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We introduce two bio-photonic applications of liquid crystals. One is the ophthalmic lenses with large aperture size. The challenge and the solutions are discussed. The other is the biosensing devices based on a switchable surface of a liquid crystal and polymer composite film, such as a sperm testing devices and high-density lipoproteins. Liquid crystals indeed have great potentials beyond displays. [ABSTRACT FROM AUTHOR]

Background: The rising cancer incidence in patients with oral leukoplakia (OL) highlights the importance of identifying potential biomarkers for high‐risk individuals and lesions because these biomarkers are useful in developing personalized management strategies for OL patients. This study systematically searched and analyzed the literature on potential saliva and serum biomarkers for OL malignant transformation. Methods: PubMed and Scopus were searched for studies published up to April 2022. The primary outcome of this study was the difference in biomarker concentrations in saliva or serum samples from healthy control (HC), OL and oral cancer (OC) populations. Cohen's d with 95% credible interval was calculated and pooled using the inverse variance heterogeneity method. Results: A total of seven saliva biomarkers were analyzed in this paper, including interleukin‐1alpha, interleukin‐6 (IL‐6), interleukin‐6‐8, tumor necrosis factor alpha (TNF‐α), copper, zinc, and lactate dehydrogenase. IL‐6 and TNF‐α exhibited statistically significant deviations in comparisons between HC versus OL and OL versus OC. A total of 13 serum biomarkers were analyzed, including IL‐6, TNF‐α, C‐reactive protein, total cholesterol, triglycerides, high‐density lipoproteins, low‐density lipoproteins, albumin, protein, β2‐microglobulin, fucose, lipid‐bound sialic acid (LSA), and total sialic acid (TSA). LSA and TSA exhibited statistically significant deviations in comparisons between HC versus OL and OL versus OC. Conclusion: IL‐6 and TNF‐α in saliva have strong predictive values for OL deterioration, and LSA and TSA concentration levels in serum also have the potential to serve as biomarkers for OL deterioration. [ABSTRACT FROM AUTHOR]

Introduction: Covid‐19 is linked with the development of cardio‐metabolic disorders, including dyslipidemia, dysregulation of high‐density lipoprotein (HDL), and low‐density lipoprotein (LDL). Furthermore, SARS‐Co‐2 infection is associated with noteworthy changes in lipid profile, which is suggested as a possible biomarker to support the diagnosis and management of Covid‐19. Methods: This paper adopts the literature review method to obtain information about how Covid‐19 affects high‐risk group patients and may cause severe and critical effects due to the development of acute lung injury and acute respiratory distress syndrome. A narrative and comprehensive review is presented. Results: Reducing HDL in Covid‐19 is connected to the disease severity and poor clinical outcomes, suggesting that high HDL serum levels could benefit Covid‐19. SARS‐CoV‐2 binds HDL, and this complex is attached to the co‐localized receptors, facilitating viral entry. Therefore, SARS‐CoV‐2 infection may induce the development of dysfunctional HDL through different mechanisms, including induction of inflammatory and oxidative stress with activation of inflammatory signaling pathways. In turn, the induction of dysfunctional HDL induces the activation of inflammatory signaling pathways and oxidative stress, increasing Covid‐19 severity. Conclusions: Covid‐19 is linked with the development of cardio‐metabolic disorders, including dyslipidemia in general and dysregulation of high‐density lipoprotein and low‐density lipoprotein. Therefore, the present study aimed to overview the causal relationship between dysfunctional high‐density lipoprotein and Covid‐19. [ABSTRACT FROM AUTHOR]

Background: Metabolic syndrome (MetS) is especially prevalent among US truck drivers. However, there has been limited research exploring associations between MetS conditions with roadway crashes among truck drivers. The objective of this paper is to assess relationships between specific combinations of individual MetS components and crashes and near‐misses. Methods: Survey, biometric, and anthropometric data were collected from 817 truck drivers across 6 diverse US states. Survey data focused on demographics and roadway safety outcomes, and anthropometric/biometric data corresponded to five MetS conditions (waist circumference blood pressure, hemoglobin A1c, triglycerides, and high‐density lipoprotein [HDL] cholesterol). Logistic regression was used to calculate odds ratios of lifetime crashes and near‐miss 1‐month period prevalence associated with: 1) specific MetS conditions regardless of presence or absence of other MetS conditions, and 2) specific MetS conditions and counts of other accompanying MetS conditions. Results: Hypertension was the MetS characteristic most strongly associated with lifetime crash and 1‐month near‐miss outcomes, while high triglycerides, low HDL cholesterol, and large waist circumference were most commonly present among groups of conditions associated with crashes and near‐misses. Overall, an increasing number of specific co‐occurring MetS conditions were associated with higher reporting of roadway crashes. Conclusions: Specific combinations and higher prevalence of MetS conditions were associated with increased frequency of reported crashes. Moreover, when the co‐occurrence of MetS conditions is aggregated, a dose–response relationship with crashes appears. These results suggest that policy changes and interventions addressing MetS may increase driver health and reduce crash risk. [ABSTRACT FROM AUTHOR]

Objective: Systemic lupus erythematosus (SLE) is an autoimmune disease with inflammation as a critical feature. Recently, high‐density lipoprotein cholesterol (HDLc) have been evidenced to have anti‐inflammatory effects, suggesting a potential link between HDL and SLE that needs to be thoroughly studied. The aim was to explore the association between SLE and HDLc through a systematic review with meta‐analysis. Methods: A systematic review with meta‐analysis was conducted to assess mean differences in HDL levels between patients with SLE and healthy controls. Both qualitative and quantitative syntheses were performed, including an assessment of heterogeneity using I2, a publication bias evaluation, a methodologic quality assessment, and a forest plot under a random effects model. Subgroup analyses were conducted based on disease activity and the report of corticosteroid dosage. Results: A total of 53 studies were included in the qualitative synthesis, and 35 studies were included in the quantitative synthesis, comprising 3,002 patients with SLE and 2,123 healthy controls. Mean HDL levels were found to be lower in patients with SLE as follows: in the meta‐analysis including all articles −6.55 (95% confidence interval [CI] −8.77 to −4.33); in patients with mild disease activity −5.46 (95% CI −8.26 to −2.65); in patients with moderate or severe disease activity −9.42 (95% CI −15.49 to −3.34); in patients using corticosteroids −5.32 (95% CI −10.35 to −0.29); and in studies with excellent methodologic quality −8.71 (95% CI −12.38 to −5.03). Conclusion: HDL levels appear to be quantitatively altered in patients with SLE, suggesting a potential contribution to immune dysregulation, highlighting the importance of HDL in autoimmune diseases. [ABSTRACT FROM AUTHOR]

Summary: We conducted a scoping review to identify definitions of metabolically healthy obesity (MHO), describe gaps in the literature, and establish a universal definition of MHO in children. We searched electronic databases from January 1980 to June 2017 and grey literature. Experimental, quasi‐experimental, or observational studies were eligible for inclusion if they (i) included a definition of MHO that identified risk factors, cut‐off values, and the number of criteria used to define MHO, and (ii) classified 2–18 year olds as overweight or obese. Two reviewers independently screened 1,711 papers for relevance and quality; we extracted data from 39 individual reports that met inclusion criteria. Most (31/39; 79%) definitions of MHO included an absence of cardiometabolic risk factors. Heterogeneity across MHO definitions, obesity criteria, and sample sizes/characteristics resulted in variable prevalence estimates (3–80%). Finally, we convened an international panel of 46 experts to complete a 4‐round Delphi process to generate a consensus‐based definition of MHO. Based on consensus (≥ 80% agreement), our definition of MHO included: high density lipoprotein‐cholesterol > 40 mg/dl (or > 1.03 mmol/l), triglycerides ≤ 150 mg/dl (or ≤ 1.7 mmol/l), systolic and diastolic blood pressure ≤ 90th percentile, and a measure of glycemia. This definition of MHO holds potential universal value to enable comparisons between studies and inform clinical decision‐making for children with obesity. [ABSTRACT FROM AUTHOR]

The present study aimed to evaluate antidiarrheal potential of prickly pear cladode and its hepatoprotective role in different groups of diarrhea‐induced mice. Mice received cefixime (4 mg/kg of bw) and different concentrations of aqueous cladode extract (250 mg/kg of bw, 500 mg/kg of bw and 1000 mg/kg of bw). Feces Salmonella typhi ATCC 19430 was used to assess antidiarrheal potential and hematological, biochemical parameters, and histopathological analyses were carried out for 17 days. The results showed that administration of Salmonella typhi ATCC 19430 in mice produced liver injuries with histological damage, whereas 1000 mg/kg of bw cladode extract reduced the Salmonella typhi ATCC 19430 load of feces earlier as compared to the other groups during 17 days. Hematological parameters, like red blood cells (RBCs) (6.19 ± 1.85 × 106/mm3) and hemoglobin (Hb) (10.06 ± 2.03 g/dL), of negative control group decreased, while white blood cells (WBCs) (13.46 × 106/mm3) increased from reference values. In lipid profile, low‐density lipoprotein (LDL) (9.0 ± 2.41 mg/dL), high‐density lipoprotein (HDL) (6.07 ± 2.45 mg/dL) and total cholesterol (TC) (35.22 ± 8.29 mg/dL) of negative control group decreased, while triglycerides (TG) (168.35 ± 71.75 mg/dL) increased from reference values. Alanine transferase (ALT) (60.30 ± 20.33 IU/L), alkaline phosphatase (ALP) (359.9 ± 100.05 IU/L) and aspartate transferase (AST) (168.77 ± 66.61 IU/L) of negative control group increased from reference values. Urea (27.36 ± 10.54 mmol/L) and creatinine (35.29 ± 12.15 mmol/L) of the negative control group increased. Cefixime also ameliorated injuries due to the administration of Salmonella typhi ATCC 19430. Conclusively, these findings indicated that pure aqueous extract of cladode showed more promising results regarding antidiarrheal potential. Hence, cladode might be used in food and supplement formulations as a functional ingredient. [ABSTRACT FROM AUTHOR]

