compensatory responses to oxidative damage. Met exposure induced structural changes such as necrosis and edema, while paradoxically activating periventricular cell proliferation. Taken together, these findings highlight the complex interplay between environmental pollutants and neurotoxicants in modulating neurotoxicity.
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Encéfalo , Modelos Animais de Doenças , Microplásticos , Estresse Oxidativo , Esquizofrenia , Peixe-Zebra , Peixe-Zebra/metabolismo , Animais , Estresse Oxidativo/efeitos dos fármacos , Microplásticos/toxicidade , Esquizofrenia/metabolismo , Esquizofrenia/induzido quimicamente , Esquizofrenia/patologia , Esquizofrenia/etiologia , Encéfalo/metabolismo , Encéfalo/efeitos dos fármacos , Encéfalo/patologia , Síndromes Neurotóxicas/metabolismo , Síndromes Neurotóxicas/etiologia , Síndromes Neurotóxicas/patologia , Ketamina/efeitos adversos , Ketamina/toxicidade , Metionina/metabolismo , Imuno-HistoquímicaRESUMO
Background: Mild Traumatic Brain Injury (mTBI) has been increasingly recognized as a public health concern due to its prevalence and potential to induce long-term cognitive impairment. We aimed to consolidate this observation by focusing on findings of neuropsychological assessments, neuroimaging, risk factors, and potential strategies for intervention to prevent and treat mTBI-associated cognitive impairments. Methods: A thorough search of PubMed, PsycINFO, and Embase databases was performed for studies published until 2024. Studies focusing on cognitive impairment after mTBI, with neurocognitive assessment as a primary outcome, were included. Results: We found consistent evidence of cognitive deficits, such as memory and attention impairments, and affected executive functions following mTBI. Neuroimaging studies corroborate these findings, highlighting structural and functional changes in the brain. Several risk factors for developing cognitive impairment post-mTBI were identified, including age, gender, genetics, and pre-existing mental health conditions. The efficacy of interventions, including cognitive rehabilitation and pharmaceutical treatment, varied across studies. Conclusions: Mild TBI can lead to significant long-term cognitive impairments, impacting an individual's quality of life. Further research is necessary to validate and standardize cognitive assessment tools post-mTBI, to elucidate the underlying neural mechanisms, and to optimize therapeutic interventions.
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Concussão Encefálica , Transtornos Cognitivos , Disfunção Cognitiva , Humanos , Concussão Encefálica/complicações , Concussão Encefálica/psicologia , Qualidade de Vida , Disfunção Cognitiva/complicações , Encéfalo , Transtornos Cognitivos/etiologiaRESUMO
Background and Objectives: Sustained virologic responses (SVRs) lead to a decrease in portal hypertension, the regression of fibrosis, and the improvement in the hepatic synthesis of procoagulant and anticoagulant factors. We aimed to assess the influence of SVR on coagulation parameters in cirrhotic patients with HCV treated with DAAs. Methods: We performed a prospective study in the Institute of Gastroenterology and Hepatology Iasi, Romania, between January 2022 and February 2024. We included patients diagnosed with compensated and decompensated HCV-related liver cirrhosis, treated with direct antivirals (PrOD ± RBV or SOF/LED ± RBV) for 12/24 weeks. Blood samples for biochemical, immunological, and coagulation tests were collected at the baseline, end of treatment (EOT), and once sustained virological response had been achieved over a period of 12/24 weeks (SVR12/24). Results: We analyzed a group of 52 patients with HCV-related liver cirrhosis, predominantly female (68.0%), and the degree of severity of cirrhosis placed the patients mainly in Child-Pugh classes B (40%) and C (36%). All patients achieved SVRs. The MELD score decreased at EOT (13.48 ± 4.273; p = 0.001) and SVR (9.88 ± 2.774; p = 0.000), compared to the baseline (14.92 ± 4.707). The FibroScan values decreased at SVR (17.596 ± 3.7276; p = 0.000) compared to the baseline (26.068 ± 7.0954). For all common coagulation parameters (platelets, INR, PT, fibrinogen, aPTT), there was a trend towards improvement during treatment, including changes which were statistically significant for the majority of patients. Factor II was low at the baseline (75.40 ± 7.506) but increased at EOT (87.40 ± 9.587) and, later, at SVR (99.12 ± 11.695; p = 0.000). The FVIII values increased at the baseline (175.52 ± 16.414) and decreased at EOT (151.48 ± 13.703) and SVR (143.40 ± 13.937). The FvW values decreased during treatment (146.84 ± 9.428, at baseline; 141.32 ± 9.690, p = 0.000, at EOT; and 126.68 ± 17.960, at SVR). In regard to the anticoagulant factors (PC, PS, ATIII), a significant improvement was brought on by SVR. Advanced stages of liver disease showed the most diminished FII activity, while at the baseline and in Child-Pugh C patients we recorded the highest values of FVIII and FvW. Conclusions: Our study proved that the "reset" of coagulopathy might be due to the improvement in liver function due to viral eradication secondary to AAD therapy.
