Prevalence and Association of Digital Eye Strain with the Quality of Sleep and Feeling of Loneliness among Female College Students in Northern India.

INTRODUCTION: Because of COVID's impact on social behavior, students have become more reliant on computer-facilitated communication to continue their studies and interact with friends. While it is known that the association between screen exposure and psychological well-being is both harmful and stronger among adolescents than younger children, what is less studied are the causal factors that may mediate the relationship. OBJECTIVES: The objectives of this study were to analyze the relationship between screen exposure and two psychological outcomes, sleep quality and loneliness, using digital eye strain as a mediating factor. Eye strain is expected to have a direct and harmful influence on psychological well-being. MATERIALS AND METHODS: A structured and validated questionnaire was transcribed and administered online. A nonrepresentative sample of 497 female college students in a North Indian city participated in the study. Digital eye strain, quality of sleep, and feeling of loneliness scores were assessed using latent class analysis. RESULTS: The selected latent model suggested that Class 2 had a high percentage of students with network issues, the problem with space and noise, and various financial hardships, which had almost doubled the rate of loneliness (53.28%) and sleep-wake difficulties (75.41%) among the students affected with computer vision syndrome (89.75%). CONCLUSION: There is an urgent need to examine the implications of digital exposure across gender and age to prevent future complications. Further, awareness for improving holistic well-being in the digital era should be promoted through various platforms.

Role of pyruvate kinase M2 in oxidized LDL-induced macrophage foam cell formation and inflammation.

Pyruvate kinase M2 (PKM2) links metabolic and inflammatory dysfunction in atherosclerotic coronary artery disease; however, its role in oxidized LDL (Ox-LDL)-induced macrophage foam cell formation and inflammation is unknown and therefore was studied. In recombinant mouse granulocyte-macrophage colony-stimulating factor-differentiated murine bone marrow-derived macrophages, early (1-6 h) Ox-LDL treatment induced PKM2 tyrosine 105 phosphorylation and promotes its nuclear localization. PKM2 regulates aerobic glycolysis and inflammation because PKM2 shRNA or Shikonin abrogated Ox-LDL-induced hypoxia-inducible factor-1α target genes lactate dehydrogenase, glucose transporter member 1, interleukin 1ß (IL-1ß) mRNA expression, lactate, and secretory IL-1ß production. PKM2 inhibition significantly increased Ox-LDL-induced ABCA1 and ABCG1 protein expression and NBD-cholesterol efflux to apoA1 and HDL. PKM2 shRNA significantly inhibited Ox-LDL-induced CD36, FASN protein expression, DiI-Ox-LDL binding and uptake, and cellular total cholesterol, free cholesterol, and cholesteryl ester content. Therefore, PKM2 regulates lipid uptake and efflux. DASA-58, a PKM2 activator, downregulated LXR-α, ABCA1, and ABCG1, and augmented FASN and CD36 protein expression. Peritoneal macrophages showed similar results. Ox-LDL induced PKM2- SREBP-1 interaction and FASN expression in a PKM2-dependent manner. Therefore, this study suggests a role for PKM2 in Ox-LDL-induced aerobic glycolysis, inflammation, and macrophage foam cell formation.

IRAK regulates macrophage foam cell formation by modulating genes involved in cholesterol uptake and efflux.

Interleukin-1 receptor-associated kinase-1 (IRAK1) is linked to the pathogenesis of atherosclerosis; however, its role in macrophage foam cell formation is not known. Therefore, the present study investigated the role of IRAK1 in lipid uptake, biosynthesis, and efflux in THP-1 derived macrophages and human monocyte-derived macrophages (HMDMs). Ox-LDL (40 µg/mL, 15 minutes-48 hours) treatment induced time-dependent increase in IRAK1, IRAK4, and Stat1 activation in THP-1 derived macrophages. IRAK1/4 inhibitor (INH) or IRAK1 siRNA significantly attenuated cholesterol accumulation, DiI-Ox-LDL binding, and uptake while cholesterol efflux to apoAI and HDL was enhanced in THP-1 derived macrophages and HMDMs. Ox-LDL treatment significantly increased the mRNA expression of CD36, LOX-1, SR-A, ABCA1, ABCG1, Caveolin-1, CYP27A1 while that of SR-BI was decreased. IRAK1/4 inhibition or IRAK1 knockdown, however, attenuated Ox-LDL-induced CD36 expression; augmented ABCA1 and ABCG1 expression while expression of others was unaffected in THP-1 derived macrophages and HMDMs. Moreover, IRAK1/4 inhibition had no significant effect on genes involved in lipid biosynthesis. In IRAK1/4 INH pre-treated THP-1 derived macrophages Ox-LDL-induced Stat1 phosphorylation and its binding to CD36 promoter was significantly attenuated while LXRα expression and its binding to the ABCA1/ABCG1 locus, NFATc2 activation and its binding to ABCA1 locus was enhanced. The present study thus demonstrates that IRAK regulates lipid accumulation by modulating CD36-mediated uptake and ABCA1-, ABCG1-dependent cholesterol efflux. Therefore, IRAK1 can be a potential target for preventing macrophage foam cell formation.