Background: Loss‐of‐function (LOF) variants of the angiopoietin‐like 3 (ANGPTL3) gene are reported to be associated with serum triglyceride (TG) and high‐density lipoprotein cholesterol (HDL‐C) concentrations and thereby affect the risk of cardiovascular disease (CVD). Objective: In the present study, we examined the association of rs10789117 in the ANGPTL 3 gene locus and the risk of CVD in the group of people who were part of the Mashhad‐Stroke and Heart‐Atherosclerotic‐Disorders (MASHAD) cohort. Methods: One thousand and two healthy individuals enrolled in this study of whom 849 subjects were healthy and 153 subjects developed CVD outcomes after 6 years of follow‐up. After a 12‐h overnight fasting, 20 mL of blood samples were collected for the measurement of fasting blood glucose and lipid profile. DNA was extracted, and the Tetra‐ARMS PCR (amplification refractory mutation system) was used for genotyping of rs10789117 in the ANGPTL3 gene. The genotype frequencies of the variant of rs10789117 in the ANGPTL3 gene were estimated using χ2 tests. Eventually, the statistical analysis was done by SPSS version 20. Results: Individuals with AC/CC genotypes (rs10789117) were found to have to greater risk of CVD events compared to AA genotype (OR = 1.43, 95%CI = 1.01–2.02, p = 0.041). There was a 1.3‐fold increase in cardiovascular events in individuals carrying the C allele of rs10789117 variant compared to non‐carriers (OR = 1.32, 95%CI = 1.06–1.72, p value = 0.038). There were significant differences between different genotypes for serum triglyceride levels within the control group, but this difference was not significant in the group with CVD. Moreover, there was a significant association between CC genotype and CVD risk in the individuals with a normal serum HDL‐C. Conclusion: We have found that a rs10789117 C>A in ANGPTL3 gene polymorphism was associated with incident CVD events, and this may be of value as a risk stratification biomarker in CVD in the Iranian population. [ABSTRACT FROM AUTHOR]

Burn survivors experience profound physiological changes following injury, which may have lasting implications for cardiovascular health. This study aims to investigate the cardiovascular risk profile among burn survivors treated at a burn center in northern Iran. This observational study was conducted from 2022 to 2023 at the burn centre affiliated with Guilan University of Medical Sciences, Rasht, Iran. This study assessed a cohort study of 210 burn survivors, focusing on individuals with ≥20% TBSA burn injuries who had recovered and returned to their daily lives. This study assessed patients' lipid profiles, Framingham General Cardiovascular Risk Score (FGCRS) and risk factors, including demographics, clinical variables and physical activity. Statistical analysis employed descriptive and inferential statistics. The mean age was 49.23 years, and the mean TBSA burned was 37.06%. The risk of cardiovascular disease in 66% of the study population was less than 10%, and in 13%, it was more than 20%. Significant associations were identified between CVD risk and sex, diabetes, hypertension, BMI, TBSA burned, years after burn, physical activity level and LDL. Of the lipid profile measures, LDL, triglycerides and TC/HDL exceeded the desirable levels. This research highlights the heightened cardiovascular risk in burn survivors, emphasizing the necessity for targeted interventions and regular monitoring. Identifying modifiable risk factors enables healthcare practitioners to develop tailored strategies, enhancing cardiovascular health in this vulnerable population and improving overall outcomes and quality of life. [ABSTRACT FROM AUTHOR]

Introduction: ANGPTLs (Angiopoietin‐like proteins) 3 and 4 play an important role in the development of type 2 diabetes. These glycoproteins affect the modulation of glucose and lipid metabolism. They inhibit lipoprotein lipase (LPL) activity and provoke lipolysis. This study was aimed to investigate the protein levels of ANGPTL3 and 4 in the serum of type 2 diabetic patients with metabolic syndrome in comparison to the type 2 diabetic patients without metabolic syndrome and the control group. Methods: Three groups of individuals were included in this study; Group I: 47 patients with type 2 diabetes and metabolic syndrome; Group II: 25 patients with type 2 diabetes without metabolic syndrome; Group III: 40 non‐diabetic healthy people without metabolic syndrome as a control group. After collection of 5 mL fasting blood samples, serum concentrations of fasting blood sugar (FBS), cholesterol (Chol), triglyceride (TG), HDL‐C (High‐density lipoprotein‐Cholesterol) and LDL‐C (Low‐density lipoprotein‐Cholesterol) were measured by the enzymatic method; blood pressure (BP), height and weight with stadiometers; and ANGPTL3 and 4 by the enzyme‐linked immunosorbent assay (ELISA). Results: The serum levels of ANGPTL3 was significantly different among our three groups (p =.000). In patients with type 2 diabetes and metabolic syndrome (Group I), ANGPTL3 and 4 levels were lower than the control group. The serum levels of the parameters evaluated in this study (except HDL‐C) was lower in the group II in comparison with the group I, and this difference was significant for TG, Chol, BP and BMI between these two groups. Also, our results revealed that there was a negative correlation between FBS, TG, Chol, LDL‐C and BMI with ANGPTL3 and 4. While, there was a significant positive correlation between ANGPTL4 and ANGPTL3. Conclusion: Altogether, our findings suggest that the decreased levels of ANGPTL3 and 4 may be a causative factor for type 2 diabetes. [ABSTRACT FROM AUTHOR]

Introduction: We investigated the association of serum uric acid to high‐density lipoprotein ratio (UHR) with the presence and severity of metabolic syndrome (MetS) among MASHAD cohort participants. Methods: In this cross‐sectional study, according to International Diabetes Federation criteria, the cohort participants were divided into MetS (+) and MetS (−) groups. MetS (+) were classified into Group 1 (those with 3 MetS criteria), Group 2 (those with 4 MetS criteria) and Group 3 (those with 5 MetS criteria). UHR was compared among the groups. Results: Data related to 9637 subjects including 3824 MetS (+) and 5813 MetS (−) were analysed. The mean UHR was significantly higher (p <.001) in the MetS (+) group compared with the MetS (−) group. UHR increased as the MetS severity increased (p <.001). ROC analysis revealed that UHR greater than 9.5% has 89.07% sensitivity and 77.03% specificity in differentiating MetS (−) from MetS (+) subjects. Conclusion: Among MASHAD cohort study participants, a significant association between UHR and MetS was found. Furthermore, there is an increase in UHR as the severity of MetS increases. Registration number of MASHAD cohort study: 85134. [ABSTRACT FROM AUTHOR]

Earlier investigations into the impact of purslane, Portulaca oleracea, on lipid profile and C‐reactive protein (CRP) produced contradictory findings. The effect of purslane consumption on lipid profiles and CRP was assessed in this comprehensive review and meta‐analysis. We conducted a thorough literature search in online databases, including PubMed, Scopus, the Cochrane library, and ISI Web of Science to find relevant randomized controlled trials up to June 2023. By incorporating 14 effect sizes from 13 RCTs, we were able to show that purslane consumption significantly decreases serum triglyceride (TG) (WMD: −16.72, 95% CI: −22.49, −10.96 mg/dL, p <.001), total cholesterol (TC) (WMD: −9.97, 95% CI: −19.86, −0.07 mg/dL, p =.048), and CRP (WMD: −1.22, 95% CI: −1.63, −0.80 mg/L, p <.001) levels in patients compared to the control group. In addition, purslane consumption significantly increases high‐density lipoprotein (HDL‐C) (WMD: 4.09, 95% CI: 1.77, 6.41 mg/dL, p =.001) levels. However, purslane consumption did not affect low‐density lipoprotein (LDL‐C) levels. According to a suggested optimal dosage, purslane consumption is considered to be safe up to 30 g/day. Purslane consumption can significantly improve cardiovascular health by improving lipid profile and inflammation status. [ABSTRACT FROM AUTHOR]

