Understanding the Influence of Web-Based Information, Misinformation, Disinformation, and Reinformation on COVID-19 Vaccine Acceptance: Protocol for a Multicomponent Study.

BACKGROUND: The COVID-19 pandemic has generated an explosion in the amount of information shared on the internet, including false and misleading information on SARS-CoV-2 and recommended protective behaviors. Prior to the pandemic, web-based misinformation and disinformation were already identified as having an impact on people's decision to refuse or delay recommended vaccination for themselves or their children. OBJECTIVE: The overall aims of our study are to better understand the influence of web-based misinformation and disinformation on COVID-19 vaccine decisions and investigate potential solutions to reduce the impact of web-based misinformation and disinformation about vaccines. METHODS: Based on different research approaches, the study will involve (1) the use of artificial intelligence techniques, (2) a web-based survey, (3) interviews, and (4) a scoping review and an environmental scan of the literature. RESULTS: As of September 1, 2022, data collection has been completed for all objectives. The analysis is being conducted, and results should be disseminated in the upcoming months. CONCLUSIONS: The findings from this study will help with understanding the underlying determinants of vaccine hesitancy among Canadian individuals and identifying effective, tailored interventions to improve vaccine acceptance among them. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/41012.

Natalizumab Modifies Catecholamines Levels Present in Patients with Relapsing- Remitting Multiple Sclerosis.

AIMS: The main aim of this study was to verify the effect of natalizumab on the levels of circulating catecholamines and indolamine and their possible relation with MS. METHODS: For this purpose, 12 healthy individuals (control group) and 12 relapsing-remitting multiple sclerosis patients (RR-MS) were selected. The patients were treated with 300 mg of natalizumab during 56 weeks (1 dose/4 weeks) (MS-56). This selection was based on the McDonalds revision criterion and scheduled to star treatment with natalizumab. Blood samples were taken before treatment (basal level) and after 56 weeks of using natalizumab. Melatonin was measured in serum and in plasma, catecholamines (dopamine, epinephrine, and norepinephrine), carbonylated proteins, 8-hydroxy-2'deoxyguanosine (8OH-dG) and the ratio reduced glutathione/oxidised glutathione (GSH/GSSG). RESULTS: The epinephrine and dopamine levels diminished in the basal group with respect to the control and did not recover normal levels with the treatment. The melatonin was decreased in RR-MS patients and went back to its normal levels with natalizumab. Norepinephrine was increased in RR-MS and decreased in MS-56 until it equalled the control group. CONCLUSION: Natalizumab normalizes altered melatonin and norepinephrine levels in MS.

Elevated melatonin levels in natalizumab-treated female patients with relapsing-remitting multiple sclerosis: relationship to oxidative stress.

Natalizumab is currently the most successful clinical treatment for multiple sclerosis. The use of this drug is associated with the reduction in the number of relapses and a slowing in disease progression, as well as an improvement in signs and symptoms displayed by the patients. To evaluate the effect of natalizumab on melatonin and its relationship with peripheral oxidative damage, we studied the serum melatonin levels in 18 patients with relapsing-remitting multiple sclerosis. Natalizumab caused significant increases in serum melatonin concentrations. This change was associated with a rise in increase of antioxidants and a reduction in oxidative stress biomarkers. In conclusion, these data may explain, at least in part, some of the beneficial effects exhibited by disease antibody such as its antioxidant capacity.

Effect of natalizumab on oxidative damage biomarkers in relapsing-remitting multiple sclerosis.

BACKGROUND: Natalizumab is a monoclonal antibody used to treat multiple sclerosis. This study sought to determine whether the protective action of natalizumab involved a reduction in oxidative damage. METHODS: Twenty-two multiple sclerosis patients fulfilling the revised McDonald criteria were assigned to treatment with 300 mg natalizumab intravenously once monthly (infusion every 4 weeks) in accordance with Spanish guidelines. Carbonylated proteins, 8-hydroxy-2'-deoxyguanosine, total glutathione, reduced glutathione, superoxide dismutase, glutathione peroxidase, and myeloperoxidase levels were measured at baseline and after 14 months' treatment, and the antioxidant gap was calculated. RESULTS: Natalizumab prompted a drop in oxidative-damage biomarker levels, together with a reduction both in myeloperoxidase levels and in the myeloperoxidase/neutrophil granulocyte ratio. Interestingly, natalizumab induced nuclear translocation of Nrf2 and a fall in serum vascular cell adhesion molecule-1 levels. CONCLUSION: These findings suggest that natalizumab has a beneficial effect on oxidative damage found in MS patients.

Electronic health record: design and implementation of a lab test request module.

