Objetivo: Analizar los cambios en la frecuencia y la incidencia de la enfermedad del ojo seco (EOS) y los tiempos de exposición a pantallas al inicio de cursos en línea, y comparar estos cambios ...entre sexos. Secundariamente, correlacionar los tiempos de exposición con la gravedad de los síntomas. Método: Se aplicaron cuatro encuestas idénticas durante 6 semanas, las cuales contenían el Ocular Surface Disease Index (OSDI) que cuantifica la gravedad de los síntomas de EOS y preguntas sobre tiempos de exposición a pantallas. Se incluyeron universitarios que transicionaron de cursos presenciales a plataformas en línea. Resultados: La frecuencia de EOS entre los 97 participantes (54 mujeres y 43 hombres) alcanzó su máximo en la semana 4 (82.47%). Las puntuaciones OSDI aumentaron significativamente (p < 0.0001) entre la situación basal (27.01 ± 17.55) y la semana 6 (37.17 ± 24.64), reflejando un empeoramiento sintomatológico y una incidencia del 8.5%. Este empeoramiento se observó en las mujeres (p < 0.0001), pero no en los hombres (p = 0.11); se encontraron diferencias significativas entre sexos en la situación basal (p = 0.01), la semana 2 (p = 0.02) y la semana 6 (p = 0.008), pero no en la semana 4 (p = 0.11). El inicio de los cursos en línea aumentó el tiempo frente a la pantalla (p < 0.0001). Las horas basales fueron 25.52 ± 11.33 y alcanzaron su máximo en la semana 2, con 34.62 ± 10.90 horas. Las puntuaciones OSDI y los tiempos de exposición de los cursos en línea se correlacionaron significativamente (semana 2, R = 0.265; semana 4, R = 0.262; semana 6, R = 0.205). Conclusiones: Los universitarios sufren síntomas graves de EOS que se correlacionaron con el inicio de los cursos en línea. Las instituciones educativas deberían fomentar la salud ocular.
A genetic component influences the development of atherosclerosis in the general population and also in rheumatoid arthritis (RA). However, genetic polymorphisms associated with atherosclerosis in ...the general population are not always involved in the development of cardiovascular disease (CVD) in RA. Accordingly, a study in North-American RA patients did not show the association reported in the general population of coronary artery disease with a series of relevant polymorphisms (TCF21, LPA, HHIPL1, RASD1-PEMT, MRPS6, CYP17A1-CNNM2-NT5C2, SMG6-SRR, PHACTR1, WDR12 and COL4A1-COL4A2). In the present study, we assessed the potential association of these polymorphisms with CVD in Southern European RA patients. We also assessed if polymorphisms implicated in the increased risk of subclinical atherosclerosis in non-rheumatic Caucasians (ZHX2, PINX1, SLC17A4, LRIG1 and LDLR) may influence the risk for CVD in RA. 2,609 Spanish patients were genotyped by TaqMan assays. Subclinical atherosclerosis was determined in 1,258 of them by carotid ultrasonography (assessment of carotid intima media thickness and presence/absence of carotid plaques). No statistically significant differences were found when each polymorphism was assessed according to the presence/absence of cardiovascular events and subclinical atherosclerosis, after adjustment for potential confounder factors. Our results do not show an association between these 15 polymorphisms and atherosclerosis in RA.
It has been suggested that increased erythrocyte membrane phosphatidylserine (PS) exposure could contribute to hypercoagulability and hemorheological disturbances in obesity. The aim of our study was ...to evaluate PS exposure in obese patients and in a control group and to correlate this with hemorheological properties, i.e., erythrocyte aggregability (EA) and deformability, and to evaluate the effect of weight loss on these parameters. An anthropometric and analytical evaluation was performed at baseline and after 3 months on a diet (very low‐calorie diet for 4 weeks and low‐calorie diet for 2 months) on 49 severe or morbid obese patients (37 women, 12 men) and 55 healthy volunteers (39 women, 16 men). PS exposure on erythrocyte membrane was performed by flow cytometry. Erythrocyte aggregation was measured using the Myrenne MA1 and the Sefam aggregometer. Erythrocyte deformability was determined in a stress diffractometer. Prothrombin fragment F1+2 (F1+2) was determined as a marker of the hypercoagulable state, and plasma malondialdehyde (MDA) as an indicator of oxidative stress. Obese patients had a higher EA index, higher PS exposure on erythrocyte membranes and higher levels of MDA and F1+2. The differences in erythrocyte aggregation and F1+2 between obese patients and the control group were maintained after adjusting for PS exposure. After 3 months of diet, a significant reduction in PS exposure on erythrocyte membrane was observed. Obese patients show increased PS exposure on erythrocyte membrane, with no effect on rheological properties. Increased PS exposure could contribute to hypercoagulability in these patients. Weight loss obtained with diet treatment reduces PS exposure on erythrocyte membrane.