The aim of this paper was to study the effect of long-term supervised exercise-induced weight maintenance on metabolic risk factors and physical fitness in obese children in early puberty. A total of 49 obese children aged 12–14 years were divided into control and exercise groups. The children in the exercise group accepted exercise intervention supervised by a professional sports teacher for 9 of the 12 months. All participants in both groups received health education once every 3 months. Anthropometry and fasting serum lipids, glucose, insulin and homeostatic model assessment for insulin resistance (HOMA-IR) were measured at months 0, 3, 9, 12 of the intervention. Physical fitness was determined before and after intervention. After the intervention (i) BMI was reduced by 0.6 ( P < 0.05) in the exercise group, but increased by 0.5 ( P < 0.05) in the control group, compared with the pre-intervention level at the end of 9-month intervention; (ii) Triglyceride levels in the exercise group significantly decreased by 23.1% by 3 months ( P < 0.05), and by 30.2% after 9 months ( P < 0.05), but increased by 50% ( P < 0.05) in the control group; high density lipoprotein-cholesterol (HDL-C) decreased more by 35% ( P < 0.05) in the controls than in the exercise group ( P < 0.05); (iii) Fasting serum glucose, insulin level and HOMA-IR decreased, respectively, by 23.1%, 36.6% and 48.5% in the exercise group at 9 months ( P < 0.05), whereas glucose levels increased by 10.9% ( P < 0.05) in the control group; (iv) Exercise performance, such as upper- and lower-limb strength, flexibility and endurance, were enhanced by 17.9%, 12.3%, 22.3% and 20.4% ( P < 0.01), respectively and (v) At 12 months, i.e. 3 months after terminating the supervised exercise, serum triglycerides, glucose, insulin and HOMA-IR level all returned to the pre-intervention level. Supervised decrement exercise can effectively slow the progress of obesity, improve insulin sensitivity and metabolic risk factors, but once the supervised exercise is stopped, the health benefits weaken or vanish. The key to helping these obese children is for them to cultivate good exercise habits which are sustained throughout their lives. [ABSTRACT FROM AUTHOR]

Objective: This study evaluated weight and cardiometabolic outcomes after a 3‐month energy‐restricted diet (−30%) containing almonds (almond‐enriched diet [AED]) or containing carbohydrate‐rich snacks (nut‐free control diet [NFD]) (Phase 1), followed by 6 months of weight maintenance (Phase 2). Methods: Participants (25–65 years old) with overweight or obesity (BMI 27.5–34.9 kg/m2) were randomly allocated to AED (n = 68) or NFD (n = 72). Results: Both groups lost weight during Phase 1 (p < 0.001) (mean [SE], −7.0 [0.5] kg AED vs. −7.0 [0.5] kg NFD, p = 0.858) and Phase 2 (p = 0.009) (−1.1 [0.5] kg AED vs. −1.3 [0.6] NFD, p = 0.756), with improvements in percentage lean mass after Phase 2 (4.8% [0.3%], p < 0.001). Reductions occurred in fasting glucose (−0.2 [0.07] mmol/L, p = 0.003), insulin (−8.1 [4.0] pmol/L, p = 0.036), blood pressure (−4.9 [0.8] mm Hg systolic, −5.0 [0.5] mm Hg diastolic, p < 0.001), total cholesterol (−0.3 [0.1] mmol/L), low‐density lipoprotein (LDL) (−0.2 [0.1] mmol/L), very low‐density lipoprotein (−0.1 [0.03] mmol/L), and triglycerides (−0.3 [0.06] mmol/L) (all p < 0.001), and high‐density lipoprotein increased (0.1 [0.02] mmol/L, p = 0.011) by the end of Phase 2 in both groups. There were group by time interactions for lipoprotein particle concentrations: very small triglyceride‐rich (−31.0 [7.7] nmol/L AED vs. −4.8 [7.9] nmol/L NFD, p = 0.007), small LDL (−109.3 [40.5] nmol/L AED vs. −20.7 [41.6] nmol/L NFD, p = 0.017), and medium LDL (−24.4 [43.4] nmol/L AED vs. −130.5 [44.4] nmol/L NFD, p = 0.045). Conclusions: An energy‐restricted AED resulted in weight loss and weight loss maintenance comparable to an energy‐restricted NFD, and both diets supported cardiometabolic health. The AED resulted in greater improvements in some lipoprotein subfractions, which may enhance reductions in cardiovascular risk. [ABSTRACT FROM AUTHOR]

The detailed molecular structure of the complex formed by the apoprotein from porcine high density lipoprotein and dimyristoyl phosphatidylcholine (lecithin) has been investigated by a range of physical techniques. The complex, an oblate ellipsoid with major axis 11.0 nm and minor axis 5.5 nm (see the accompanying paper), is comprised of a section of lecithin bilayer with apoprotein at the surface. The main site of interaction between protein and lipid is in the lipid glycerophosphorytcholine group region; as with native high density lipoprotein the surface of the particle consists of a mosaic of lecithin polar groups and protein. The formation of this mosaic reduces the cooperativity of the lecithin chain motions and changes the curvature of the lipid-water interface, as compared to a bilayer. Otherwise, there are no major changes in lecithin motions indicating that no strong binding of lipid to protein occurs. The interaction involves the intercalation of amphipathic, 60 % α-helical, apoprotein molecules among the lecithin molecules so that the protein resides at the lipid-water interface. The apoprotein has a high affinity for the lipid-water interface but specific lipid-protein interactions are not involved. [ABSTRACT FROM AUTHOR]

Amphipathic helical repeals arc considered as the structural units of numerous apolipoproteins and have been described as being responsible for the interaction of apolipoproteins with phospholipids in high-density lipoproteins (HDL). Furthermore. apolipoproteins. and especially apolipoprotein Al (apoAl), are involved in various biological functions of these circulating particles in plasma. Studies with synthetic peptides corresponding to domains of the apoAl sequence have however shown that short 39-residue fragments do not interact strongly enough with phospholipids to generate particles that correctly mimic the physicochemical properties of HDL reconstituted with native apoAl [Vanloo, B., Demoor, L., Boutil- Ion. C.. Lins, L.. Baert, J,, Fruchart, J. C.. Tartar. A. & Rosseneu, M. (1995) Association of synthetic peptide fragments of human apolipoprotein A-I with phospholipids. i. Lipid Res. 36. 1686-1696.1. Here we show that synthetic branched multirneric peptides. often used as carriers for the design of synthetic vaccines (multiple-antigen peptides). can be used to mimic the physicochemical properties of apoAl in HDL. This type of molecule is obtained by using a small core matrix of Lys residues bearing radially branched synthetic peptides as dendritic arms. We compared the lipid-binding capacities and the structural properties of a linear peptide corresponding to residues 145--183 of apoAl [apoAl-(145-183)-peptide) with those of two multimeric peptides consisting respectively of three [trimeric apoAl-(145-183)j and four copies [tetrameric apoAl-( 145- 183)] of the selected sequence. branched on a covalent core matrix. This paper provides evidence for the increased abilities of the multimeric peptides to associate with phospholipids compared with the short linear peptides. Moreover, the trimeric apoAl-(145 - 183) peptide was most efficient in mimicking the physicochemical and structural properties of native apoAl in reconstituted HDL. As tools adequate to unravel the structure/function relationship of separate apolipoprotein domains are still missing. these multirneric peptides might constitute an alternative approach to linear peptides which are poor mimetics and to protein mutants which are difficult to produce and only provide information about the total sequence. [ABSTRACT FROM AUTHOR]

Adult bovine aortic endothelial (ABAE) cells, exposed to serum-free medium, specifically bind 125I-labeled human high-density lipoprotein (125I-HDL). Addition of human lipoprotein-deficient serum (LPDS) reduces the specific binding of 125I-HDL in a concentration-dependent manner, such that LPDS at a concentration of 6 mg protein/ml almost completely inhibits the specific binding of 125I-HDL. ABAE cultures exposed to 125I-labeled LPDS (125I-LPDS) specifically bind two peptides, which appear as minor iodinated components in 125I-LPDS. The binding of these two components is abolished in the presence of excess amounts of unlabeled LPDS or HDL. Preincubation of ABAE cells with 25-hydroxycholesterol (25-HC) results in an increase in the binding of the two 125I-LPDS components, similar to the increase observed in 125I-HDL binding in the presence of 25-HC. These two LPDS components comigrate on sodium dodecyl sulfate/polyacrylamide gel electrophoresis (SDS-PAGE) with apolipoproteins A-I and A-IV of molecular masses 28 kDa and 43 kDa respectively. Furthermore, these two proteins were transfered from the SDS gel to nitrocellulose paper and interacted specifically with anti-(A-I) and anti-(A-IV) sera respectively. When ABAE cultures, pretreated with 25-HC in the presence of LPDS, are subjected to cell-surface iodination, the A-IV appears as one of the major proteins on the cell surface accessible to iodination. The interaction of A-IV with the cell surface of 25-HC-treated cells is not specific to ABAE cells and appears also in human skin fibroblasts. Analysis of the relative amounts of various apolipoproteins in the 125I-HDL bound to ABAE cells demonstrates a decrease in the relative amount of iodinated A-II concomitant with increase in the relative amounts of the other iodinated apolipoproteins, when compared to the composition of the native 125I-HDL. These changes are similar whether the binding is done in the presence or absence of LPDS. It indicates that the decrease in 125I-HDL binding in the presence of LPDS is not due to displacement of the iodinated apolipoproteins A-I and A-IV in the 125I-HDL by unlabeled A-I and A-IV present in LPDS. The results indicate that free apolipoproteins A-I and A-IV, present in LPDS, can displace HDL on the cell surface of ABAE cells. Thus, free A-I and A-IV, present in plasma, control the binding of HDL to endothelial cells and may regulate the process of cholesterol removal from the cells performed by HDL. [ABSTRACT FROM AUTHOR]