Curcuma oil attenuates accelerated atherosclerosis and macrophage foam-cell formation by modulating genes involved in plaque stability, lipid homeostasis and inflammation.

In the present study, the anti-atherosclerotic effect and the underlying mechanism of curcuma oil (C. oil), a lipophilic fraction from turmeric (Curcuma longa L.), was evaluated in a hamster model of accelerated atherosclerosis and in THP-1 macrophages. Male golden Syrian hamsters were subjected to partial carotid ligation (PCL) or FeCl3-induced arterial oxidative injury (Ox-injury) after 1 week of treatment with a high-cholesterol (HC) diet or HC diet plus C. oil (100 and 300 mg/kg, orally). Hamsters fed with the HC diet were analysed at 1, 3 and 5 weeks following carotid injury. The HC diet plus C. oil-fed group was analysed at 5 weeks. In hyperlipidaemic hamsters with PCL or Ox-injury, C. oil (300 mg/kg) reduced elevated plasma and aortic lipid levels, arterial macrophage accumulation, and stenosis when compared with those subjected to arterial injury alone. Similarly, elevated mRNA transcripts of matrix metalloproteinase-2 (MMP-2), MMP-9, cluster of differentiation 45 (CD45), TNF-α, interferon-γ (IFN-γ), IL-1ß and IL-6 were reduced in atherosclerotic arteries, while those of transforming growth factor-ß (TGF-ß) and IL-10 were increased after the C. oil treatment (300 mg/kg). The treatment with C. oil prevented HC diet- and oxidised LDL (OxLDL)-induced lipid accumulation, decreased the mRNA expression of CD68 and CD36, and increased the mRNA expression of PPARα, LXRα, ABCA1 and ABCG1 in both hyperlipidaemic hamster-derived peritoneal and THP-1 macrophages. The administration of C. oil suppressed the mRNA expression of TNF-α, IL-1ß, IL-6 and IFN-γ and increased the expression of TGF-ß in peritoneal macrophages. In THP-1 macrophages, C. oil supplementation prevented OxLDL-induced production of TNF-α and IL-1ß and increased the levels of TGF-ß. The present study shows that C. oil attenuates arterial injury-induced accelerated atherosclerosis, inflammation and macrophage foam-cell formation.

PKCδ-IRAK1 axis regulates oxidized LDL-induced IL-1ß production in monocytes.