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Antivirais , Cirrose Hepática , Resposta Viral Sustentada , Humanos , Feminino , Masculino , Cirrose Hepática/tratamento farmacológico , Cirrose Hepática/sangue , Cirrose Hepática/complicações , Antivirais/uso terapêutico , Pessoa de Meia-Idade , Estudos Prospectivos , Romênia , Idoso , Coagulação Sanguínea/efeitos dos fármacos , Hepacivirus/efeitos dos fármacos , Hepatite C/tratamento farmacológico , Hepatite C/complicações , Hepatite C/sangue , Hepatite C Crônica/tratamento farmacológico , Hepatite C Crônica/complicações , Hepatite C Crônica/sangue , AdultoRESUMO
Dementia represents a clinical syndrome characterised by progressive decline in memory, language, visuospatial and executive function, personality, and behaviour, causing loss of abilities to perform instrumental or essential activities of daily living. The most common cause of dementia is Alzheimer's disease (AD), which accounts for up to 80% of all dementia cases. Despite that extensive studies regarding the etiology and risk factors have been performed in recent decades, and how the current knowledge about AD pathophysiology significantly improved with the recent advances in science and technology, little is still known about its treatment options. In this controverted context, a nutritional approach could be a promising way to formulate improved AD management strategies and to further analyse possible treatment strategy options based on personalised diets, as Nutritional Psychiatry is currently gaining relevance in neuropsychiatric disease treatment. Based on the current knowledge of AD pathophysiology, as well as based on the repeatedly documented anti-inflammatory and antioxidant potential of different functional foods, we aimed to find, describe, and correlate several dietary compounds that could be useful in formulating a nutritional approach in AD management. We performed a screening for relevant studies on the main scientific databases using keywords such as "Alzheimer's disease", "dementia", "treatment", "medication", "treatment alternatives", "vitamin E", "nutrition", "selenium", "Ginkgo biloba", "antioxidants", "medicinal plants", and "traditional medicine" in combinations. Results: nutrients could be a key component in the physiologic and anatomic development of the brain. Several nutrients have been studied in the pursuit of the mechanism triggered by the pathology of AD: vitamin D, fatty acids, selenium, as well as neuroprotective plant extracts (i.e., Ginkgo biloba, Panax ginseng, Curcuma longa), suggesting that the nutritional patterns could modulate the cognitive status and provide neuroprotection. The multifactorial origin of AD development and progression could suggest that nutrition could greatly contribute to the complex pathological picture. The identification of adequate nutritional interventions and the not yet fully understood nutrient activity in AD could be the next steps in finding several innovative treatment options for neurodegenerative disorders.
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Ischemic strokes occur when the blood supply to a part of the brain is interrupted or reduced due to arterial blockage, and it often leads to damage to brain cells or death. According to a myriad of experimental studies, oxidative stress is an important pathophysiological mechanism of ischemic stroke. In this narrative review, we aimed to identify how the alterations of oxidative stress biomarkers could suggest a severity-reflecting diagnosis of ischemic stroke and how these interactions may provide new molecular targets for neuroprotective therapies. We performed an eligibility criteria-based search on three main scientific databases. We found that patients with acute ischemic stroke are characterized by increased oxidative stress markers levels, such as the total antioxidant capacity, F2-isoprostanes, hydroxynonenal, total and perchloric acid oxygen radical absorbance capacity (ORACTOT and ORACPCA), malondialdehyde (MDA), myeloperoxidase, and urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine. Thus, acute ischemic stroke is causing significant oxidative stress and associated molecular and cellular damage. The assessment of these molecular markers could be useful in diagnosing ischemic stroke, finding its causes, predicting its severity and outcomes, reducing its impact on the cellular structures of the brain, and guiding preventive treatment towards antioxidant-based therapy as novel therapeutic alternatives.