Background: Childhood maltreatment (CM) is associated with both dietary fat intake and obesity in later life. There is less information on associations with metabolic risk factors and specific types of CM such as physical, sexual and emotional abuse, as well as neglect. Aims: To assess the association between five types of self‐reported CM and a range of obesity and metabolic indicators in a subsample of a birth cohort. Methods: This was a study of 1689 adults born in a major metropolitan maternity hospital in Australia and followed up 30 years later. Body mass index, bioimpedance and fasting lipid levels/insulin resistance were measured. Details on self‐reported CM were collected using the Child Trauma Questionnaire. We adjusted for birth weight, parental income and relationship at participants' birth, as well as maternal age and alcohol or tobacco use. We also adjusted for participants' smoking, depression, educational level, marital and employment status at follow up. Results: One‐fifth reported maltreatment (n = 362), most commonly emotional neglect (n = 175), followed by emotional abuse (n = 128), physical neglect (n = 123), sexual (n = 121) and physical abuse (n = 116). On adjusted analyses, there were significant associations for CM, particularly neglect or emotional abuse, and one or more of the following outcomes: obesity, the total cholesterol/high‐density lipoprotein cholesterol (TC/HDL‐C) ratio and HDL levels. Results for other outcomes were more equivocal. Conclusions: Of child maltreatment types, emotional abuse and neglect show the strongest associations with obesity and several cardiometabolic risk factors, therefore highlighting the public health importance of early intervention to reduce childhood adversity. [ABSTRACT FROM AUTHOR]

Increasing air pollution is associated with serious human health problems. P‐coumaric acid (PC) is a herbal phenolic compound that exhibits beneficial pharmacological potentials. Here, the protective effect of PC on liver injury induced by air pollution was examined. Thirty‐two adult male Wistar rats (200‐250 g) were divided randomly into four groups (n = 8). The groups were; Control (rats received DMSO and then exposed to clean air), PC (rats received PC and then exposed to clean air), DMSO + Dust (rats received DMSO and then exposed to dust), and PC + Dust (the animals received PC and then exposed to dust). The clean air, DMSO, PC, and dust were administrated 3 days a week for 6 consecutive weeks. The rats were anesthetized and their blood samples and liver sections were taken to conduct molecular, biomedical, and histopathological tests. Dust exposure increased the liver enzymes, bilirubin, triglyceride, cholesterol, and the production of liver malondialdehyde, and decreased in liver total anti‐oxidant capacity and serum high‐density lipoprotein. It also increased the mRNA expression of inflammatory‐related cytokines, decreased the mRNA expression of SIRT‐1, decreased the expression levels of miR‐20b5p, and MEG3 while increased the expression levels of miR‐34a, and HOTAIR. Dust exposure also increased the liver content of three cytokines TNF‐α, NF‐κB, HMGB‐1, and ATG‐7 proteins. PC enhanced liver function against adverse effects of dust through recovering almost all the studied variables. Exposure to dust damaged the liver through induction of oxidative stress, inflammation, and autophagy. PC protected the liver against dust‐induced cytotoxicity. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) is a group of chronic diseases caused by kidney damage from multiple causes. Metabolic syndrome (MS) manifests as dysfunction of endothelial cells and chronic functional inflammatory states, and may be involved in pathological changes related to renal impairment. Based on longitudinal data analysis of the association between estimated glomerular filtration rate (eGFR), proteinuria and MS in patients with CKD, this study aims to provide new ideas for the pathophysiological mechanism of CKD and a theoretical basis for the early prevention and effective intervention of MS‐related kidney damage. A total of 126 patients with CKD were divided into non‐MS group and MS group. According to the eGFR level, 126 patients with CKD were divided into G1 group, G2 group, G3a group, G3b group, G4 group and G5 group. Serum markers such as eGFR, urine protein, and triglycerides (TG) were collected. The correlation between eGFR, urine protein and MS‐related indexes was analysed, and the risk factors affecting CKD complicated by MS were analysed. In patients with CKD, the levels of urine protein, abdominal circumference, TG, systolic blood pressure (SBP), diastolic blood pressure (DBP), and fasting blood glucose (FPG) were increased with the course of the disease, but the levels of eGFR and high density lipoprotein (HDL‐C) were decreased (p < 0.05). Abdominal circumference, TG, SBP, DBP, FP were significantly negatively correlated with eGFR, but HDL‐C was positively correlated with eGFR (p < 0.05). Diabetes, hyperlipidemia, UA, and SBP were independent risk factors affecting CKD complicated MS, and eGFR were independent protective factors (p < 0.05). The combination of diabetes, hyperlipidemia, UA, SBP, and eGFR exhibited higher prediction value for the CKD patients complicated by MS. There was a certain correlation between between MS components with eGFR and urinary protein in patients with CKD. The early intervention treatment of MS was helpful in delaying the development of CKD and reducing proteinuria. [ABSTRACT FROM AUTHOR]

Background: To compare OCs(oral contraceptives) + metformin and OCs alone for metabolic effects in nonobese polycystic ovary syndrome (PCOS) patients. Methods: The search was performed in PubMed, EMBASE, the Cochrane Library and clinicaltrials.gov for all published studies up to 30 April 2022 and was limited to English‐language articles. All randomized controlled trials (RCTs) comparing OCs + metformin and OCs alone for reproductive‐age women with PCOS were included. Data were processed using Revman 5.3 software. Results: Of 396 studies identified, 14 RCTs were included for analysis comprising 707 women. OCs+metformin significantly modified fasting glucose (MD = −0.21 [95% confidence interval (CI) = −0.31, −0.12], p <.00001) and fasting insulin (MD = −2.54 [95%CI = −4.04, −1.04], p =.0009) at study completion compared with OCs alone in nonobese PCOS subjects. There was no statistic difference in the homoeostasis model assessment of insulin resistance (HOMA‐IR), high‐density lipoprotein (HDL), low‐density lipoprotein (LDL), total cholesterol or triglycerides at study end between the two groups. Conclusions: Metformin, via its positive effects on insulin clearance, in combination with OCs, improved glucose metabolism and offered a good treatment alternative in nonobese women with PCOS. [ABSTRACT FROM AUTHOR]

High‐fat diets (HFD) adversely affect organ systems. Several studies have examined HFD‐related disorders in animals but only in a few organs and time points. Herein, we evaluated disease development with time‐dependent HFD‐induced pathological, cardiovascular, and morphological changes in rabbits with lipid metabolism similar to that in humans for 9 weeks. The body weights and waist ratio of the HFD group were higher than those in the control group. HFD significantly increased the total cholesterol, low‐density lipoprotein, high‐density lipoprotein, and phospholipid levels after 3 weeks. Liver enzyme levels increased with hepatomegaly, steatosis, and fibrosis after 3 or 6 weeks. RBCs and hemoglobin decreased, while platelets increased in the HFD group with atherosclerosis and inflammatory cell infiltration in the aorta after 6 weeks. Ejection fraction and fractional shortening values decreased in the HFD group after 9 weeks. Creatinine increased with glomerulosclerosis in the kidneys of the HFD groups after 3 weeks, indicating renal dysfunction. Lipid accumulation was found in the pancreas after 9 weeks. Lipid accumulation and hypertrophy were observed in the adrenal glands after 3 weeks. Overall, our findings provide global reference data on the time‐dependent effects of HFD on the body and may serve as a guide for future HFD risk prevention. [ABSTRACT FROM AUTHOR]

Summary: Sleep is essential for the maintenance of health and systemic homeostasis. Decreased sleep time and sleep quality have been associated with a wide range of diseases. To evaluate the effects of obstructive sleep apnea (OSA) and total or selective rapid eye movement (REM) sleep deprivation on male reproductive function, we performed a three‐arm parallel study with one pre‐defined OSA group and a group of healthy volunteers who were then randomised into total or REM sleep deprivation groups. Questionnaires were completed and overnight polysomnography was undertaken, and blood and sperm samples were collected at the Sleep Institute, São Paulo, Brazil. OSA was diagnosed using questionnaires and polysomnography. Male sexual function was assessed through the questionnaires, blood tests, and semen samples. Data showed an association between OSA and lower circulating levels of total and free testosterone and high‐density lipoproteins, as well as a lower proportion of healthy sperm cells and decreased sperm concentration, in comparison to volunteers. Volunteers subjected to either total or REM sleep deprivation had increased circulating levels of thyroid‐stimulating hormone, insulin, and higher homeostatic model assessment of insulin resistance (HOMA‐IR) values. Both sleep‐deprived groups also shown decreased cholesterol, and low‐density lipoproteins when compared to their baseline levels, but had no alterations in their spermograms. We observed a reduction in total testosterone following total sleep deprivation, but no effect after REM sleep deprivation. OSA was associated with a hormonal imbalance, which is probably linked with impaired reproductive function and associated comorbidities, such as sleep fragmentation/loss and obesity. [ABSTRACT FROM AUTHOR]

