Assessing the effects of common topical exposures on skin bacteria associated with atopic dermatitis.

BACKGROUND: While patients and families struggling with atopic dermatitis (AD) have documented concerns for a contributory role of skin care products in AD pathology, nearly all the skin microbiome studies to date have asked participants to avoid topical products (such as soaps or select medications) for the preceding days to weeks prior to sample collection. Thus, given the established role of the microbiome in AD, the interactions between topical exposures, dysbiosis and AD remains underrepresented in the academic literature. OBJECTIVES: To address this knowledge gap, we expanded our previous evaluations to test the toxicological effects of a broader range of common chemicals, AD treatment lotions, creams and ointments using both health- and AD-associated strains of Roseomonas mucosa and Staphylococcus spp. METHODS: Use of in vitro culture techniques and mouse models were deployed to identify chemicals with dysbiotic or pre-biotic potential. A proof-of-concept study was subsequently performed in healthy volunteers to assess global microbiome shifts after exposure to select chemicals using dermatologic patch testing. RESULTS: Numerous chemicals possessed antibiotic properties, including many not marketed as anti-microbials. Through targeted combination of potentially beneficial chemicals, we identified combinations which promoted the growth of health-associated isolates over disease-associated strains in bacterial culture and enhanced microbe-specific outcomes in an established mouse model of AD; the most promising of which was the combination of citral and colophonium (often sold as lemon myrtle oil and pine tar). Additional studies would likely further optimize the combination of ingredients use. Similar results were seen in the proof-of-concept human studies. CONCLUSIONS: Our results could offer a systematic, multiplex approach to identify which products carry dysbiotic potential and thus may guide formulation of new topicals to benefit patients with AD.

Ecological Drawbacks of Nanomaterials Produced on an Industrial Scale: Collateral Effect on Human and Environmental Health.

Currently, hundreds of different nanomaterials with a broad application in products that make daily lives a little bit easier, in every aspect, are being produced on an industrial scale at thousands of tons per year. However, several scientists, researchers, politics, and ordinary citizens have stated their concern regarding the life cycle, collateral effects, and final disposal of these cutting-edge materials. This review summarizes, describes, and discusses all manuscripts published in the Journal Citation Reports during the last 10 years, which studied the toxicity or the effects of nanomaterials on human and environmental health. It was observed that 23.62% of the manuscripts analyzed found no ecological or human risks; 54.39% showed that several nanomaterials have toxicological effects on the ecosystems, human, or environmental health. In comparison, only 21.97% stated the nanomaterials had a beneficial impact on those. Although only 54.39% of the manuscripts reported unfavorable effects of nanomaterials on ecosystems, human, or environmental health, it is relevant because the potential damage is invaluable. Therefore, it is imperative to make toxicological studies of nanomaterials with holistic focus under strictly controlled real conditions before their commercialization, to deliver to the market only innocuous and environmentally friendly products.

"ST-elevation myocardial infarction associated with air pollution levels in Mexico City".

Background Coronary heart disease has multiple risk factors, including air pollution. Numerous pathophysiological mechanisms have been identified with increasing levels of air pollution, mainly with ozone (O3), nitrogen dioxide (NO2), sulphur dioxide (SO2), particulate matter (PM10), fine particulate matter (PM2.5) and carbon monoxide (CO). In Mexico, the pollution level is reported using an air quality index called IMECA. Methods All patients with STEMI admitted at Hospital Español were collected between 2012 and 2019 (N = 348). We conducted a retrospective analysis using the air pollution exposure at the time of each event (lag0), the previous 24 h (lag1), 48 h (lag2), 72 h (lag3) and 5-day cumulative lag. The level of air pollution was analyzed independently using IMECA and particle concentrations. The data was divided in two groups: days with one of more STEMI's (MI group) and days free of events (Control group), using ANCOVA to evaluate the difference between means of both groups taking into account confounders. Results: For days with one or more cardiovascular event, a significant increase in SO2 was observed at lag1; similar increase was found in CO, PM2.5, SO2 at lag2. For the 5-day cumulative lag, SO2 and PM2.5 showed a significant increase. No differences were found using the IMECA levels in both groups. Conclusions: The elevated concentrations levels of CO, SO2 and PM2.5 showed significant association with STEMI at different time points before the event. Ozone, PM10 and NO2 showed no difference between groups. IMECA levels showed no association with STEMI in our study.

Cervical Spinal Cord Degeneration in Spinocerebellar Ataxia Type 7.