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AVC Isquêmico , Acidente Vascular Cerebral , Humanos , Antioxidantes/uso terapêutico , Antioxidantes/metabolismo , AVC Isquêmico/diagnóstico , AVC Isquêmico/tratamento farmacológico , AVC Isquêmico/prevenção & controle , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/tratamento farmacológico , Estresse Oxidativo/fisiologia , BiomarcadoresRESUMO
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases. Its incidence is progressively rising and it is possibly becoming a worldwide epidemic. NAFLD encompasses a spectrum of diseases accounting for the chronic accumulation of fat within the hepatocytes due to various causes, excluding excessive alcohol consumption. In this study, we aimed to focus on finding evidence regarding the implications of oxidative stress and inflammatory processes that form the multifaceted pathophysiological tableau in relation to thrombotic events that co-occur in NAFLD and associated chronic liver diseases. Recent evidence on the pathophysiology of NAFLD suggests that a complex pattern of multidirectional components, such as prooxidative, proinflammatory, and prothrombotic components, better explains the multiple factors that promote the mechanisms underlying the fatty acid excess and subsequent processes. As there is extensive evidence on the multi-component nature of NAFLD pathophysiology, further studies could address the complex interactions that underlie the development and progression of the disease. Therefore, this study aimed to describe possible pathophysiological mechanisms connecting the molecular impairments with the various clinical manifestations, focusing especially on the interactions among oxidative stress, inflammation, and coagulation dysfunctions. Thus, we described the possible bidirectional modulation among coagulation homeostasis, oxidative stress, and inflammation that occurs in the various stages of NAFLD.
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Transtornos da Coagulação Sanguínea , Hepatopatia Gordurosa não Alcoólica , Dermatopatias , Humanos , Hepatopatia Gordurosa não Alcoólica/complicações , Coagulação Sanguínea , Inflamação , Estresse OxidativoRESUMO
ABSTRACT: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly contagious new ß-coronavirus that primarily affects the lungs. Because of its unprecedented spread, in a relatively short interval, it is declared a global pandemic. Binding to the angiotensin-converting enzyme 2 receptors, SARS-CoV-2 is easily disseminated through air. Apart from the established clinical panel, individuals exposed to prolonged chronic stress also manifest gastrointestinal (GI) symptoms similar to those exhibited by SARS-CoV-2-infected patients.The present study aims to assess the incidence of GI deficiencies and prevalence of anxiety among healthy medical staff by applying the Visual Analog Scale for Irritable Bowel Syndrome (VAS-IBS) and Hamilton Anxiety Rating Scale (HAM-A) during this global crisis.We found significant differences on several items of the VAS-IBS: regarding the incidence of diarrhea (p = 0.04), bloating/gases (p = 0.02), and nausea/vomiting (p = 0.01) from the physical spectrum. After stratification based on age of the participants and after we applied Kruskal-Wallis test because of heterogeneity between groups, we noted two situations in which the null hypothesis is rejected: nausea/vomiting in women between 20 and 30 years, and between 30 and 40, and between 40 and 50 years, respectively (p = 0.026/0.029). Anxiety was prevalent among young and middle-class people after the centralization of HAM-A data, where 40.4% of the participants had various forms of anxiety: mild (n = 13; 13.82%), severe (n = 13; 13.82%), and moderate (n = 12; 12.76%).This study demonstrates that VAS-IBS is a reliable tool for assessing the incidence of GI deficiencies, as well as HAM-A for anxiety.