Acorn is a nutritious fruit with the reported potential of ameliorating diseases, including diabetes. This research aimed to assess the effects of acorn muffin consumption on glycemic, lipid indices, and appetite in patients with type 2 diabetes. Sixty‐six subjects were dichotomized to receive either one muffin containing 10 grams of acorn flour or a placebo muffin containing white wheat flour (no bran), per day, for 8 weeks. Acorn muffin consumption improved glycated hemoglobin (p =.06, mean difference [MD] = −0.65), triglyceride (p =.06, MD = −36.38), and high‐density lipoprotein (p =.05, MD = 1.30), albeit only marginally significantly. Among appetite parameters, hunger, desire to eat, and prospective to eat were significantly lower, and satiety and fullness were significantly higher, in the acorn muffin group. In conclusion, acorn muffins could be utilized as an adjuvant therapy to control appetite and ameliorate glycated hemoglobin in patients with type 2 diabetes. However, further investigations are required for a more comprehensive conclusion. [ABSTRACT FROM AUTHOR]

Autophagy defects accelerate aging, while stimulation of autophagy decelerates aging. Acyl‐coenzyme A binding protein (ACBP), which is encoded by a diazepam‐binding inhibitor (DBI), acts as an extracellular feedback regulator of autophagy. As shown here, knockout of the gene coding for the yeast orthologue of ACBP/DBI (ACB1) improves chronological aging, and this effect is reversed by knockout of essential autophagy genes (ATG5, ATG7) but less so by knockout of an essential mitophagy gene (ATG32). In humans, ACBP/DBI levels independently correlate with body mass index (BMI) as well as with chronological age. In still‐healthy individuals, we find that high ACBP/DBI levels correlate with future cardiovascular events (such as heart surgery, myocardial infarction, and stroke), an association that is independent of BMI and chronological age, suggesting that ACBP/DBI is indeed a biomarker of "biological" aging. Concurringly, ACBP/DBI plasma concentrations correlate with established cardiovascular risk factors (fasting glucose levels, systolic blood pressure, total free cholesterol, triglycerides), but are inversely correlated with atheroprotective high‐density lipoprotein (HDL). In mice, neutralization of ACBP/DBI through a monoclonal antibody attenuates anthracycline‐induced cardiotoxicity, which is a model of accelerated heart aging. In conclusion, plasma elevation of ACBP/DBI constitutes a novel biomarker of chronological aging and facets of biological aging with a prognostic value in cardiovascular disease. [ABSTRACT FROM AUTHOR]

Summary: Background: Living in single parent and blended families or as an only child—compared to living in two‐parent biological families or with siblings, respectively—is associated with a higher body mass index (BMI) in cross‐sectional studies. However, longitudinal research addressing the children's BMI in this context is scarce. Further, little is known about the association between family structure and metabolic health. Objectives: This study aimed at investigating the association between both aspects of family structure with BMI and a metabolic score (MetS). Methods: Cross‐sectional data from 7804 children participating in the European multi‐center I.Family study (2013/2014) and longitudinal data from 5621 children who also participated previously in the IDEFICS study (2007–2010) were used. Family structure was assessed by a detailed interview. BMI z‐score and the MetS were based on measured anthropometry, blood pressure, high‐density lipoprotein, blood glucose, and triglycerides. Linear regressions were performed to model associations between family structure with BMI and MetS. Results: Children from single‐parent families had higher BMI z‐scores in the cross‐sectional (β = 0.09, 95% confidence interval [CI]: 0.001 to 0.18) and longitudinal analyses compared to those from two‐parent families. Cross‐sectionally, the number of siblings was associated with lower BMI z‐scores (β = −0.07, 95% CI: −0.10 to −0.03) and lower MetS (β = −0.14, 95% CI: −0.26 to −0.01). Longitudinally, only children between baseline and follow‐up had higher BMI z‐scores at follow‐up (β = 0.07, 95% CI: 0.01 to 0.14) compared to stable siblings. Conclusion: Obesity prevention measures should focus on single‐parent households and families with an only child. [ABSTRACT FROM AUTHOR]

Cholesterol levels have been repeatedly linked to Alzheimer's Disease (AD), suggesting that high levels could be detrimental, but this effect is likely attributed to Low‐Density Lipoprotein (LDL) cholesterol. On the other hand, High‐Density Lipoproteins (HDL) cholesterol levels have been associated with reduced brain amyloidosis and improved cognitive function. However, recent findings have suggested that HDL‐functionality, which depends upon the HDL‐cargo proteins associated with HDL, rather than HDL levels, appears to be the key factor, suggesting a quality over quantity status. In this report, we have assessed the HDL‐cargo (Cholesterol, ApoA‐I, ApoA‐II, ApoC‐I, ApoC‐III, ApoD, ApoE, ApoH, ApoJ, CRP, and SAA) in stable healthy control (HC), healthy controls who will convert to MCI/AD (HC‐Conv) and AD patients (AD). Compared to HC we observed an increased cholesterol/ApoA‐I ratio in AD and HC‐Conv, as well as an increased ApoD/ApoA‐I ratio and a decreased ApoA‐II/ApoA‐I ratio in AD. Higher cholesterol/ApoA‐I ratio was also associated with lower cortical grey matter volume and higher ventricular volume, while higher ApoA‐II/ApoA‐I and ApoJ/ApoA‐I ratios were associated with greater cortical grey matter volume (and for ApoA‐II also with greater hippocampal volume) and smaller ventricular volume. Additionally, in a clinical status‐independent manner, the ApoE/ApoA‐I ratio was significantly lower in APOE ε4 carriers and lowest in APOE ε4 homozygous. Together, these data indicate that in AD patients the composition of HDL is altered, which may affect HDL functionality, and such changes are associated with altered regional brain volumetric data. [ABSTRACT FROM AUTHOR]

Background and Purpose: Metabolic and vascular dysfunction are common features of obesity. Aryl hydrocarbon receptor (AhR) regulates lipid metabolism and vascular homeostasis, but whether vascular AhR are activated in obesity or have a protective and/or harmful effects on vascular function in obesity are unknown. Our study addresses whether AhR activation contributes to obesity‐associated vascular dysfunction and the mechanisms involved in these AhR effects. Experimental Approach Male AhR KO (Ahr−/−) and WT mice were fed either control or a HF (high‐fat) diet for 10 weeks. Metabolic and inflammatory parameters were measured in serum and adipose tissue. Vascular reactivity (isometric force) was evaluated using a myography. Endothelial NOS (eNOS) and AhR protein expression was determined by western blot, Cyp1A1 and Nos3 gene expression by RT‐PCR and.NO production was quantified by DAF fluorescence. Key Results: HF diet increased total serum HDL and LDL, as well as vascular AhR protein expression and proinflammatory cytokines in the adipose tissue. HF diet decreased endothelium‐dependent vasodilation. AhR deletion protected mice from HF diet‐induced dyslipidaemia, weight gain and inflammatory processes. HF diet‐induced endothelial dysfunction was attenuated in Ahr−/− mice. Vessels from Ahr−/− mice exhibited a greater NO reserve. In cultured endothelial cells, lysophosphatidylcholine (LPC) a major component of LDL and oxidized LDL [oxLDL]) reduced Nos3 gene expression and NO production. Antagonism of the AhR inhibited LPC effects on endothelial cells and induced decreased endothelium‐dependent vasodilation. Conclusion and Implications: AhR deletion attenuates HF diet‐induced dyslipidaemia and vascular dysfunction by improving eNOS/NO signalling. Targeting AhRs may prevent obesity‐associated vascular dysfunction. [ABSTRACT FROM AUTHOR]

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The triglyceride glucose (TyG) index and triglyceride/high lipoprotein density cholesterol (TG/HDL‐C) are two important risk markers to evaluate the insulin resistance and cardiovascular diseases (CVDs). To assess the association between TG/HDL‐C and TyG index and CVDs. The Mashhad stroke and heart association disorder cohort study started in 2010 and has been continued until 2020. During 6‐year follow‐up of 9704 participants, 235 events including 118 acute coronary syndrome (ACS), 83 chronic coronary syndrome, 27 myocardial infarction, and 27 cardiac death were confirmed. SPSS software (version 21) was used for statistical analysis and figures were drawn by GraphPad Prism 6 software. The prevalence of ACS and cardiac death were higher in the fourth quartile of serum TG/HDL‐C (>4.43) and higher prevalence of ACS was considered in subjects classified in the fourth quartile of TyG index (>8.98). A high TyG index was associated with an increased risk of ACS and cardiac death [1.362 (95% confidence interval [CI]: [1.013–1.831]) and 2.3 (95% CI: [1.247–4.241])] respectively; based on Cox regression analysis elevated TyG and TG/HDL‐C increased the chance of CVD by [1.634 (95% CI: 1.304–2.047) and 1.068 (95% CI: 1.031–1.105)], respectively. Our results strongly showed that TyG index and TG/HDL‐C are independent risk factors for incident CVD, suggesting that TyG index and TG/HDL‐C may be as an important unique biomarker for predicting CVD outcomes and progression. [ABSTRACT FROM AUTHOR]