BACKGROUND: The electronic health record (EHR) has become a fundamental tool in health care. The ordering and inclusion of lab tests and results is one of the most frequently requested services by EHR users. We have designed, developed and implemented in Andalusia, an autonomous community in the south of Spain (8.3 million inhabitants), a unified lab test request module for the Andalusian public health system EHR. PURPOSE: After implementing the module in 27 laboratories, our objective is to assess its impact on healthcare activities and to ascertain whether its functional design addresses the needs and expectations of users. METHODS: We surveyed laboratory and healthcare professionals to assess their opinion of the module's operation in daily practices and the effect it has had on pre- and post-analytical quality indicators (before and after lab test module implementation). RESULTS: All the laboratories surveyed noted that the implementation of the laboratory module in the EHR improved the analytical process, highlighting better safety in patient identification, less programming or container errors and shorter response times. Clinical professionals gave the module a rating of 7.8 out of 10, positively highlighting the speed at which results are delivered and their integration in the EHR. In terms of the model's drawbacks, laboratories have highlighted its rigidity in solving errors and clinical professionals have noted the requirement of adapting to a new nomenclature. It is also necessary to expand coding to all the tests available in clinical laboratories. CONCLUSIONS: The results of our survey indicate that the functional design of our analytical testing module is suitable for user needs, allowing to integrate information from multiple laboratories in a single region. Based on our experience, the key aspects for the success of this project have been: a design conceived for both laboratories and clinical professionals, the involvement of laboratories as a key element of the project, as well as sufficient time of local piloting before widespread implementation which is basic for the success of a computer application that affects so many potential users of the health care system.

Nuevas herramientas en salud / New tools in healthcare

No disponible

Nuevas herramientas en salud / New tools in healthcare

No disponible

Oxidative stress and inflammation biomarkers in the blood of patients with Huntington's disease.

OBJECTIVES: Huntington's disease (HD) is a neurodegenerative disorder for which there is no effective treatment. Oxidative stress and inflammation are known to be involved in HD, but the precise relationship between the two remains unclear. The aim of this study was to analyze oxidative stress and inflammation biomarkers in blood of patients with HD with a view to identifying potential links between them. METHODS: Blood samples were collected from 13 patients with HD and from 10 age- and sex-matched controls, and the following were measured: C-reactive proteins, myeloperoxidase (MPO)/white blood cell (WBC) ratio, interleukin-6 (IL-6), thioredoxin reductase-1 (TrRd-1), thioredoxin-1 (Trx-1), total nitrites (NOx), nitric oxide synthase (NOS) and nitrotyrosine. RESULTS: Results showed that HD is associated to a reduction of TrRd-1 and Trx-1 levels in plasma and erythrocytes, and with an increase in the MPO/WBC ratio. A positive correlation was observed between global oxidative stress (GOS) and MPO/WBC. No changes were found in NOS and Nox levels with respect to controls. CONCLUSION: Oxidative damage may be linked to the inflammatory response in HD, via a peripheral immune response.

Natalizumab y reducción de los niveles de proteínas carboniladas en pacientes con esclerosis múltiple / Natalizumab and reduction of carbonylated proteins in patients with multiple sclerosis

Introducción. Es conocida la especial sensibilidad del sistema nervioso central al daño oxidativo, así como la relación entre éste y la respuesta inflamatoria. Recientes estudios han mostrado que el estrés oxidativo está presente en la instauración y evolución de la esclerosis múltiple (EM). Uno de los más recientes tratamientos en este proceso es el natalizumab,un anticuerpo monoclonal. Objetivo. Evaluar si el efecto terapéutico del natalizumab se asocia con la gravedad de la enfermedad y el daño oxidativo. Pacientes y métodos. Se reclutó para el estudio a 20 pacientes con EM remitente recurrente (EMRR) incluidos en terapia con natalizumab y distribuidos según la Expanded Disability Status Scale (EDSS) en dos grupos: EMRR-1 (EDSS < 5) yEMRR-2 (EDSS ≥ 5). Se obtuvieron muestras sanguíneas para un estudio del perfil oxidativo.Resultados. Los datos mostraron un descenso en las proteínas carboniladas tras el tratamiento con natalizumab. La reducciónde daño oxidativo valorada como oxidación de proteínas es significativa entre la situación previa del paciente (basal) y tras 14 meses de tratamiento. El decremento más significativo coincidió con los pacientes de mayor gravedad en el proceso. Si bien no ha sido posible establecer una correlación, la significación estadística es mayor para pacientes del grupo EMRR-2 tratados con natalizumab. Por su parte, los sistemas antioxidantes no mostraron cambios estadísticamentesignificativos. Conclusión. El natalizumab induce una reducción en los niveles de proteínas carboniladas (AU)