Dyslipidemia is commonly found in T1D adults and increases the risk of CVD. There is no research on dyslipidemia in T1D adults in Spain so far.
The aim of the study was to evaluate the prevalence and ...the pattern of dyslipidemia and its relationship with other risk factors or comorbidities.
Methods: A multicentric, cross-sectional study in Spain included 1252 adults with T1D who visited Diabetes Clinic from December 2017 to December 2018. Cut-off points for abnormal lipid levels (total cholesterol (TC) ≥200 mg/dL, LDL ≥130 mg/dL, HDL ≤35 mg/dL, and triglycerides (TG) ≥150 mg/dL) were taken from the Third Report of the National Cholesterol Education Program and the ADA. Dyslipidemia was defined by the presence of one or more abnormal serum lipid concentrations.
Results: Among 1252 patients 50,3% were male. Median age 40,5+/-13 years old and the median duration of diabetes was 20+/-13 years. Median A1c 7,96+/-2,49% and BMI 25,7+/-4,6kg/m2 The overall lipid profile was TC 188+/-42 mg/dL, LDL 109+/-36 mg/dL, HDL 59+/-17 mg/dL and TG 96+/-96 mg/dL. The prevalence of dyslipidemia was 43,5%. The most frequent dyslipidemia found wash high TC (34,6%), followed by high LDL (26,6%), high TG (11,3%) and low HDL (1,8%). Comparison between the dyslipidemic (D) group and normolipidemic (No D) group age was significantly higher in the D group P< 0,001). The frequency of dyslipidemia was higher in male, current smokers and hypertension. There were no differences between the D and No D groups in terms of A1c, BMI, family background, hypoglycemic treatment or duration of diabetes. The prevalence of microvascular complications was higher in the D group (p< 0,0001), there were no differences in macrovascular complications.
Conclusions: Our study was the first report of lipid data in Spanish T1D adults. We have shown that the overall lipid pattern was comparable to that in nondiabetic individuals. There is high prevalence of dyslipidemia which was associated with age, sex (male), smoking and comorbidities but not with glycemic control.
Disclosure
M. Rodriguez Carnero: None. D. Bellido Guerrero: None. C. Tejera: None. M. López de la Torre: None. A. Soto González: None. F.J. Escalada: Advisory Panel; Self; Merck Sharp & Dohme Corp., Novo Nordisk A/S, Sanofi. Consultant; Self; Esteve, Lilly Diabetes. Speaker's Bureau; Self; Amgen Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Janssen Pharmaceuticals, Inc., Merck Sharp & Dohme Corp., Novo Nordisk A/S, Sanofi. A. Hernandez-Mijares: None. L. Suarez Gutierrez: None. C. Morales: Other Relationship; Self; AstraZeneca, Janssen Pharmaceuticals, Inc., Lilly Diabetes, Merck Sharp & Dohme Corp., Novo Nordisk A/S, Sanofi. L. Gutiérrez Carrasqu: None. A. Cadenas: Advisory Panel; Self; Janssen Pharmaceuticals, Inc. O. Díaz Trastoy: None. J. Amigó-Farran: None. I. Gonzalez molero: None. V. Bellido: None. F. Arrieta: None. F. Tinahones: Advisory Panel; Self; Lilly Diabetes, Novo Nordisk A/S, Regeneron Pharmaceuticals, Sanofi-Aventis. Consultant; Self; AstraZeneca. Research Support; Self; AstraZeneca. Speaker's Bureau; Self; Danone Nutricia Research, Lilly Diabetes, Novo Nordisk A/S, Regenerative Medical Solutions, Sanofi-Aventis.
Introduction: Cardiovascular disease (CVD) is the major cause of mortality in T1D. Lipid-lowering treatment (LLT) with statins prevent major cardiovascular events and dead in a broad spectrum of ...patients. However, evidence of CVD risks factors and its management are based on subgroup analyses and extrapolations of effects demonstrates in other populations.