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Dor Abdominal/epidemiologia , Transtornos de Ansiedade/epidemiologia , COVID-19 , Constipação Intestinal/epidemiologia , Diarreia/epidemiologia , Síndrome do Intestino Irritável/epidemiologia , Náusea/epidemiologia , Doenças Profissionais/epidemiologia , Recursos Humanos em Hospital/estatística & dados numéricos , Vômito/epidemiologia , Adulto , Feminino , Humanos , Pessoa de Meia-Idade , Prevalência , Escalas de Graduação Psiquiátrica , Psicometria , Índice de Gravidade de Doença , Adulto JovemRESUMO
During and following the processing of a plant's raw material, considerable amounts are wasted, composted, or redistributed in non-alimentary sectors for further use (for example, some forms of plant waste contribute to biofuel, bioethanol, or biomass production). However, many of these forms of waste still consist of critical bioactive compounds used in the food industry or medicine. Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders. The primary treatment is based on symptomatology alleviation and controlled dietary management. Thus, this review aimed to describe the possible relevance of molecules residing in plant waste that can be used to manage IBS and co-occurring symptoms. Significant evidence was found that many forms of fruit, vegetable, and medicinal plant waste could be the source of some molecules that could be used to treat or prevent stool consistency and frequency impairments and abdominal pain, these being the main IBS symptoms. While many of these molecules could be recovered from plant waste during or following primary processing, the studies suggested that enriched food could offer efficient valorization and prevent further changes in properties or stability. In this way, root, stem, straw, leaf, fruit, and vegetable pomaces were found to consist of biomolecules that could modulate intestinal permeability, pain perception, and overall gastrointestinal digestive processes.
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Síndrome do Intestino Irritável , Dor Abdominal , Indústria Alimentícia , Frutas , Síndrome do Intestino Irritável/tratamento farmacológico , VerdurasRESUMO
Recently, increased interest and efforts were observed in describing the possible interaction between sleep and emotions. Human and animal model studies addressed the implication of both sleep patterns and emotional processing in neurophysiology and neuropathology in suggesting a bidirectional interaction intimately modulated by complex mechanisms and factors. In this context, we aimed to discuss recent evidence and possible mechanisms implicated in this interaction, as provided by both human and animal models in studies. In addition, considering the affective component of brain physiological patterns, we aimed to find reasonable evidence in describing the two-way association between comorbid sleep impairments and psychiatric disorders. The main scientific literature databases (PubMed/Medline, Web of Science) were screened with keyword combinations for relevant content taking into consideration only English written papers and the inclusion and exclusion criteria, according to PRISMA guidelines. We found that a strong modulatory interaction between sleep processes and emotional states resides on the activity of several key brain structures, such as the amygdala, prefrontal cortex, hippocampus, and brainstem nuclei. In addition, evidence suggested that physiologically and behaviorally related mechanisms of sleep are intimately interacting with emotional perception and processing which could advise the key role of sleep in the unconscious character of emotional processes. However, further studies are needed to explain and correlate the functional analysis with causative and protective factors of sleep impairments and negative emotional modulation on neurophysiologic processing, mental health, and clinical contexts.
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Emoções , Sono , Tonsila do Cerebelo/fisiologia , Animais , Encéfalo/fisiologia , Emoções/fisiologia , Humanos , Imageamento por Ressonância Magnética , Modelos Animais , Sono/fisiologiaRESUMO
Harlequin syndrome (HS) is a rare autonomic disorder. The causes and risk factors of the disease are not fully understood. Some cases of HS are associated with traumatic injuries, tumors, or vascular impairments of the head. Symptoms of HS can also occur in some autoimmune disorders, ophthalmic disorders, sleep disorders, and with certain organic lesions. In this context, a thorough review of the pathophysiology of HS in relation to neurological, ophthalmological, and dermatological conditions is necessary. In this mini-review, we aim to review the pathophysiological changes and underlying mechanisms in primary and secondary HS. Additionally, we discuss possible management approaches for patients with HS in light of the discussed pathological mechanisms. The main symptoms of HS that are correlated with autonomic nervous system impairments include sudden unilateral flushing of the face, neck, chest, and rarely arm, with concurrent contralateral anhidrosis. Despite reported co-occurring syndromes (such as cluster headaches), several studies have shown that HS could frequently overlap with other syndromes that are disruptive to the idiopathic nerve pathways. HS usually does not require any medical treatment. In some severe cases, symptomatic treatments could be needed. However, total symptomatic relief may not be achieved in many cases of HS. We therefore suggest an approach to comprehensive management of HS, which may lead to better long-term control of HS.
