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This study investigated the prevalence of sensory atypicalities of mothers and fathers of individuals with Autism and explored the relationship between levels of emotional distress (parental distress, anxiety, and depression) and sensory processing patterns. There is limited evidence connecting these variables, and research in this area remains scarce. 251 parents participated in the study. 170 parents of individuals with Autism completed questionnaires on sensory experiences, parental distress, anxiety, and depression. A control group of 81 parents of individuals with typical development completed the sensory questionnaire. The relationship between sensory atypicality and emotional distress was examined only in the Autism group. Mothers and fathers of individuals with Autism showed a higher prevalence of sensory atypicality, especially in hyposensitive patterns. Relationships were found between specific sensory patterns and the levels of emotional distress. The hypo-reactive and hyposensitive quadrant, 'Low Registration', displayed significant predictive capacity for both anxiety and depression, while 'Sensory Sensitivity' was predominantly related to parental distress. Awareness of specific sensory patterns could facilitate the identification of those potentially vulnerable to experiencing anxiety, depression, or parental distress. • A high prevalence of sensory atypicality is identified in mothers and fathers of individuals with Autism. • Certain sensory atypicality profiles in parents of individuals with Autism appear related to anxiety, depression, and/or parental distress. • People with a hypo-reactive and hyposensitive profile may show particular vulnerability to high levels of emotional distress. [ABSTRACT FROM AUTHOR]

Childhood obesity with its growing prevalence worldwide presents one of the most important health challenges nowadays. Multiple mechanisms are involved in the development of this condition, as well as in its associations with various cardiometabolic complications, such as insulin resistance, diabetes, metabolic dysfunction-associated steatotic liver disease and cardiovascular diseases. Recent findings suggest that childhood obesity and associated dyslipidemia at least partly originate from epigenetic modifications that take place in the earliest periods of life, namely prenatal and perinatal periods. Hence, alterations of maternal metabolism could be fundamentally responsible for fetal and neonatal metabolic programming and consequently, for metabolic health of offspring in later life. In this paper, we will review recent findings on the associations among intrauterine and early postnatal exposure to undesirable modulators of metabolism, development of childhood obesity and later cardiometabolic complications. Special attention will be given to maternal dyslipidemia as a driven force for undesirable epigenetic modulations in offspring. In addition, newly proposed lipid biomarkers of increased cardiometabolic risk in obese children and adolescents will be analyzed, with respect to their predictive potential and clinical applicability. [Display omitted] • Childhood obesity poses short-term and long-term impact on cardiometabolic health. • Maternal dyslipidemia could predispose offspring to obesity. • Obesity-related dyslipidemia in childhood increases cardiometabolic risk in adulthood. • Omics-based biomarkers could improve evaluation of dyslipidemia in childhood. [ABSTRACT FROM AUTHOR]

• EAE induced increased astro- and microgliosis. • Treatment with theta burst stimulation attenuates reactive gliosis and downregualtes vimentin expression. • Both TBS protocols significantly reduced paralysis time. • Vimentin could be used as a potential biomarker of the disease. Multiple sclerosis (MS) is a chronic neurodegenerative disease caused by inflammatory processes in the central nervous system (CNS). Decades of research led to discovery of several disease-modifying therapeutics strategies with moderate success. Experimental autoimmune encephalomyelitis (EAE) is currently the most commonly used experimental model for MS and for studying various therapeutic approaches. Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive neurostimulation technique with multiple beneficial effects on healthy as well as CNS with pathology. However, the molecular and cellular mechanisms of rTMS on acute EAE are scarce. Our study demonstrated beneficial effects of theta-burst stimulation (TBS), an experimental paradigm of rTMS, on disease course of acute EAE. TBS treatment attenuated reactive gliosis, restored myelin sheet and down-regulated expression of vimentin in EAE rats. These effects were reflected through reduced clinical parameters, shorter duration of illness and days spent in paralysis. Based on our research, rTMS deserves further considerations for its neuroprotective effect on EAE, and is an excellent candidate for further research and points that it could be used for more than for simple symptomatic therapy. [ABSTRACT FROM AUTHOR]