Introduction. The sensitivity of the central nervous system to oxidative damage and its relationship with inflammatory response are well known. Recent studies have shown that oxidative stress is present in the establishment and developmentof multiple sclerosis (MS). One of the most recent treatments in this process is natalizumab, a monoclonal antibody. Aim. To evaluate whether the therapeutic effect of natalizumab is associated with the severity of the disease and the oxidative damage. Patients and methods. Researchers recruited twenty patients with relapsing-remitting MS (RRMS) undergoing therapy with natalizumab and distributed, according to the Expanded Disability Status Scale (EDSS), in two groups: RRMS-1 (EDSS< 5) and RRMS-2 (EDSS ≥ 5). Blood samples were taken for an oxidative profile study. Results. Data showed a decrease in carbonylated proteins following treatment with natalizumab. The reduction in oxidative damage rated as protein oxidation is significant between the previous (baseline) situation of the patient and after 14 months’ treatment. The most significant decrease coincided with the patients with the highest levels of severity in the process.Although it has not been possible to establish a correlation, the statistical significance is higher for patients in the RRMS-2 group treated with natalizumab. The antioxidant systems, on the other hand, did not display any tatistically significant changes.Conclusions. Natalizumab brings about a reduction in carbonylated protein levels (AU)

Peripheral oxidative stress in relapsing-remitting multiple sclerosis.

OBJECTIVES: To evaluate levels of oxidative stress in blood samples in patients with relapsing-remitting MS (RR-MS). DESIGN AND METHODS: Peripheral blood samples were collected from 24 RR-MS patients and 15 healthy controls. Levels of the following were measured: carbonylated proteins, 8-hydroxy-2'deoxyguanosine (8OHdG), total glutathione, reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG ratio, superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GRd), glutathione-S-transferase (GST), myeloperoxidase (MPO), antioxidant gap, total antioxidant capacity (PAO), global oxidative stress (GOS), serum vascular cell adhesion molecule-1 (sVCAM-1) and serum inter-cellular adhesion molecule 1 (sICAM-1). RESULTS: Values for carbonylated proteins, 8OHdG, total glutathione, GSH, GSH/GSSG ratio, SOD, GRd and GOS were significantly higher in RR-MS patients than in healthy controls. By contrast, PAO, GSSG, GPx and GST were lower in RR-MS patients. CONCLUSION: Oxidative stress plays a major role in MS, and is observed prior to relapse.

Melatonin improves 3-nitropropionic acid induced behavioral alterations and neurotrophic factors levels.

OBJECTIVE: This study sought to determine whether melatonin causes changes in neurotrophic factors and it protects against the mycotoxin 3-nitropropionic acid (3-NP) in brain tissue. METHODS: Rats were given 3-NP over four consecutive days (20 mg/kg BW), while melatonin was administered over 21 days (1 mg/kg/BW), starting after the last injection of 3-NP. RESULTS: Rats treated with 3-NP displayed significant changes in neurotrophic factor (BDNF and GDNF) levels, together with alterations in behavior; they also displayed extensive oxidative stress and a massive neuronal damage. CONCLUSIONS: Melatonin improved behavioral alterations, reduced oxidative damage, lowered neurotrophic factor levels and neuronal loss in 3-NP-treated rats. These results suggest that melatonin exerts a neuroprotective action.

Changes in body mass index are associated with changes in inflammatory and endothelial dysfunction biomarkers in obese prepubertal children after 9 months of body mass index SD score loss.

The metabolic syndrome is associated with insulin resistance, a systemic low-grade inflammatory state, and endothelial dysfunction. These disorders may arise at a very early age in obese children. The aim of this study was to confirm changes in endothelial dysfunction and inflammatory biomarkers in obese prepubertal children and to evaluate the effect of body mass index (BMI) modification on these biomarkers. Biomarkers for inflammation, endothelial dysfunction, and insulin resistance were measured in obese children (47) and healthy controls (47). Baseline pretreatment levels of insulin (P = .019), homeostasis model assessment of insulin resistance (P = .004), soluble intercellular adhesion molecule (sICAM) (P = .003), and C-reactive protein (CRP) (P < .001) were significantly higher in obese children than in controls. After 9 months of treatment, obese children with lowered BMI SD score (SDS-BMI) displayed a significant decrease in insulin (P = .011), homeostasis model assessment of insulin resistance (P = .012), CRP (P = .006), and interleukin-6 (IL-6) (P = .045) levels compared with obese children with stable SDS-BMI; they also displayed a nonsignificant drop in sICAM levels. Similarly, obese children with lowered SDS-BMI displayed a decrease in CRP (P = .005) and IL-6 (P = .065) compared with baseline levels before treatment. In the total obese group, changes in SDS-BMI correlated positively with changes in CRP (P = .035), IL-6 (P = .027), and sICAM-1 (P = .038) levels. Only SDS-BMI was an independent predictive factor for CRP (P = .031), IL-6 (P = .027), and sICAM-1 (P = .033). Prepubertal obese children displayed alterations indicative of endothelial dysfunction, insulin resistance, and inflammatory state. Lowering of the SDS-BMI after 9 months of treatment was associated with an improvement in these variables compared with those in obese children with stable SDS-BMI status.