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Doenças do Sistema Nervoso Autônomo , Rubor , Hipo-Hidrose , Disautonomias Primárias , Doenças do Sistema Nervoso Autônomo/patologia , Face/patologia , Rubor/patologia , Humanos , Hipo-Hidrose/complicações , Hipo-Hidrose/diagnóstico , Disautonomias Primárias/patologia , Doenças Raras/patologiaRESUMO
Alzheimer's disease (AD) is a progressive neurodegenerative disorder, associated with extensive neuronal loss, dendritic and synaptic changes resulting in significant cognitive impairment. An increased number of studies have given rise to the neuroinflammatory hypothesis in AD. It is widely accepted that AD brains show chronic inflammation, probably triggered by the presence of insoluble amyloid beta deposits and neurofibrillary tangles (NFT) and is also related to the activation of neuronal death cascade. In the present study we aimed to investigate the role of YKL-40 levels in the cerebrospinal fluid (CSF) in the diagnosis of AD, and to discuss whether there are further potential roles of this protein in the management and treatment of AD. We conducted an online search on PubMed, Web of Science, and the Cochrane library databases from 1990 to 2021. The quantitative analysis showed that the levels of YKL-40 were significantly higher in Alzheimer's disease compared to controls, to mild cognitive impairment (MCI) AD (MCI-AD) and to stable MCI. They were also increased in MCI-AD compared to stable MCI. The present study shows that the CSF levels of YKL-40 could be potentially used as a biomarker for the prognosis of mild cognitive impairment and the likelihood of progression to AD, as well as for the differential diagnosis between AD and MCI.
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Doença de Alzheimer , Doença de Alzheimer/diagnóstico , Peptídeos beta-Amiloides , Biomarcadores , Proteína 1 Semelhante à Quitinase-3 , Diagnóstico Diferencial , HumanosRESUMO
Keratoconus (KC) is a controversial ophthalmological disease, often considered both multifactorial and multigenic with poor or not entirely understood etiopathogenesis. Corneal collagen crosslinking (CXL) procedure is the most common surgical therapy for KC which both slows corneal thinning and halts disease progression. While extensive studies provide consistent evidence on systemic oxidative stress in KC patients and animal models, little is known on the tear fluid oxidative stress markers such as antioxidant enzymes activity or lipid peroxidation markers. Also, little is known considering the oxidative status dynamics following CXL. In this way, we aimed to evaluate three oxidative stress markers in the tears of KC patients before and after CXL procedure. Total superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzymatic activity and malondiladehyde (MDA) levels were assessed from the tears of 20 kC patients who received the recommendation for CXL procedure. Significantly decreased SOD activity (p = 0.0014) was observed in KC patients tears, as compared to age and sex-matched controls which could lead to significant lipid peroxidation boost (p < 0.001). Significantly higher GPx enzyme activity was observed in KC patients, as compared to control (p < 0.001), suggesting a compensatory response to intense lipid peroxidation. Following CXL, SOD activity significantly decreases and GPx activity extensively increases, as compared to baseline KC levels and controls (p < 0.001). This work provides additional evidence on oxidative stress status in the tears of KC considering general oxidative stress markers dynamics both before and after the CXL procedure. We also demonstrated that the CXL procedure could have further relevance in the management of this disorder.
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Biomarcadores/metabolismo , Colágeno/metabolismo , Substância Própria/efeitos dos fármacos , Reagentes de Ligações Cruzadas , Ceratocone/tratamento farmacológico , Estresse Oxidativo/fisiologia , Fármacos Fotossensibilizantes/uso terapêutico , Adulto , Substância Própria/metabolismo , Proteínas do Olho/metabolismo , Feminino , Glutationa Peroxidase/metabolismo , Humanos , Ceratocone/metabolismo , Masculino , Malondialdeído/metabolismo , Riboflavina/uso terapêutico , Superóxido Dismutase/metabolismo , Lágrimas/enzimologia , Raios UltravioletaRESUMO
Background: Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, exhibiting complex and controversial pathological features. Both oxidative stress and inflammation-related reactive oxygen species production may be involved in IBS pathological development. Thus, we focused on several aspects regarding the causes of oxidative stress occurrence in IBS. Additionally, in the molecular context of oxidative changes, we tried to discuss these possible neurological implications in IBS. Methods: The literature search included the main available databases (e.g., ScienceDirect, Pubmed/Medline, Embase, and Google Scholar). Articles in the English language were taken into consideration. Our screening was conducted based on several words such as "irritable bowel syndrome", "gut brain axis", "oxidative stress", "neuroendocrine", and combinations. Results: While no consistent evidence suggests clear pathway mechanisms, it seems that the inflammatory response may also be relevant in IBS. The mild implication of oxidative stress in IBS has been described through clinical studies and some animal models, revealing changes in the main markers such as antioxidant status and peroxidation markers. Moreover, it seems that the neurological structures involved in the brain-gut axis may be affected in IBS rather than the local gut tissue and functionality. Due to a gut-brain axis bidirectional communication error, a correlation between neurological impairment, emotional over-responsiveness, mild inflammatory patterns, and oxidative stress can be suggested. Conclusions: Therefore, there is a possible correlation between neurological impairment, emotional over-responsiveness, mild inflammatory patterns, and oxidative stress that are not followed by tissue destruction in IBS patients. Moreover, it is not yet clear whether oxidative stress, inflammation, or neurological impairments are key determinants or in which way these three interact in IBS pathology. However, the conditions in which oxidative imbalances occur may be an interesting research lead in order to find possible explanations for IBS development.