• Data on atrial fibrillation (AF) recurrence after multiple-procedure pulmonary vein isolation (PVI) are rare. • After up to two procedures (PVI only), left atrial volume predicts AF recurrence. • Burden based classification (AF burden score) predicts AF recurrence as well. • But conventional classification (paroxysmal or persistent) does not. Catheter ablation of atrial fibrillation (AF) by means of pulmonary vein isolation (PVI) focuses on the PVs as the putative trigger of AF. However, which classification should be used to identify patients that are most suitable for PVI is uncertain. The aim of the study was to evaluate rhythm-, burden-, and anatomically-based classification schemes to predict success rates after up to two procedures of an ablation strategy strictly aimed at isolation of the PVs. Patients with paroxysmal or non-longstanding persistent AF undergoing PVI-only ablation with the option of one repeat PVI in case of AF recurrence were included. An AF burden score (AFB) was determined based on frequency, episode duration, and number of previous cardioversions and then categorized as minimal, mild, moderate, or severe. Two- and three-dimensional anatomical assessment of the left atrium (LA) was performed based on pre-interventional imaging by computed tomography or magnetic resonance imaging. Of 195 patients analyzed, 24 presented with recurrence after the last intervention (12%, median follow up: 16 ± 11 months). In multivariable analysis, a more than 6-fold increase of risk for AF recurrence was identified for patients with a severe compared to a mild AFB [hazard ratio: 6.241 (95% confidence interval: 1.914–20.167, p = 0.002)]. In contrast to univariable analysis, no other parameter was associated with recurrence in multivariable analysis. Burden-based (AFB) classification was identified as a significant predictor for AF recurrence even after repeat PVI, while neither anatomical parameters nor the established rhythm-based classification of paroxysmal and persistent AF did. [ABSTRACT FROM AUTHOR]

Abstract Obesity, a pandemic of the modern world, is intimately associated with dyslipidemia, which is mainly driven by the effects of insulin resistance and pro-inflammatory adipokines. However, recent evidence suggests that obesity-induced dyslipidemia is not a unique pathophysiological entity, but rather has distinct characteristics depending on many individual factors. In line with that, in a subgroup of metabolically healthy obese (MHO) individuals, dyslipidemia is less prominent or even absent. In this review, we will address the main characteristics of dyslipidemia and mechanisms that induce its development in obesity. The fields, which should be further investigated to expand our knowledge on obesity-related dyslipidemia and potentially yield new strategies for prevention and management of cardiometabolic risk, will be highlighted. Also, we will discuss recent findings on novel lipid biomarkers in obesity, in particular proprotein convertase subtilisin/kexin type 9 (PCSK9), as the key molecule that regulates metabolism of low-density lipoproteins (LDL), and sphingosine-1-phosphate (S1P), as one of the most important mediators of high-density lipoprotein (HDL) particles function. Special attention will be given to microRNAs and their potential use as biomarkers of obesity-associated dyslipidemia. Highlights • Obesity is mainly driven by insulin resistance and pro-inflammatory adipokines. • Vitamin D deficiency affects adipose tissue function and lipid status in obesity. • Metabolically healthy obesity is characterised by a favorable lipid profile. • Further data on PCSK9 and S1P in obesity might upgrade therapeutic approaches. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: End-stage renal disease (ESRD) is characterized by profound dyslipidemia and enhanced oxidative stress. The patients also show evidence of exhausted and/or deficient anti-oxidative defense enzymes, one of them being glutathione-S-transferase (GST). This study investigates relationship between GST gene polymorphism and low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subclasses in ESRD. Design and methods: GSTM1, T1, and P1 genotypes were determined by polymerase chain reaction–restriction fragment length polymorphism in 160 patients undergoing hemodialysis. LDL and HDL subclasses were separated by gradient gel electrophoresis and biochemical parameters were measured by routine laboratory methods. Results: GSTM1-positive patients had higher proportion of small, dense LDL III particles than those with GSTM1-null genotype (P <0.05). Similarly, GSTP1-Ile/Ile patients had higher proportion of LDL III (P <0.05), but more HDL 2b and less HDL 3a particles than GSTP1-Ile/Val and Val/Val carriers (P <0.05). LDL subclass distribution in smokers with GSTM1-null genotype was shifted towards smaller particles, as compared to GSTM1-positive and GSTM1-null non-smokers. Smokers with GSTP1-Ile/Val and Val/Val genotypes had smaller LDL size than their non-smoking counterparts (P <0.05). Both smokers and non-smokers with GSTP1 Ile/Ile genotype had more LDL III particles than non-smokers carrying Val allele. Non-smokers with GSTP1 Ile/Ile genotype had more HDL 2b subclasses than non-smokers with GSTP1-Ile/Val and Val/Val (P <0.05), but less HDL 3a particles than smokers with GSTP1-Ile/Val and Val/Val genotypes (P <0.05). GSTT1 gene polymorphism had no effect on lipoprotein subclass distributions. Conclusions: Our results demonstrate significant associations between low activity GST genotypes and proatherogenic lipoprotein particles in hemodialysis patients which might further increase their cardiovascular disease risk. [Copyright &y& Elsevier]