This study examined the role of interleukin (IL)-1 receptor-associated kinase (IRAK) and protein kinase C (PKC) in oxidized LDL (Ox-LDL)-induced monocyte IL-1ß production. In THP1 cells, Ox-LDL induced time-dependent secretory IL-1ß and IRAK1 activity; IRAK4, IRAK3, and CD36 protein expression; PKCδ-JNK1 phosphorylation; and AP-1 activation. IRAK1/4 siRNA and inhibitor (INH)-attenuated Ox-LDL induced secreted IL-1ß and pro-IL-1ß mRNA and pro-IL-1ß and mature IL-1ß protein expression, respectively. Diphenyleneiodonium chloride (NADPH oxidase INH) and N-acetylcysteine (free radical scavenger) attenuated Ox-LDL-induced reactive oxygen species generation, caspase-1 activity, and pro-IL-1ß and mature IL-1ß expression. Ox-LDL-induced secretory IL-1ß production was abrogated in the presence of JNK INH II, Tanshinone IIa, Ro-31-8220, Go6976, Rottlerin, and PKCδ siRNA. PKCδ siRNA attenuated the Ox-LDL-induced increase in IRAK1 kinase activity, JNK1 phosphorylation, and AP-1 activation. In THP1 macrophages, CD36, toll-like receptor (TLR)2, TLR4, TLR6, and PKCδ siRNA prevented Ox-LDL-induced PKCδ and IRAK1 activation and IL-1ß production. Enhanced Ox-LDL and IL-1ß in systemic inflammatory response syndrome (SIRS) patient plasma demonstrated positive correlation with each other and with disease severity scores. Ox-LDL-containing plasma induced PKCδ and IRAK1 phosphorylation and IL-1ß production in a CD36-, TLR2-, TLR4-, and TLR6-dependent manner in primary human monocytes. Results suggest involvement of CD36, TLR2, TLR4, TLR6, and the PKCδ-IRAK1-JNK1-AP-1 axis in Ox-LDL-induced IL-1ß production.

Vagus nerve stimulation modulates distinct acetylcholine receptors on B cells and limits the germinal center response.

Acetylcholine is produced in the spleen in response to vagus nerve activation; however, the effects on antibody production have been largely unexplored. Here, we use a chronic vagus nerve stimulation (VNS) mouse model to study the effect of VNS on T-dependent B cell responses. We observed lower titers of high-affinity IgG and fewer antigen-specific germinal center (GC) B cells. GC B cells from chronic VNS mice exhibited altered mRNA and protein expression suggesting increased apoptosis and impaired plasma cell differentiation. Follicular dendritic cell (FDC) cluster dispersal and altered gene expression suggested poor function. The absence of acetylcholine-producing CD4+ T cells diminished these alterations. In vitro studies revealed that α7 and α9 nicotinic acetylcholine receptors (nAChRs) directly regulated B cell production of TNF, a cytokine crucial to FDC clustering. α4 nAChR inhibited coligation of CD19 to the B cell receptor, presumably decreasing B cell survival. Thus, VNS-induced GC impairment can be attributed to distinct effects of nAChRs on B cells.

Curcuma oil ameliorates hyperlipidaemia and associated deleterious effects in golden Syrian hamsters.

Essential oil components from turmeric (Curcuma longa L.) are documented for neuroprotective, anti-cancer, anti-thrombotic and antioxidant effects. The present study aimed to investigate the disease-modifying potential of curcuma oil (C. oil), a lipophilic component from C. longa L., in hyperlipidaemic hamsters. Male golden Syrian hamsters were fed a chow or high-cholesterol (HC) and fat-rich diet with or without C. oil (30, 100 and 300 mg/kg) for 28 d. In HC diet-fed hamsters, C. oil significantly reduced plasma total cholesterol, LDL-cholesterol and TAG, and increased HDL-cholesterol when compared with the HC group. Similar group comparisons showed that C. oil treatment reduced hepatic cholesterol and oxidative stress, and improved liver function. Hyperlipidaemia-induced platelet activation, vascular dysfunction and repressed eNOS mRNA expression were restored by the C. oil treatment. Furthermore, aortic cholesterol accumulation and CD68 expression were also reduced in the C. oil-treated group. The effect of C. oil at 300 mg/kg was comparable with the standard drug ezetimibe. Delving into the probable anti-hyperlipidaemic mechanism at the transcript level, the C. oil-treated groups fed the chow and HC diets were compared with the chow diet-fed group. The C. oil treatment significantly increased the hepatic expression of PPARa, LXRa, CYP7A1, ABCA1, ABCG5, ABCG8 and LPL accompanied by reduced SREBP-2 and HMGCR expression. C. oil also enhanced ABCA1, ABCG5 and ABCG8 expression and suppressed NPC1L1 expression in the jejunum. In the present study, C. oil demonstrated an anti-hyperlipidaemic effect and reduced lipid-induced oxidative stress, platelet activation and vascular dysfunction. The anti-hyperlipidaemic effect exhibited by C. oil seems to be mediated by the modulation of PPARa, LXRa and associated genes involved in lipid metabolism and transport.

Circulating MicroRNAs: Diagnostic Value as Biomarkers in the Detection of Non-alcoholic Fatty Liver Diseases and Hepatocellular Carcinoma.