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Síndrome do Intestino Irritável/complicações , Estresse Oxidativo/fisiologia , Encéfalo/fisiopatologia , Humanos , Síndrome do Intestino Irritável/etiologia , Síndrome do Intestino Irritável/fisiopatologia , Modelos Neurológicos , Doenças Neurodegenerativas/sangue , Doenças Neurodegenerativas/etiologia , Sistemas NeurossecretoresRESUMO
Irritable bowel syndrome (IBS) remains to date an intriguing functional gastrointestinal disorder. Recent studies described a multitude of exogenous factors that work together in IBS, gradually impairing intestinal lining cellular metabolism, including oxidative status balance, with or without a genetic background. Although the current biomarkers support the differentiation between IBS subtypes and other functional gastrointestinal disorder, they are mostly non-specific, referring to clinical, biochemical, and inflammatory imbalances. Since IBS could be also the result of deficient signaling pathways involving both gastrointestinal secretion and neuro-vegetative stimulation, IBS makes no exception from the oxidative hypothesis in the pathological mechanisms. Regarding the oxidative stress implication in IBS, the previous research efforts showed controversial results, with some animal models and patient studies reporting clear oxidative imbalance both on systemic and local levels, but still with no concrete evidence to point to a direct correlation between oxidative stress and IBS. Additionally, it seems that a major role could be also attributed to gut microbiota and their ability to shape our bodies and behaviors. Moreover, the genetic features study in IBS patients showed that several genetic similarities point to a possible correlation of IBS with affective spectrum disorders. Thus, we focus here the discussion on the assumption that IBS could in fact be more likely a stress-related disorder rather than a gastrointestinal one.
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Trato Gastrointestinal/fisiopatologia , Síndrome do Intestino Irritável/fisiopatologia , Estresse Oxidativo/fisiologia , Estresse Psicológico/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Humanos , Síndrome do Intestino Irritável/psicologia , Transdução de Sinais/fisiologia , Estresse Psicológico/complicaçõesRESUMO
Background and objectives: Oxidative stress shows evidence of dysregulation in cirrhotic patients with hepatic encephalopathy (HE), although there are still controversies regarding the connections between oxidative stress and ammonia in these patients. The aim of this study was to evaluate the oxidative stress implication in overt HE pathogenesis of cirrhotic patients. Materials and Methods: We performed a prospective case-control study, which included 40 patients divided into two groups: group A consisted of 20 cirrhotic patients with HE and increased systemic ammoniemia, and group B consisted of 20 cirrhotic patients with HE and normal systemic ammoniemia. The control group consisted of 21 healthy subjects matched by age and sex. The activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA) levels (lipid peroxidation marker), and ammoniemia were evaluated. Results: We found a significant decrease in SOD and GPx activity and also a significant increase of MDA levels in cirrhotic patients with HE as compared to the healthy age-matched control group (1.35 ± 0.08 vs. 0.90 ± 0.08 U/mL, p = 0.002; 0.093 ± 0.06 vs. 0.006 ± 0.008 U/mL, p = 0.001; and 35.94 ± 1.37 vs. 68.90 ± 5.68 nmols/mL, p = 0.0001, respectively). Additionally, we found significant correlations between the main oxidative stress markers and the levels of systemic ammonia (r = 0.452, p = 0.005). Patients from group A had a significant increase of MDA as compared with those from group B (76.93 ± 5.48 vs. 50.06 ± 5.60 nmols/mL, p = 0.019). Also, there was a compensatory increase in the activity of both antioxidant enzymes (SOD and GPx) in patients with increased systemic ammoniemia (group A), as compared to HE patients from group B. Conclusions: Our results demonstrated a significant decrease in antioxidants enzymes activities (SOD and GPx), as well as a significant increase in MDA concentrations, adding new data regarding the influence of oxidative stress in HE pathogenesis in cirrhotic patients.