Metabolic cardiovascular syndrome in obese prepubertal children: the role of high fasting insulin levels.

The aim of this study was to detect the presence and degree of impairment of cardiovascular disease (CVD) risk factors, grouped as metabolic cardiovascular syndrome (MCS), in obese prepubertal children. We also assessed the influence of high fasting insulin levels in this pathological status. A cross-sectional study was performed on obese children based on fasting blood samples. Subjects were 61 obese children (aged 6 to 9 years) and an equal number of non-obese children paired by age and sex. The obese children presented the following characteristics in comparison to the non-obese group: significantly high levels of insulin (8.2 +/- 0.52 v 6.12 +/- 0.34 microU/mL), triglycerides (TG) (0.79 +/- 0.04 v 0.60 +/- 0.02 mmol/L), uric acid (0.24 +/- 0.005 v 0.21 +/- 0.004 mmol/L), systolic (SBP) (94.59 +/- 1.06 v 88.85 +/- 1.2 mm Hg) and diastolic (56.49 +/- 1.07 v 52.21 +/- 1.06 mm Hg) blood pressure (DBP), and low levels of high-density lipoprotein cholesterol (HDL-C) (1.30 +/- 0.04 v 1.46 +/- 0.03 mmol/L), and nonesterified fatty acids (0.407 +/- 0.02 v 0.505 +/- 0.02 mmol/L). The hyperinsulinemic obese children showed the same types of differences when compared with the normoinsulinemic group. In the obese group, having adjusted for age, waist/hip ratio (WHR), body mass index (BMI), and sex hormone-binding globulin (SHBG), insulin was an independent prediction factor for triglycerides (P =.0004), apolipoprotein A-I (Apo-AI) (P =.005), and alanine aminotransferase (ALT) (P =.029). BMI was an independent prediction factor for HDL-C (P =.001) and triglycerides (P =.027). However, insulin was an independent prediction factor in the control group for triglycerides (P =.0002) and SBP (P =.012), just as BMI was for HDL-C (P =.011) and uric acid (P =.041). We conclude that the cluster of CVD risk factors associated with MCS and intra-abdominal fat is present in obese prepubertal children. This situation seems to depend, to a large extent, on the insulin basal level. The apparent association between BMI and MCS is due to the correlation between BMI and insulin, and to the fact that insulin associates with MCS. Within the obese group, hyperinsulinemic children present the greatest impairment in the parameters considered to be constituents of MCS.

Elevated plasma total homocysteine levels in hyperinsulinemic obese subjects.

Homocysteine has been associated with the oxidative stress in the pathogenesis of atherosclerosis. Oxidative stress caused by triglycerides and free fatty acids is known to cause insulin resistance and hyperinsulinemia. On the other hand, insulin resistance may increase homocysteine levels. Since obesity is associated with insulin resistance and hyperinsulinemia, we aimed to study the possible association of homocysteine with hyperinsulinemia in obese subjects. 20 obese male subjects (body mass index >29), aged 33--55 (mean 45 years old) were studied. A fasting blood sample was obtained for the study and the subjects undertook an oral glucose tolerance test with samples taken at 1 and 2 h after glucose. Subjects were divided in two groups according to the fasting insulin levels, < 9 &mgr;U/ml or normoinsulinemic (group 1) and >9 &mgr;U/ml or hyperinsulinemic (group 2). Glucose, insulin, homocysteine, folate, B(12,) total cholesterol, HDL-cholesterol and triglycerides levels were determined in fasting blood samples. In oral glucose tolerance test, glucose, insulin and homocysteine levels were measured. Hyperinsulinemic obese subjects (group 2) had higher levels of insulin and glucose at 1 h and 2 h postglucose, compared with group 1. Fasting total homocysteine and triglyceride levels were also increased in this group, whereas folate and B(12) levels were similar in both groups. Fasting homocysteine significantly correlated with fasting insulin (r = 0.6, p <0.01). Homocysteine levels slightly but significantly decreased after glucose loading in normoinsulinemic but not in hyperinsulinemic obese subjects. These results show that higher homocysteine levels are observed in the hyperinsulinemic obese subjects and suggest that homocysteine could play a role in the higher risk of cardiovascular disease in obesity.