Non-alcoholic fatty liver disease (NAFLD), a metabolic-related disorder, is the most common cause of chronic liver disease which, if left untreated, can progress from simple steatosis to advanced fibrosis and eventually cirrhosis or hepatocellular carcinoma, which is the leading cause of hepatic damage globally. Currently available diagnostic modalities for NAFLD and hepatocellular carcinoma are mostly invasive and of limited precision. A liver biopsy is the most widely used diagnostic tool for hepatic disease. But due to its invasive procedure, it is not practicable for mass screening. Thus, noninvasive biomarkers are needed to diagnose NAFLD and HCC, monitor disease progression, and determine treatment response. Various studies indicated that serum miRNAs could serve as noninvasive biomarkers for both NAFLD and HCC diagnosis because of their association with different histological features of the disease. Although microRNAs are promising and clinically useful biomarkers for hepatic diseases, larger standardization procedures and studies are still required.

Perception of college-going girls towards corneal donation in North India: A latent class analysis study.

Purpose: To assess the perception of college-going girls toward corneal donation in Northern India. Methods: An online survey with a pre-structured, pre-validated questionnaire was conducted on 1721 college-going girls in Northern India. The knowledge and attitude scores were regressed, and latent class analysis was carried out. Results: The average of scores for all participants was computed individually for the knowledge questions and the attitude questions, and based on this score, total participants were divided into two groups: Better corneal donation behaviors (BCDB) and poor corneal donation behaviors. The binomial logistic regression model of knowledge domain for predicting BCDB, age of the participant, their awareness about corneal donation, and willingness to discuss eye donation among family members were found significant. Similarly, for the attitude domain, awareness about corneal donation, knowledge about hours within which ideal eye donation needs to be undertaken, and knowledge about eye donation during coronavirus disease 2019 (COVID-19) pandemic were found to be significant. Latent class analysis identified one subset of participants having poorer knowledge and attitude scores and that they were more from a rural background, were having more than first order as birth order, were belonging to SC/ST classes, had illiterate or secondary education of father and mother, and were living in rented houses. Conclusion: The findings of the study significantly contribute to devising a mechanism to improve knowledge and influencing the attitude about eye donation among the youth, especially young women, who can act as counselors and motivators for the masses as well as their own families, in the generations to come.

How technological innovation and electricity consumption affect environmental quality? A road map towards achieving environmental sustainability.

Still the world witnessed an upturn in environmental degradation in spite of commitment to climate change across the nations. However, this study attempts to examine linkages among environmental degradation, technological innovation, and electricity consumption in India from 1981 to 2018 using time series data. To examine the long-run equilibrium relationship among the studied variables, we used robust econometric methods such as the autoregressive distributed lag (ARDL), fully modified ordinary least square (FMOLS), and dynamic ordinary least square (DOLS) methods. Furthermore, Granger causality also investigates through the vector error correction model (VECM) model, to assess inter-connotation among the underlying variables. From our empirical findings, urbanization, financial development, and technological innovation have a negative impact on carbon emissions, indicating long-term improvements in environmental quality. While economic development and electricity consumption are deteriorating environmental quality in India. The study's findings suggest that policymakers should prioritize renewable energy, which decreases environmental damage without impeding economic growth.

Clinical Efficacy of Remdesivir and Favipiravir in the Treatment of COVID-19 Patients: Scenario so far.

The novel SARS-CoV-2 is a new disease that has caused severe destruction to human lives across the globe, including infection, mortality and financial crises, for which, scientific researchers have been directed towards the development of treatment and controlling measures against coronavirus. Currently, there has been no approved drug for the treatment of the disease, but several antiviral drugs have shown therapeutic effects from which, remdesivir and favipiravir are two such drugs. These drugs have shown some therapeutic potential in the treatment of COVID-19 by inhibiting viral enzyme RNA-dependent RNA polymerase. The purpose of this systematic review is to provide an overview of the effectiveness of these two drugs based on the clinical trials reported in current published data.

Association of screen time, quality of sleep and dry eye in college-going women of Northern India.