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Amônia/sangue , Encefalopatia Hepática/enzimologia , Cirrose Hepática/enzimologia , Estresse Oxidativo , Idoso , Biomarcadores/sangue , Estudos de Casos e Controles , Feminino , Glutationa Peroxidase/sangue , Encefalopatia Hepática/sangue , Encefalopatia Hepática/complicações , Humanos , Cirrose Hepática/sangue , Cirrose Hepática/complicações , Masculino , Malondialdeído/sangue , Pessoa de Meia-Idade , Estudos Prospectivos , Superóxido Dismutase/sangueRESUMO
Background and objectives: Oxidative stress and inflammation have been implicated in the etiology of irritable bowel syndrome (IBS), a common gastrointestinal functional disease. This study aimed to further characterize the contention-stress rat model by exploring a possible correlation between oxidative stress markers measured in brain tissues with behavioral components of the aforementioned model. Thus, it is hereby proposed a possible IBS animal model relevant to pharmacological and complementary medicine studies. Materials and Methods: Wild-type male Wistar rats (n = 5/group) were chronically exposed to 6-hour/day contention, consisting of isolating the animals in small, vital space-granting plastic devices, for seven consecutive days. Following contention exposure, temporal lobes were extracted and subjected to biochemical analyses to assess oxidative stress-status parameters. Results: Our results show increased brain oxidative stress in contention-stress rat model: decreased superoxide dismutase and glutathione peroxidase activities and increased malondialdehyde production in the IBS group, as compared to the control group. Furthermore, the biochemical ratios which are used to evaluate the effectiveness of an antioxidant system on oxidative stress could be described in this model. Conclusions: The correlations between the behavioral patterns and biochemical oxidative stress features could suggest that this may be a complex model, which can successfully mimic IBS symptomatology further providing evidence of a strong connection between the digestive system, enteric nervous system, and the central nervous system.
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Antidepressivos Tricíclicos/farmacologia , Antioxidantes/farmacologia , Encéfalo/metabolismo , Síndrome do Intestino Irritável/metabolismo , Nortriptilina/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Animais , Antidepressivos Tricíclicos/administração & dosagem , Antidepressivos Tricíclicos/uso terapêutico , Biomarcadores/metabolismo , Glutationa Peroxidase/metabolismo , Humanos , Síndrome do Intestino Irritável/tratamento farmacológico , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Malondialdeído/metabolismo , Modelos Animais , Nortriptilina/administração & dosagem , Nortriptilina/uso terapêutico , Estresse Oxidativo/fisiologia , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismoRESUMO
INTRODUCTION: Oxytocin (OT) is a well-known neuropeptides which together with vasopressin, melatonin, insulin and other hormones can alter both behavior and physiological or neuronal functions. This growing interest on OT roles is also based on the demonstrated beneficial effects as a stress reliever and a social bonding agent. The association between old age and OT was only vaguely studied. Little or few is known on the effect of the OT hormone on the old body. Hereby, we present our preliminary results in the research on behavioral changes regarding the intraperitoneal administration of OT in aged rats. SUBJECTS AND METHODS: OT was administered for 8 days in Wistar aged rats in parallel with saline administration for control group. Behavioral markers were assessed in some specific behavioral tasks, such as the Y-Maze test for short-term working memory, Open Field test, Elevated Plus Maze, and Forced Swim test for anxious and depressive behavior assessment, and Three-chambered Maze test for sociability assessment. RESULTS: Increased mobility and decreased anxiety behaviors were reported for the aged intraperitoneal OT-treated animals, as compared with controls, during FST and OFT, and respectively FST, EPM, and OFT. Also, decreased depressive-like behaviors were observed in the same animal group during FST and ST. Moreover, a decrease in anxiolytic behavior was observed as exposed to stressful stimuli (such as grooming behavior in OFT, and forced grooming behavior in ST), and as exposed to social stimuli (such as grooming behavior in TCT). Similarly, significant differences were obtained regarding the social behavior of the intraperitoneal OT-treated animal as compared to control group, the animals showing increased sociability and social preference for the stranger animal in TCT. However, no significant effects on the working memory (assessed as spontaneous alternation in YMT) were observed. CONCLUSIONS: Intraperitoneal administration of OT in aged rats has clear effects on anxious and depressive behavior, but no significant effects on the working memory. Also, several beneficial effects of OT on social preferences and sociability were observed.