Sevelamer, has been shown to have many pleiotropic actions on lipid panel, various inflammatory markers, and blood glucose levels in chronic kidney disease patients. We conducted a systematic review and meta‐analysis to compare these pleiotropic effects of sevelamer to other phosphate binders used in chronic kidney disease patients. The relevant randomized controlled trials published from 1 January 2001 to 31 November 2019 on the following databases: Cochrane Central Register of Controlled Trials published in The Cochrane Library, PubMed, Scopus and Google Scholar were identified. All the included studies were independently assessed for eligibility and risk of bias. The modified data extraction form of Cochrane was used. This review included 44 studies for qualitative analysis and 28 reports for quantitative analysis. A meta‐analysis of three studies (n = 180) showed that glycated haemoglobin had significantly decreased in sevelamer‐treated patients (MD: 0.5%; p = <.001). Compared with calcium‐based phosphate binders, sevelamer showed a significant reduction in low‐density lipoprotein (MD: −19.43 mg/dL; p = <.001) and total cholesterol (MD: −19.98 mg/dL; p <.001). A significant increase in high‐density lipoprotein (MD: 1.29 mg/dL; p =.05) was also prominent in sevelamer treated patients. However, we were not able to observe a significant change in other biochemical parameters such as TG, CRP, hs‐CRP, FGF‐23, IL‐6 and albumin as, no statistically significant difference was observed. SUMMARY AT A GLANCE: This meta‐analysis on the pleiotropic effects of sevelamer in CKD beyond phosphate control showed that glycated haemoglobin and low‐density lipoprotein and total cholesterol were significantly reduced, whereas high‐density lipoprotein cholesterol was increased when compared with calcium‐based phosphate binders. [ABSTRACT FROM AUTHOR]

Aims: To compare anthropometrics, and lipid and glucose metabolism in the 9‐year‐old offspring of mothers treated with metformin or insulin for gestational diabetes mellitus (GDM). Materials and Methods: This was a Finnish two‐centre, 9‐year follow‐up study of two open‐label, randomized controlled trials comparing the effects observed in the offspring of mothers who received metformin and insulin treatment for GDM. Measurements included anthropometrics, blood pressure, lipoproteins, and oral glucose tolerance tests. This study was registered with ClinicalTrials.gov, number NCT02417090. Results: At the age of 9 years 172 children (55% of the original study cohort, 82 from the metformin and 90 from the insulin group) participated in the study. No differences were found between the 9‐year‐old offspring groups in anthropometric variables, including body mass index and waist‐to‐height ratio. The offspring in the metformin group had higher high‐density lipoprotein (HDL) cholesterol concentrations (1.72 vs. 1.54 mmol/L; P = 0.039) but lower low‐density lipoprotein cholesterol (2.39 vs. 2.58 mmol/L; P = 0.046) and apolipoprotein B concentrations (0.63 vs. 0.67 g/L; P = 0.043) than the offspring in the insulin group. The difference in HDL cholesterol concentration was found to be significant only in boys (P = 0.003). The 2‐hour glucose value in the oral glucose tolerance test was 0.6‐mmol/L lower in boys from the metformin group than in those from the insulin group (P = 0.015). Conclusions: Metformin treatment for GDM is associated with similar offspring growth and glucose metabolism but a more favourable lipid profile at the age of 9 years as compared to insulin treatment. [ABSTRACT FROM AUTHOR]

Background and Purpose: Statins (HMG CoA reductase inhibitors) have beneficial effects independent of reducing cholesterol synthesis and this includes their ability to acutely activate endothelial nitric oxide synthase (eNOS). The mechanism by which this occurs is largely unknown and thus we characterized the pathways by which statins activate NOS, including involvement of scavenger receptor-B1 (SR-B1), which is expressed in endothelial cells and maintains cholesterol concentrations.Experimental Approach: Nitric oxide production was monitored in bovine aortic endothelial cells (BAECs) exposed to lovastatin (LOV) or pravastatin (PRA) for 10-20 min, alone or following pre-exposure to the end product of HMG-CoA reductase (mevalonate), G protein inhibitors (pertussis/cholera toxins), phospholipase C (PLC) inhibitor (U-73122), or intracellular and extracellular calcium chelators - BAPTA-AM and EGTA (respectively), or a function blocking antibody to SR-B1.Key Results: Both statins increased NO production in a rapid, dose-dependent and HMG-CoA reductase-independent manner. Inhibiting Gi protein or PLC almost completely blocked statin-induced NO generation. Additionally, removing extracellular calcium inhibited statin-induced NO production. COS-7 cells co-transfected with eNOS and SR-B1 increased NO production when exposed to LOV or high-density lipoprotein (HDL), an agonist of SR-B1. These effects were not observed in COS-7 cells with eNOS alone or co-transfected with bradykinin receptor 2, indicating specificity for SR-B1. Further, pretreatment of BAEC with blocking antibody for SR-B1 blocked NO responses to statins and HDL.Conclusions and Implications: LOV and PRA acutely activate eNOS through pathways that include the cell surface receptor SR-B1, Gi protein, phosholipase C and entry of extracellular calcium into endothelial cells. [ABSTRACT FROM AUTHOR]

Background and Purpose: Hyperlipidaemia interferes with cardioprotective mechanisms, but the cause of this phenomenon is largely unknown, although hyperlipidaemia impairs the cardioprotective NO-cGMP system. However, it is not known if natriuretic peptide-cGMP-protein kinase G (PKG) signalling is affected by hyperlipidaemia. Therefore, we investigated the cardioprotective efficacy of cGMP-elevating agents in hearts from normal and hyperlipidaemic rats.Experimental Approach: Male Wistar rats were rendered hyperlipidaemic by feeding with 2% cholesterol-enriched chow for 12 weeks. Hearts isolated from normal and hyperlipidaemic rats were perfused (Langendorff mode) and subjected to 30 min occlusion of the left main coronary artery, followed by 120 min reperfusion. 8-Br-cGMP (CG, 10 nM), B-type natriuretic peptide-32 (BNP, 10 nM), S-nitroso-N-acetyl-penicillamine (SNAP, 1 microM) were perfused from 10 min prior to coronary occlusion until the 15th min of reperfusion. Infarct size (% of ischaemic risk zone) was determined by triphenyltetrazolium staining.Key Results: Treatment with CG, SNAP or BNP decreased infarct size significantly in normal hearts from its control value of 41.6 +/- 2.9% to 15.5 +/- 2.4%, 23.3 +/- 3.0% and 25.3 +/- 4.6%, respectively (P < 0.05). Protection by BNP was abolished by co-perfusion of PKG inhibitors KT5823 (600 nM) or Rp-8pCPT-PET-cGMPs (1 microM), confirming its PKG dependence. In hearts from hyperlipidaemic rats, CG, SNAP or BNP failed to decrease infarct size. Hyperlipidaemia did not alter basal myocardial PKG content, but decreased its activity as assessed by phosphorylation of cardiac troponin I.Conclusions and Implications: This is the first demonstration that defects in the cardioprotective cGMP-PKG system could be a critical biochemical anomaly in hyperlipidaemia. [ABSTRACT FROM AUTHOR]

Okra (Abelmoschus esculentus) is a traditionally important vegetable herb used to treat numerous illnesses, including diabetes mellitus, in many rural parts of Bangladesh and the South Asian subcontinent. However, the scientific evidence for the aforementioned properties has not been adequately validated. Hence, the aim of this study was to explore the antidiabetic, antilipidemic activity of okra mucilage powder, and to compare its effectiveness with the isolated peel–seed of okra after mucilage extraction in Swiss albino mice. After extraction, both mucilage and peel–seed were made into powder. In addition, crude protein, mineral contents, and in vitro antioxidant activity of mucilage and peel–seed powder were assessed. After acute toxicity test, methanolic extracts of both powders were administered to alloxan‐induced diabetic mice for 3 weeks. Blood glucose levels were assessed weekly. Finally, blood samples were collected on day 21 to estimate blood glucose level, total protein (TP), and lipid profile levels. Okra mucilage powder showed less amount of protein, calcium, magnesium, phosphorus, potassium, sodium, and iron compared with peel–seed powder. In terms of antioxidant activity, the IC50 value and total phenolic content were found higher in okra mucilage powder in contrast to peel–seed powder. However, total flavonoid content was higher in peel–seed powder than mucilage powder. Three‐week administration of mucilage and peel–seed suspensions at a dose of 150 mg/kg and 200 mg/kg significantly (p <.05) reversed the abnormal changes of bodyweights, water consumption, feed consumption, and fasting blood glucose levels of diabetic subjects. Cholesterol, triglycerides, low‐density lipoproteins, high‐density lipoproteins, and total protein were found to be significantly (p <.05) improved after mucilage and peel–seed treatment. Thus, Okra can be recommended as a potential source of antidiabetic drug candidate for the effective management of diabetes mellitus and its complications. [ABSTRACT FROM AUTHOR]