PURPOSE: To evaluate the association of daily screen time and quality of sleep with the prevalence of dry eye among college-going women. METHODS: This study was a cross-sectional, comparative questionnaire-based study of 547 college-going women in northern India. A 10-item Mini Sleep Questionnaire was used to check the quality of sleep, and the Standard Patient Evaluation of Eye Dryness (SPEED) scale was used to examine the prevalence of dry eye among college-going women. RESULTS: Multinomial logistic regression showed a significant association between dry eye with daily screen time spent (P < 0.05) and the quality of sleep (P < 0.05) among college-going girls. Using Latent Class Analysis, two latent classes were selected based on the Bayesian Information Criteria. It was found that the majority population falls in class two and was having Severe Sleep-Wake difficulty. It was seen that the participants in class two belonged to the age bracket of 18-21 years, were from stream Humanities, education of father and mother equal to graduation, father working only, belonging to the nuclear family, having one sibling, hailing from the urban locality, spending more than 6 h daily on-screen, a majority of them using mobile phones, not using eye lubricants, and reported an increase in screen time during COVID-19. CONCLUSION: Dry eye and sleep quality are essential global health issues, and coupled with increased screen time, may pose a challenge in the present era. Preventive strategies need to be incorporated in school and college curriculums to promote physical, social, and psychological well-being and quality of life.

Follicular dendritic cell dysfunction contributes to impaired antigen-specific humoral responses in sepsis-surviving mice.

Sepsis survivors exhibit impaired responsiveness to antigen (Ag) challenge associated with increased mortality from infection. The contribution of follicular dendritic cells (FDCs) in the impaired humoral response in sepsis-surviving mice is investigated in this study. We demonstrated that mice subjected to sepsis from cecal ligation and puncture (CLP mice) have reduced NP-specific high-affinity class-switched Ig antibodies (Abs) compared with sham-operated control mice following immunization with the T cell-dependent Ag, NP-CGG. NP-specific germinal center (GC) B cells in CLP mice exhibited reduced TNF-α and AID mRNA expression compared with sham-operated mice. CLP mice showed a reduction in FDC clusters, a reduced binding of immune complexes on FDCs, and reduced mRNA expression of CR2, ICAM-1, VCAM-1, FcγRIIB, TNFR1, IKK2, and LTßR compared with sham-operated mice. Adoptive transfer studies showed that there was no B cell-intrinsic defect. In summary, our data suggest that the reduced Ag-specific Ab response in CLP mice is secondary to a disruption in FDC and GC B cell function.

Constitutive Vagus Nerve Activation Modulates Immune Suppression in Sepsis Survivors.

Patients surviving a septic episode exhibit persistent immune impairment and increased mortality due to enhanced vulnerability to infections. In the present study, using the cecal ligation and puncture (CLP) model of polymicrobial sepsis, we addressed the hypothesis that altered vagus nerve activity contributes to immune impairment in sepsis survivors. CLP-surviving mice exhibited less TNFα in serum following administration of LPS, a surrogate for an infectious challenge, than control-operated (control) mice. To evaluate the role of the vagus nerve in the diminished response to LPS, mice were subjected to bilateral subdiaphragmatic vagotomy at 2 weeks post-CLP. CLP-surviving vagotomized mice exhibited increased serum and tissue TNFα levels in response to LPS-challenge compared to CLP-surviving, non-vagotomized mice. Moreover, vagus nerve stimulation in control mice diminished the LPS-induced TNFα responses while having no effect in CLP mice, suggesting constitutive activation of vagus nerve signaling in CLP-survivors. The percentage of splenic CD4+ ChAT-EGFP+ T cells that relay vagus signals to macrophages was increased in CLP-survivors compared to control mice, and vagotomy in CLP-survivors resulted in a reduced percentage of ChAT-EGFP+ cells. Moreover, CD4 knockout CLP-surviving mice exhibited an enhanced LPS-induced TNFα response compared to wild-type mice, supporting a functional role for CD4+ ChAT+ T cells in mediating inhibition of LPS-induced TNFα responses in CLP-survivors. Blockade of the cholinergic anti-inflammatory pathway with methyllcaconitine, an α7 nicotinic acetylcholine receptor antagonist, restored LPS-induced TNFα responses in CLP-survivors. Our study demonstrates that the vagus nerve is constitutively active in CLP-survivors and contributes to the immune impairment.