Objectives: The aim of the study was to analyze the differences between T1D adults on lipid-lowering treatment (T group) and without treatment (No T group). We pay special attention to CVD risk factors, comorbidities and which factors are associated with receiving lipid-lowering treatment.
Research design and Methods: A multicentric, cross-sectional study in Spain included 1252 T1D adults who visited Diabetes Clinic from December 2017 to December 2018.
Results: Among 1252 patients 344 were on LLT. In terms of lipid profile LDL (131 vs. 100 mg/dL), HDL (57 vs. 60 mg/dL), total cholesterol (213 vs. 178 mg/dL) and triglycerides (125 vs. 85 mg/dL) levels were statistically significant while compared between T and No T groups. T group was older (48 vs. 37 years old) and the median duration of diabetes was higher (25 vs. 18 years)than No T group (p< 0.000). BMI in T group was 27 kg/m2 higher than no T group (25 kg/m2) (p < 0,0001). There was a trend toward higher prevalence of microvascular (57% vs. 23,8%) and macrovascular complications (13,7% vs. 3,6%) in T group than in No T (p < 0,000). A positive association was found between sex (male), smoking, high blood pressure and to be on treatment. There were no differences between the T group and No T group in terms of A1c (A1c 7,90% vs. 7,99%) or fasting glucose (157 vs.161 mg/dl).
Conclusions: This multicentric study shows that starting LLT is associated with LDL > 100 mg/dL, aged, sex (male), duration of diabetes, high BMI, comorbidities, smoking and a high blood pressure. Our results show compliance with the recommendations of 2014 AHA/ADA scientific statement type 1 diabetes mellitus and Cardiovascular Disease.
Disclosure
M. Rodriguez Carnero: None. D. Bellido Guerrero: None. C. Tejera: None. M. López de la Torre: None. A. Soto González: None. F.J. Escalada: Advisory Panel; Self; Merck Sharp & Dohme Corp., Novo Nordisk A/S, Sanofi. Consultant; Self; Esteve, Lilly Diabetes. Speaker's Bureau; Self; Amgen Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Janssen Pharmaceuticals, Inc., Merck Sharp & Dohme Corp., Novo Nordisk A/S, Sanofi. A. Hernandez-Mijares: None. L. Suarez Gutierrez: None. C. Morales: Other Relationship; Self; AstraZeneca, Janssen Pharmaceuticals, Inc., Lilly Diabetes, Merck Sharp & Dohme Corp., Novo Nordisk A/S, Sanofi. L. Gutiérrez Carrasqu: None. A. Cadenas: Advisory Panel; Self; Janssen Pharmaceuticals, Inc. O. Díaz Trastoy: None. J. Amigó-Farran: None. I. Gonzalez molero: None. V. Bellido: None. F. Arrieta: None. F. Tinahones: Advisory Panel; Self; Lilly Diabetes, Novo Nordisk A/S, Regeneron Pharmaceuticals, Sanofi-Aventis. Consultant; Self; AstraZeneca. Research Support; Self; AstraZeneca. Speaker's Bureau; Self; Danone Nutricia Research, Lilly Diabetes, Novo Nordisk A/S, Regenerative Medical Solutions, Sanofi-Aventis.
MUC5B rs35705950 (G/T) is strongly associated with idiopathic pulmonary fibrosis (IPF) and also contributes to the risk of interstitial lung disease (ILD) in rheumatoid arthritis (RA-ILD) and chronic ...hypersensitivity pneumonitis (CHP). Due to this, we evaluated the implication of MUC5B rs35705950 in antisynthetase syndrome (ASSD), a pathology characterised by a high ILD incidence. 160 patients with ASSD (142 with ILD associated with ASSD ASSD-ILD+), 232 with ILD unrelated to ASSD (comprising 161 IPF, 27 RA-ILD and 44 CHP) and 534 healthy controls were genotyped. MUC5B rs35705950 frequency did not significantly differ between ASSD-ILD+ patients and healthy controls nor when ASSD patients were stratified according to the presence/absence of anti Jo-1 antibodies or ILD. No significant differences in MUC5B rs35705950 were also observed in ASSD-ILD+ patients with a usual interstitial pneumonia (UIP) pattern when compared to those with a non-UIP pattern. However, a statistically significant decrease of MUC5B rs35705950 GT, TT and T frequencies in ASSD-ILD+ patients compared to patients with ILD unrelated to ASSD was observed. In summary, our study does not support a role of MUC5B rs35705950 in ASSD. It also indicates that there are genetic differences between ILD associated with and that unrelated to ASSD.