Summary: Inflammation and immune dysfunction have been increasingly recognized as crucial mechanisms in atherogenesis. Modifications in cell lipid metabolism, plasma dyslipidaemia and particularly low high‐density lipoprotein (HDL) levels occur both in atherosclerosis and in autoimmune rheumatic diseases (which are strongly associated with an increased risk of atherosclerosis), suggesting the presence of a crucial link. HDL, the plasma lipoprotein responsible for reverse cholesterol transport, is known for its several protective effects in the context of atherosclerosis. Among these, HDL immunomodulatory effects are possibly the less understood. Through the efflux of cholesterol from plasma cell membranes with the consequent disruption of lipid rafts and the interaction with the cholesterol transporters present in the plasma membrane, HDL affects both the innate and adaptive immune responses. Animal and human studies have demonstrated a predominance of HDL anti‐inflammatory effects, despite some pro‐inflammatory actions having also been reported. The HDL role on the modulation of the immune response is further suggested by the detection of low levels together with a dysfunctional HDL in patients with autoimmune diseases. Here, we review the current knowledge of the immune mechanisms of atherosclerosis and the modulatory effects HDL may have on them. [ABSTRACT FROM AUTHOR]

Previous findings have highlighted the association between oxidized high‐density lipoprotein (ox‐HDL) and polycystic ovary syndrome (PCOS) development; however, the underlying mechanism remains unclear. Under such context, the present study aimed to investigate the mechanism underlying the involvement of ox‐HDL in PCOS in relation to the p65/micro‐RNA‐34a (miR‐34a)/FOS axis. PCOS rat models were established with the injection of dehydroepiandrosterone (6 mg/100 g body weight). Both PCOS‐modelled rats and granulosa cells (GCs) were received treatment with ox‐HDL in order to identify its role in PCOS. Next, apoptosis and viability of GCs were detected with the application of TdT‐mediated dUTP Nick‐End Labeling and flow cytometry and Cell counting kit‐8, respectively. A series of assays were performed to determine the interaction among ox‐HDL, p65, miR‐34a, FOS and nuclear factor‐κB (NF‐κB). The results revealed high expression of ox‐HDL in PCOS, and enhanced endocrine disorders and ovarian damage in rats. ox‐HDL promoted apoptosis of GCs and decreased its viability. ox‐HDL activated NF‐κB pathway and induced p65 phosphorylation to promote miR‐34a expression. miR‐34a targeted and inhibited FOS expression. In conclusion, our findings suggested that ox‐HDL promoted the activation of p65 and transcription of miR‐34a, which stimulated apoptosis of GCs and inhibited expression of FOS, resulting in the overall acceleration of PCOS development. [ABSTRACT FROM AUTHOR]

Differential miRNA plasma profiles associated with the spontaneous loss of HIV-1 control: miR-199a-3p and its potential role as a biomarker for quick screening of elite controllers People living with HIV (PLWH) who are able to maintain suppressed viral load (VL) for years in the absence of antiretroviral therapy (ART) are known as elite controllers (ECs). From the 23 miRNAs, 22 miRNAs were positively correlated with viral load (VL), seven miRNAs were positively correlated with CD4 SP + sp T-cell counts, and 11 miRNAs were positively correlated with CD8 SP + sp T-cell counts (Table S3). Then, we also evaluated the plasma miRNA profile in TCs under the postloss condition and we found 38 miRNAs differentially expressed among groups, suggesting that viremia strongly influences the plasma miRNA profile of ECs (Figure 2A, Table S4). [Extracted from the article]

Objective: Abnormal blood lipid levels are common in bipolar disorder (BD) and correlate with mood symptoms and neurocognition. However, studies have not examined the lipid–brain structure association in BD or youth. Methods: This study examined low‐density lipoprotein (LDL‐C), high‐density lipoprotein (HDL‐C), triglycerides, and total cholesterol (TC) levels in relation to brain structure utilizing T1‐weighted images, among participants ages 13–20 with BD (n = 55) and healthy controls (HC; n = 47). General linear models investigated group differences in the association of lipids with anterior cingulate cortex (ACC), hippocampus, and inferior parietal lobe structure, controlling for age, sex, body mass index, and intracranial volume. For significant associations, post hoc within‐group analyses were undertaken. Exploratory vertex‐wise analyses further investigated group differences in the lipid–brain structure association. Results: There were significant group differences in the association of LDL‐C (β = −0.29 p = 0.001), and TC (β = −0.21 p = 0.016), with hippocampal volume, and triglycerides with ACC volume (β = −0.25 p = 0.01) and area (β = −0.26 p = 0.004). Elevated lipids were associated with smaller brain structure to a significantly greater extent in BD vs HC. Post hoc analyses revealed that elevated LDL‐C (β = −0.27 p = 0.007) and reduced HDL‐C (β = 0.24 p = 0.01) were associated with smaller hippocampal volume in the BD group. Exclusion of BD second‐generation antipsychotic users did not alter these results. Vertex‐wise analyses further showed that elevated lipids were associated with smaller brain structure to a significantly greater extent in BD vs HC, across the cortex. Conclusion: Elevated lipids are associated with smaller brain structure in BD. Research evaluating lipid–brain structure associations prospectively and whether lipid optimization has salutary effects on brain structure is necessary. [ABSTRACT FROM AUTHOR]

The morphology and structural organisation of the complexes formed from the apoprotein of porcine high-density lipoprotein and dimyristoyl phosphatidylcholine (lecithin) have been studied using the technique of small-angle X-ray scattering. Scattering measurements made in solvents of varying electron density were interpreted in terms of a scattering-equivalent model for the structure of the complex. This model is described by an oblate ellipsoidal morphology with dimensions at 20 °C: major axis 11.0 nm, minor axis 5.5 nm. Within this overall shape the lipid hydrocarbon chains are organised in an apolar core whilst the lipid polar head groups and protein are located in a outer shell 0.85 nm in thickness. The oblate morphology demonstrates that the structure of the complex is directed by the fundamental bilayer organisation of the lecithin. The dimension of the minor axis (5.5 nm) indicates that phospholipid hydrocarbon chains are orientated perpendicular to the interface. [ABSTRACT FROM AUTHOR]

Elaborates procedures for the isolation of two lipoprotein fractions from plasma high-density lipoproteins, characterized by apolipoprotein A-I and apolipoprotein A-I together with apolipoprotein A-II. Polyacrylamide gel electrophoresis; Immuno-double-diffusion; Amino acid compositions; Immunoelectrophoresis.

Background: More than 11 million people were estimated to have been infected by Schistosoma japonicum in China before the 1950s. However, few studies have been conducted to evaluate the longitudinal effects of previous schistosome infection (PSI). Objective: We aimed to evaluate the association of PSI with fatty liver and coronary heart disease in China. Methods: A cross‐sectional study was conducted in regions which were all reportedly heavily endemic for S japonicum in China. All data were collected using a questionnaire administered and health examinations by well‐trained medical professionals. 2867 participants aged 40 years and older were enrolled. Among these, 731 patients with PSI were selected as study subjects and 2136 subjects served as controls. Comparisons between groups were performed with or without an adjustment for a covariate, using Student's t tests for continuous variables and chi‐square testing for categorical variables. Multivariable logistic models were used to estimate the associations between PSI and fatty liver or coronary heart disease. Results: The PSI participants had significantly lower levels of triglyceride, low‐density lipoprotein cholesterol, fasting blood glucose, uric acid, serum creatinine, urea nitrogen, platelet, total protein and globulin as well as a lower prevalence of fatty liver (13.3% vs 53.6%, P <.001) and coronary heart disease (3.4% vs 6.0%, P <.05) compared with the uninfected, contemporaneous controls (without PSI), whereas the PSI participants had higher levels of high‐density lipoprotein cholesterol, direct bilirubin and a higher prevalence of hepatic dysfunction compared with those without PSI (P <.05). Conclusion: We found PSI significantly negatively associated with fatty liver and coronary heart disease. However, further studies on schistosomiasis may provide new directions for prevention and treatment of fatty liver and coronary heart disease. [ABSTRACT FROM AUTHOR]

Ever since the discovery of P-gp in 1975, ATP-binding cassette transporters have captivated basic researchers, microbiologists, and clinicians alike. The role of ABC transporters in health and disease As this special issue highlights, ABC transporters handle a wide range of structurally dissimilar endo- and xenobiotics in the human body, especially in tissue barriers and metabolizing or secretory organs [18-21]. Understanding ABC transporter function from structure Looking back at the previous ABC Special Issue published by FEBS Letters, the current wealth of ABC transporter structures seems overwhelming. ABC transporters and the environment A further emerging theme in this special issue is the interplay between ABC transporters and their environment. [Extracted from the article]