BACKGROUND AND PURPOSE: Spinocerebellar ataxia type 7 is an autosomal dominant neurodegenerative disease caused by a cytosine-adenine-guanine (CAG) repeat expansion. Clinically, spinocerebellar ataxia type 7 is characterized by progressive cerebellar ataxia, pyramidal signs, and macular degeneration. In vivo MR imaging studies have shown extensive gray matter degeneration in the cerebellum and, to a lesser extent, in a range of cortical cerebral areas. The purpose of this study was to evaluate the impact of the disease in the spinal cord and its relationship with the patient's impairment. MATERIALS AND METHODS: Using a semiautomated procedure applied to MR imaging data, we analyzed spinal cord area and eccentricity in a cohort of 48 patients with spinocerebellar ataxia type 7 and compared them with matched healthy controls. The motor impairment in the patient group was evaluated using the Scale for Assessment and Rating of Ataxia. RESULTS: Our analysis showed a significantly smaller cord area (t = 9.04, P < .001, d = 1.31) and greater eccentricity (t = -2.25, P =. 02, d = 0.32) in the patient group. Similarly, smaller cord area was significantly correlated with a greater Scale for Assessment and Rating of Ataxia score (r = -0.44, P = .001). A multiple regression model showed that the spinal cord area was strongly associated with longer CAG repetition expansions (P = .002) and greater disease duration (P = .020). CONCLUSIONS: Our findings indicate that cervical spinal cord changes are progressive and clinically relevant features of spinocerebellar ataxia type 7, and future investigation of these measures as candidate biomarkers is warranted.

Ataxia Severity Correlates with White Matter Degeneration in Spinocerebellar Ataxia Type 7.

BACKGROUND AND PURPOSE: There is a scarcity of information on the effect of white matter degeneration in patients with spinocerebellar ataxia type 7. Therefore, we investigated the WM integrity in a large group of patients with spinocerebellar ataxia type 7 by using Tract-Based Spatial Statistics. MATERIALS AND METHODS: Thirty-three patients with a molecular diagnosis of spinocerebellar ataxia type 7 and their age- and sex-matched healthy controls participated in this study. The patients' ataxia severity was evaluated with the Scale for the Assessment and Rating of Ataxia. Voxelwise analyses of diffusion metrics, including fractional anisotropy and mean diffusivity, were performed with Tract-Based Spatial Statistics. The correlation between WM abnormalities and ataxia severity was then calculated. RESULTS: Tract-Based Spatial Statistics analysis revealed WM abnormalities in the cerebellum and the cerebellar peduncles, as well as in other major cortical and subcortical pathways. Further analysis between the Scale for the Assessment and Rating of Ataxia score and WM mean diffusivity showed significant associations only in key areas related to motor control and visuospatial processing, including the cerebellar WM, the middle occipital WM, the superior cerebellar peduncle, and bilateral anterior thalamic radiation. No significant associations between fractional anisotropy and the Scale for the Assessment and Rating of Ataxia were found. CONCLUSIONS: These results suggest a significant contribution of local cerebellar and cerebellar-midbrain connections to ataxic impairment in spinocerebellar ataxia type 7. The results also suggest an involvement of cortical WM abnormalities including tracts within the occipital and frontal cortices. These findings contribute to a more comprehensive view of the clinical impact of the white matter degeneration in spinocerebellar ataxia type 7.

Primary aldosteronism can alter peripheral levels of transforming growth factor beta and tumor necrosis factor alpha.

UNLABELLED: Primary aldosteronism (PA) is the most common secondary cause of hypertension that has recently been implicated in alterations of the immune system and progression of cardiovascular disease. OBJECTIVE: To study the cytokines transforming growth factor beta1 (TGF-beta1), tumor necrosis factor alpha (TNF-alpha), and interleukin 10 (IL-10) in patients with PA and essential hypertensives (EH) and evaluate its association with the renin-angiotensin-aldosterone system. PATIENTS AND METHODS: We studied 26 PA and 52 EH patients as controls, adjusted by their blood pressure, body mass index, age, and gender. In both groups, PA and EH, we measured serum aldosterone (SA), plasma renin activity (PRA), and cytokines TGF- beta1, TNF-alpha, and IL-10. In addition, 17 PA patients were treated for 6 months with spironolactone, a mineralocorticoid receptor (MR) antagonist. RESULTS: PA patients had lower levels of TGF-beta1 (17.6+/-4.1 vs 34.5+/-20.5 pg/ml, p<0.001) and TNF-alpha (17.0+/-4.4 vs 35.6+/-21.7 pg/ml, p<0.001) and similar IL-10 levels (99.7+/-18.7 vs 89.4+/-49.5 pg/ml, p: ns), as compared with EH controls. TGF-beta1 and TNF-alpha levels showed a remarkable correlation with SA/PRA ratio in the total group (PA+EH). The treatment of PA patients with spironolactone increased the TGF-beta1 levels (18.3+/-5.9 to 28.4+/-6.3 pg/ml, p<0.001), while TNF-alpha, and IL-10 remained unchanged. CONCLUSION: Our results showed that PA patients have lower TGF-beta1 and TNF-alpha cytokine serum levels than EH. TGF-beta1 levels were restored with spironolactone, showing a MR-dependent regulation. In this way, the chronic aldosterone excess modifies the TGF-beta1 levels, which could produce an imbalance in the immune system homeostasis that may promote an early proinflammatory cardiovascular phenotype.