Objective: To compare erythrocyte aggregation (EA) in patients with severe obesity without other cardiovascular risk factors with a control group, using the Myrenne and the Sefam aggregometers, and ...to evaluate the effect of weight loss on this parameter.
Research Methods and Procedures: This was a longitudinal, clinical intervention study of a very low‐calorie diet for 4 weeks followed by a low‐calorie diet for 2 months. In 67 severely obese patients, an anthropometric and analytical evaluation plasmatic lipids, fibrinogen (Fbg), and EA was performed at baseline and 3 months after diet. The same determinations were performed in 67 normal‐weight volunteers. EA was measured with the Myrenne MA1, which determines EA at stasis (EA0) and at a low shear of 3 seconds−1 (EA1), and the Sefam aggregometer, which determines aggregation index at 10 seconds−1 (IA10), aggregation time (Ta), and disaggregation threshold (γD). Insulin resistance (IR) was calculated by homeostasis model assessment.
Results: Obese patients showed higher Fbg levels, EA0, EA1, IA10, and γD values, and lower Ta values. Differences between obese patients and control group for EA0, EA1, Ta, IA10, and γD disappeared after adjusting for BMI or for homeostasis model assessment but were maintained after adjusting for Fbg or low‐density lipoprotein‐cholesterol. Obese patients with IR showed higher EA0 and EA1 values. After weight loss, EA1 showed a significant improvement.
Discussion: Obese patients show increased EA. Erythrocyte hyperaggregation does not seem to be related to a high Fbg level or to an abnormal lipid profile but to IR. Hyperagreggation improves after weight loss.
The objective of this investigation was to study the effect of nonsurgical periodontal treatment, with or without systemic administration of doxycycline, on the metabolic control of patients with ...type 1 diabetes. Sixty type 1 diabetic subjects with moderate to severe periodontitis were recruited. Periodontal parameters were measured, and blood samples were obtained to evaluate glycosylated hemoglobin (HbA1c). Group 1 (30 patients) was treated with scaling, root planning, and chlorhexidine rinses for 3 months in conjunction with systemic administration of doxycycline (100 mg once a day for 15 days). Group 2 (30 patients) received the same periodontal treatment but without the use of doxycycline. The paired Student
t
-test was used to detect differences between glycosylated hemoglobin means before and 3 months after periodontal treatment in group 1 and group 2 separately. Changes in mean HbA1c after treatment were 0.07% in group 1 and –0.06% in group 2, which were not statistically significant after 3 months. Significant changes were not found even in patients with the best response to periodontal treatment. Periodontal treatment in type 1 diabetic patients after 3 months follow-up did not improve metabolic control of diabetes as measured by glycosylated hemoglobin.
INTRODUCTIONThe aim of this study was to determine whether whole body periodic acceleration (pGz) could improve muscle recovery after unaccustomed eccentric exercise (EE).
METHODSDownhill treadmill ...running was used to elicit EE-induced muscle damage in mice, and pGz treatment (480 cycles per minute, 1 h·d) was applied daily for 10 d after the initial EE bout (day 0). Every 2 d during the pGz treatment course starting at day 0, we 1) assessed intracellular Ca and Na concentrations and membrane potential (as indicators of intracellular ion dysfunction) in vivo in gastrocnemius muscle from anesthetized animals and 2) quantified creatine kinase (CK), tumor necrosis factor α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), and interleukin-10 (IL-10) concentrations in plasma or muscle lysates (as indicators of muscle damage and inflammation).
RESULTSEE significantly increased intracellular Ca and Na, CK, TNF-α, MCP-1, IL-6, and IL-10, all of which peaked on day 2 with the exception of IL-10 and declined slowly over 10 d of recovery. pGz treatment after the EE bout mitigated ion dyshomeostasis and expedited recuperation to control values after 6 d of treatment. pGz treatment also accelerated the normalization of CK, TNF-α, MCP-1, and IL-6 while further increasing IL-10 concentrations. The nitric oxide synthase inhibitor L-N-nitroarginine methyl ester, administered in drinking water before and maintained throughout the treatment course, was sufficient to abrogate the salutary effects of pGz after EE.
CONCLUSIONSThe present study demonstrates whole body periodic acceleration as an effective therapeutic strategy to accelerate muscle recovery after EE-induced skeletal muscle injury, as indicated by a faster normalization of all the studied parameters.
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