Abstract: Objective: Dyslipidemia is commonly seen in patients with end-stage renal disease (ESRD). This prospective study investigates whether small-sized high-density lipoprotein (HDL) particles alone or in combination with high sensitivity C-reactive protein (hsCRP) are independent determinants of ESRD mortality. Design and methods: We performed 36months follow-up study in 122 haemodialysis (HD) patients. HDL size and subclass distribution were determined by gradient gel electrophoresis. Baseline characteristics of the patients were evaluated for the prediction of mortality. Results: Cox regressions analysis showed that patients with small-sized HDL particles had 2.8-fold higher risk of lethal outcome (P <0.05). Concomitant presence of small-sized HDL particles and increased hsCRP concentration were significantly associated with reduced survival rate (HR=3.907; P <0.05). Observed relationships persisted after adjustment for serum lipid and lipoprotein concentrations. Conclusions: Our results indicate that small-sized HDL particles alone and combined with elevated hsCRP concentrations are independent predictors of reduced survival in HD patients. [Copyright &y& Elsevier]

Abstract: Objective: Small, dense low-density lipoprotein (sdLDL) and small-sized high-density lipoprotein (HDL) particles are established risk factors for ischemic heart disease. However, their clinical significance for acute ischemic stroke (AIS) is uncertain. This study evaluates associations of LDL and HDL particle sizes and subclasses with AIS risk and short-term mortality after AIS. Methods: Two hundred AIS patients hospitalised for first-in-a-lifetime stroke and 162 apparently healthy controls were included in the study. LDL and HDL particles were separated by gradient gel electrophoresis and serum lipid parameters were measured by standard laboratory methods. Baseline characteristics of LDL and HDL particles were evaluated for the prediction of AIS and short-term mortality after AIS. Results: AIS patients had significantly more LDL III and IVb, but less LDL I and II particles. They also had significantly smaller HDL size, more HDL 3a, 3b and 3c and less HDL 2b subclasses. The relative content of both sdLDL and small-sized HDL particles was significantly increased in patients (P <0.001 and P <0.001, respectively). In addition, sdLDL was significantly higher in AIS fatalities (n =25) compared with survivors (n =175, P <0.05). Increased sdLDL was a significant predictor of AIS (OR=4.31; P <0.001) and in-hospital mortality after AIS (OR=5.50; P <0.05). The observed relationships persisted after adjustment for conventional risk factors. Conclusions: AIS is associated with adverse distributions of LDL and HDL subclasses. In addition, short-term mortality after AIS is associated with increased sdLDL particles. Our results indicate that sdLDL is an independent predictor of both AIS onset and consecutive short-term mortality. [Copyright &y& Elsevier]