The Iowa (G26R) mutation in human apolipoprotein A‐I (apoA‐I), the major protein of plasma high‐density lipoprotein, is associated with systemic amyloidosis, and the N‐terminal 1–83 fragment of apoA‐I carrying this mutation has a strong propensity to form amyloid fibrils. Here, we generated and characterized novel monoclonal antibodies (mAbs) that display selective reactivity to apoA‐I amyloid fibrils. By immunizing BALB/c and A/J mice with apoA‐I 1‒83/G26R fibrils conjugated with hemocyanin and the hybridoma production, four IgM class mAbs were obtained. The generated mAbs exhibited strong reactivity to amyloid fibrils formed by the 1–83 fragment of apoA‐I, but not to the monomeric 1–83 fragment or full‐length apoA‐I. The apparent dissociation constant of the mAbs to apoA‐I fibrils was determined to be within the nM range. A time‐dependent aggregation assay demonstrated that the mAbs preferentially react with mature fibrils over non‐fibrillar aggregates formed by apoA‐I 1–83/G26R. In addition, dot blotting and ELISA using deletion or proline substituted variants of apoA‐I 1‒83/G26R suggest that the generated mAbs react to common structural features in apoA‐I amyloid fibrils. Indeed, the mAbs also recognized amyloid fibrils formed by α‐synuclein that has no sequence identity to apoA‐I. Thus, our newly generated anti‐apoA‐I fibril mAbs may be utilized for not only diagnosis of apoA‐I‐related amyloidosis but also structural analysis of amyloid fibrils as novel conformation‐selective antibodies. [ABSTRACT FROM AUTHOR]

Aim: Very low carbohydrate high fat diets (VLCHF) are increasingly popular for weight loss and diabetes management, but the risk implications of long‐term adherence to a high‐fat‐diet remain unclear, especially in high‐risk populations. This review aimed to examine adherence, weight loss, diabetes‐ and cardiovascular disease (CVD)‐related risk markers in adults consuming VLCHF diets. Methods: Online databases were searched for randomised controlled trials ≥3 months duration that met a pre‐defined macronutrient prescription: VLCHF ≤25%E carbohydrate, >35%E fat; low fat (LF) ≥45%E carbohydrate, ≤30%E fat; and reported energy, saturated fat (SFA), weight, blood glucose, cholesterol and blood pressure (BP). Studies were excluded if the macronutrient prescription was not targeted (n = 32); not met (n = 17) or not reported (n = 13). Results: Eight studies included: 1217 commenced; 922 completed overweight and obese adults. Diets were isocaloric moderately energy‐restricted, closely monitored with ongoing support from dietitians, physicians, and/or nurses. Four studies reported non‐adherence beyond 3 months (n = 3) and 6 months (n = 1) despite interventions of 12, 15 and 24 months. VLCHF diets were high in fat and SFA (fat 49%‐56%E; SFA 11%‐21%E) compared to LF diets (fat 13%‐29%E; SFA 5%‐11%E). All groups achieved significant weight loss and improvements in BP and blood glucose. LDL‐C reduction favoured LF, P <.05; increased HDL‐C and reduced triglyceride levels favoured VLCHF, P <.05. Conclusions: VLCHF and LF diets with moderate energy restriction demonstrate similar weight loss and improvements to BP to 3 months. However, adherence is likely poor without intensive support from health professionals. Dietary SFA should be monitored to ensure recommended intakes, but longer‐term studies with high adherence are required to confirm the level of CVD‐risk and potential harms. [ABSTRACT FROM AUTHOR]

Background: The association of migraine with vascular comorbidities is long‐established. The contribution of the "traditional" cardiovascular risk factors to this connection remains unclear. Objective: To determine‐quantify the differences in the serum lipid concentrations between lipid‐lowering agents–naïve individuals with migraine and healthy controls (HC). Methods: The study protocol was not preregistered with an online systematic review‐protocol registry. A literature search involving MEDLINE, EMBASE, CENTRAL, Google Scholar, and the OpenGrey database was performed. Case–control, cross‐sectional, or cohort studies involving HC and participants with migraine (with and without aura regardless of the use of prophylactic treatment) that quantitatively assessed serum low‐density lipoprotein cholesterol (LDL‐C) (primary index) and/or total cholesterol (TC) and/or high‐density lipoprotein cholesterol (HDL‐C) and/or triglycerides (TG) (secondary indices) were retrieved. Articles including participants with known dyslipidemia (or under lipid‐lowering medications) or with secondary causes of dyslipidemia (aside from the subjectively assessed lifestyle parameters) were excluded. Studies with abstracts and full texts not published in English and articles reporting the implementation of other study designs (reviews, meta‐analyses, commentaries, case reports, etc.) were excluded as well. Conference abstracts and English abstracts from studies with full texts not published in English were evaluated as part of the gray literature. Each step of the review process was performed by two investigators independently, and relevant data were abstracted based on standardized extraction forms. Any discrepancies were resolved by a third investigator. Results: Seventeen studies (16 case–control and 1 cross‐sectional) fulfilled the eligibility criteria. Retrieved articles involved adult participants, principally during the fourth decade of life. Results were compatible with higher LDL‐C levels in migraine individuals (1370) than in HC (1215) [12 studies, mean difference (MD) = 10.4 mg/dl, 95% confidence interval (CI) = (1.6, 19.2)]. Similarly, higher TC levels were determined in migraine patients [14 studies, migraine = 1325, HC = 1213, MD = 10.6 mg/dl, 95% CI = (1.8, 19.3)], as were TG levels [15 studies, migraine = 1526, HC = 1262, MD = 11.8 mg/dl, 95% CI = (3.6, 20.0)]. HDL‐C concentrations were not different between the two groups [14 studies, migraine = 1488, HC = 1328, MD = −0.4 mg/dl, 95% CI = (−2.2, 1.5)]. Prespecified sensitivity analysis following the exclusion of studies not presenting comparable body mass index values between the groups nullified the significant difference regarding LDL‐C levels [MD = 5.3 mg/dl, 95% CI = (−0.1, 10.8)]. Subgroup analyses as well as the direct comparison of migraine with aura and migraine without aura individuals were compatible with no difference regarding lipid concentrations, but only a small fraction of the retrieved studies presented relevant figures. Conclusions: Although our results are of limited generalizability, since most retrieved studies were performed in Turkey (nine studies), TC abnormalities may provide part of the explanation for the unfavorable cardiovascular profile of migraine patients. Lifestyle may be partly or entirely accountable for the determined increased serum TC. Additional studies that will completely address the effect that lifestyle parameters exert on lipid concentrations are required to better capture existing abnormalities. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to determine the impact of weight gain prevention interventions on changes in cardiovascular risk factors over 6 years.Methods: The Study of Novel Approaches to Weight Gain Prevention (SNAP) randomized 599 participants (ages 18-35; 46% with BMI 21-25; 54% with BMI 25-30) to Large Changes (produce buffer by losing 5-10 pounds initially), Small Changes (daily small changes in intake and activity) or Control and followed 355 participants with ongoing intervention and assessments through 6 years.Results: There were no significant differences among interventions for changes in weight or cardiovascular disease (CVD) risk factors from baseline to 6 years. However, 44% of participants gained ≥5%, and only 14% lost ≥5% over 6 years. Weight changes, from baseline to year 6, were significantly associated with changes in risk factors, especially insulin and high-density lipoprotein cholesterol. Earlier weight changes (e.g., weight cycling) had no beneficial or adverse effect on changes in CVD risk factors at 6 years, independent of 6-year weight changes.Conclusions: Despite participation in a weight gain prevention trial, almost half of these young adults gained ≥5% or more over 6 years, with significant worsening in CVD risk factors. Greater attention to long-term weight gain prevention in young adults is needed. [ABSTRACT FROM AUTHOR]

Objective: The effects of anticonvulsants on lipids are the subject of considerable concern and investigation, but there are almost no data on this issue from randomized trials. We evaluated serum lipid profiles in adults with newly diagnosed epilepsy, following randomization to lacosamide (LCM) or carbamazepine (CBZ) monotherapy. Methods: We analyzed data from a Phase 3, international, randomized, double‐blind trial of LCM vs CBZ for the initial treatment of focal epilepsy. Serum lipid profiles in patients not taking lipid‐lowering agents and providing blood samples under fasting conditions before treatment, and following 3 or 12 months of treatment with LCM or CBZ at various doses were analyzed. Results: At 12 months, 271 patients satisfied the inclusion criteria for the analysis. No change was observed in LCM‐treated patients for total cholesterol, cholesterol fractions, or triglycerides. CBZ‐treated patients showed an increase of 21.1 mg/dL in total cholesterol, 12.6 mg/dL in low‐density lipoprotein (LDL) cholesterol, 12.5 mg/dL in non–high density lipoprotein (non‐HDL) cholesterol, and 8.5 mg/dL in HDL cholesterol; triglycerides remained unchanged. The proportion of patients with elevated total cholesterol levels (above the upper limit of the reference range) did not change in the LCM treatment group (37.0% at Baseline; 34.8% at 12 months), but increased from 30.8% (at Baseline) to 49.6% (at 12 months) in the CBZ treatment group. Significance: This study provides Class II evidence that CBZ elevates serum lipids, whereas LCM has no effect on lipids. It supports LCM as an appropriate choice for new‐onset focal epilepsy. [ABSTRACT FROM AUTHOR]