Assuntos
Envelhecimento/efeitos dos fármacos , Comportamento Animal/efeitos dos fármacos , Ocitocina/farmacologia , Animais , Injeções Intraperitoneais , Masculino , Memória de Curto Prazo/efeitos dos fármacos , Ratos , Ratos Wistar , Comportamento SocialRESUMO
Due to Alzheimer's disease (AD) great aggressiveness, many worldwide health associations began to globalize research efforts in order to find a suitable treatment and to clarify once and for all its controversial aetiology. Moreover, the animal modelling research is one of the best tools to evaluate molecular mechanisms and to correlate them with clinical features and behaviours. However, in order to provide valuable scientific data correlated to low error sources, a rigorous algorithm of selecting the proper animal model for testing is required. An ideal animal model for AD research has probably not yet been developed, but by a careful selection of the existent models or even by developing new models suitable to research conditions, consistent progress in this area of research can be achieved. This paper aims to show and centralize some of the valuable information gathered along the past years of failure and success in Alzheimer's disease animal modelling, in order to provide a theoretical ground for new and innovative aspects in this rather new area of research.
Assuntos
Doença de Alzheimer/tratamento farmacológico , Doença de Alzheimer/genética , Modelos Animais de Doenças , Animais , Animais Geneticamente Modificados , Humanos , Fenótipo , RoedoresRESUMO
INTRODUCTION: Various manifestations ranging from physical symptoms to cognitive and emotional impairments could often be seen following head concussions that lead to mild traumatic brain injury (mTBI). These symptoms are commonly comprising the post-concussion syndrome (PCS) and their resolution could be influenced by multiple factors. Personality traits have been suggested as potential risk factors for the emergence and persistence of PCS. In this study, we aimed to investigate the possible predisposition to PCS given by certain personality traits. METHODS: Prospective cohort studies, observational studies, and cross-phenotype polygenic risk score analyses were selected from the main scientific databases (PubMed/Medline, Scopus, EMBASE, Web of Science) based on multiple-step screening, using keywords (such as "personality traits", "post-concussion syndrome", "traumatic brain injury", "anxiety", "depression", "resilience", and "somatization") and inclusion/exclusion criteria (English written studies available in full text presenting relevant data on TBI patients and their personality traits; reviews, animal studies, and studies not written in English, not available in full text, or not presenting full demographical and clinical data were excluded). The investigated personality traits included emotional reserve, somatic trait anxiety, embitterment, mistrust, parental anxiety, state anxiety, trait anxiety, anxiety sensitivity, pain catastrophizing, helplessness, sports-concussion symptom load, and cognitive resilience. RESULTS: The reviewed data from 16 selected studies suggested that personality traits play an essential role in the development and persistence of PCS. Emotional reserve, cognitive resilience, and lower levels of somatic trait anxiety were associated with better outcomes in PCS. However, higher levels of anxiety sensitivity, pain catastrophizing, helplessness, and sports-concussion symptom load were associated with worse outcomes in PCS. Parental anxiety was not associated with persistent symptoms in children following concussion. Despite the statistical analysis regarding the included publications bias was low, further studies should further investigate the correlation between TBI and some personality traits, as some of the selected studies did not included healthy individuals and their psychological profiles for comparison and correlation analysis. CONCLUSION: Personality traits may help predict the development and persistence of PCS following mTBI. Understanding the personality traits roles in PCS could assist the development of targeted interventions for the prevention and treatment of PCS. Further research is needed to better understand the complex interactions between personality traits, neurobiological factors, and psychosocial factors in PCS.