Abstract: Objective: Small, dense low-density lipoprotein-cholesterol (sdLDL-C) is a recently recognised marker of cardiovascular disease risk. On the other hand, the usefulness of sdLDL-apoB concentration determination in clinical practice offers grounds for further exploration. This study investigates the associations of sdLDL-C and sdLDL-apoB with serum lipid parameters and LDL size in healthy men and women. Methods: The concentrations of sdLDL-C and sdLDL-apoB were measured after heparin–magnesium precipitation of serum samples from ninety-five asymptomatic subjects (47 men, 30 premenopausal and 18 menopausal women). LDL size was determined by gradient gel electrophoresis and serum lipid and lipoprotein parameters were measured by routine laboratory methods. Results: Compared to premenopausal women, men had higher sdLDL-C (P <0.001) and sdLDL-apoB concentrations (P <0.001). No difference in the sdLDL-C concentration was found between men and menopausal women. Menopause status was associated with higher concentrations of both sdLDL-C (P <0.01) and sdLDL-apoB (P <0.05). Subjects with the LDL B phenotype had elevated sdLDL-C (P <0.01) and sdLDL-apoB concentrations (P <0.001). LDL size and triglycerides were independent determinants of both sdLDL-C and sdLDL-apoB concentrations. Conclusion: Gender and menopausal status have significant impact on sdLDL-C and sdLDL-apoB concentrations. The variability in sdLDL-C and sdLDL-apoB levels is considerably influenced by changes in LDL size and triglyceride concentration. Our results suggest that the characterisation of sdLDL particles by evaluating sdLDL-C could be complemented with sdLDL-apoB determination. [Copyright &y& Elsevier]

Background and Aims: Lipoprotein (a) [Lp(a)] consists of low-density lipoprotein (LDL) and apolipoprotein (a) [apo(a)]. Both Lp(a) constituents are well-recognized risk factors for coronary artery disease (CAD). This study investigates the interrelationship of apo(a) and LDL size, as well as their possible synergistic effect on the increase of CAD risk. Methods: One hundred nine CAD patients and 102 apparently healthy subjects were included in the study. Lp(a) concentration was measured using immunoturbidimetry. The sizes of apo(a) isoforms were determined by SDS-agarose gel electrophoresis followed by immunoblotting. LDL particle size was determined by gradient gel electrophoresis. Results: We found an inverse correlation between apo(a) size and Lp(a) concentration (r 2 = 31%, p <0.001 in the control group and r 2 = 35%, p <0.001 in the CAD group). Individuals with smaller apo(a) isoforms and small, dense LDL (sdLDL) >50% had the highest risk of CAD development (OR = 4.23, p = 0.017). The synergy index (SIM) for the combination of smaller apo(a) isoforms and sdLDL >50% was 1.2. Adjustment for Lp(a) and triacylglycerol concentrations eliminated smaller apo(a)/sdLDL >50% related risk (p = 0.233 and p = 0.09, respectively). Conclusions: Smaller apo(a) isoforms appear to be superior to sdLDL for the assessment of CAD risk. Their combined effect is synergistic. [Copyright &y& Elsevier]

Abstract Background Previous studies revealed decreased level of high-density lipoprotein cholesterol (HDL C) as important factor for development of colorectal cancer (CRC). Quantity and structure of HDL particles depend on activities of lipid transfer proteins lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP), but this topic is largely unexplored in CRC. The main objective of this study was to investigate activities of LCAT and CETP in patients with CRC. Additionally, we analyzed activity of paraoxonase-1 (PON-1), as a main carrier of HDL-antioxidant function. Materials and methods Ninety-nine CRC patients and 101 healthy individuals were included. LCAT and CETP activities were assessed by measuring rates of formation and transfer of cholesteryl esters. PON-1 paraoxonase and arylesterase activities were measured. Results Lower levels of HDL-C (p <.001) were observed in cohort of patients, alongside with decreased LCAT (p <.050) and increased CETP activity (p <.050). Both PON-1 activities were diminished in CRC (p <.050 and p <.001 respectively). Univariate logistic regression singled out HDL-C level (OR = 0.218, p <.001), CETP activity (OR = 1.010, p <.01) and mass (OR = 0.994, p <.001) as possible markers of elevated CRC risk. CETP mass maintained its predictive significance when adjusted for traditional risk factors and level of oxidative stress (OR = 0.993, p <.001; OR = 0.982, p <.050, respectively). Conclusion Our results demonstrated increased CETP and decreased LCAT and PON-1 activities in CRC patients. In preliminary analysis CETP mass was identified as potential significant predictor of CRC development, suggesting that alterations in HDL-C levels, alongside with changes in HDL structure might have a role in carcinogenesis. Highlights • High CETP, low LCAT activity and reduced HDL-C were observed in CRC. • Diminished PON-1 activity and high PAB values suggest high rate of OS. • CETP activity and mass are possible candidate markers for CRC development. [ABSTRACT FROM AUTHOR]