A Standardized Chemically Modified Curcuma longa Extract Modulates IRAK-MAPK Signaling in Inflammation and Potentiates Cytotoxicity.

The TLR/IL-1R pathway is a critical signaling module that is misregulated in pathologies like inflammation and cancer. Extracts from turmeric (Curcuma longa L.) enriched in curcumin and carbonyls like turmerones have been shown to exert potent anti-inflammatory effects. The present study evaluated the anti-inflammatory activity, cytotoxic effect and the underlying mechanism of a novel chemically modified, non-carbonyl compound enriched Curcuma longa L. (C. longa) extract (CMCE). CMCE (1 or 10 µg/mL; 14 h) significantly decreased LPS (50-100 ng/mL) induced TNF-α and IL-1ß production in THP-1 cells, human, and mouse whole blood as measured by ELISA. LPS-induced IRAK1, MAPK activation, TLR4 expression, TLR4-MyD88 interaction, and IκBα degradation were significantly reduced in CMCE pre-treated THP-1 cells as assessed by Western blotting. CMCE (30, 100, and 300 mg/kg; 10 days p.o.) pre-treated and LPS (10 mg/kg) challenged Swiss mice exhibited attenuated plasma TNF-α, IL-1ß, nitrite, aortic iNOS expression, and vascular dysfunction. In a PI permeability assay, cell lines derived from acute myeloid leukemia were most sensitive to the cytotoxic effects of CMCE. Analysis of Sub-G1 phase, Annexin V-PI positivity, loss of mitochondrial membrane potential, increased caspase-3, and PARP-1 activation confirmed CMCE induced apoptosis in HL-60 cells. IRAK inhibition also sensitized HL-60 cells to CMCE induced cytotoxicity. The present study defines the mechanism underlying the action of CMCE and suggests a therapeutic potential for its use in sepsis and leukemia.

Evaluation of non-surgical therapy on glutathione levels in chronic periodontitis.

OBJECTIVE: To compare the levels of glutathione (GSH), both oxidized and reduced forms in patients with and without chronic periodontitis in gingival crevicular fluid (GCF). MATERIALS AND METHODS: Twenty GCF samples from maxillary quadrants were collected using capillary micropipettes from the chronic periodontitis patients (test group) at baseline before treatment, at 1-month, 3 months, and 6 months after scaling and root planing and samples from 20 patients without chronic periodontitis (control group) from maxillary quadrants were also collected. GSH, oxidized glutathione (GSSG) levels and GSH: GSSG ratios were determined using the spectrophotometric method. STATISTICAL ANALYSIS: Results were concluded for the test over control groups using paired Student's t-test. RESULTS: Lower concentrations of GSH (P < 0.001) and GSSG (P < 0.001) were detected in GCF in patients with chronic periodontitis (test group) than patients without chronic periodontitis (control group) at baseline. Treatment had a significant effect in improving the GSH and reducing GSSG levels postscaling and root planing at 1-month and 3 months but not significant effect at 6 months. Scaling and root planing increased the GSH: GSSG ratio (P < 0.001) in the test group as compared to the control group (P < 0.001). CONCLUSIONS: The concentrations of GSH within GCF are reduced in chronic periodontitis patients. Scaling and root planing (nonsurgical therapy) restores GSH concentration in GCF post 1-month and 3 months along with redox balance (GSH: GSSG ratio), but at 6 months the balance is not maintained. Adjunctive use of micronutritional supplements to boost antioxidant concentration in tissues by preserving GSH or by elevating its level at the inflamed sites is recommended, as nonsurgical periodontal therapy alone is not able to maintain redox balance for longer duration.

Silymarin ameliorates fructose induced insulin resistance syndrome by reducing de novo hepatic lipogenesis in the rat.

High dietary fructose causes insulin resistance syndrome (IRS), primarily due to simultaneous induction of genes involved in glucose, lipid and mitochondrial oxidative metabolism. The present study evaluates effect of a hepatoprotective agent, silymarin (SYM) on fructose-induced metabolic abnormalities in the rat and also assessed the associated thrombotic complications. Wistar rats were kept on high fructose (HFr) diet throughout the 12-week study duration (9 weeks of HFr feeding and subsequently 3 weeks of HFr plus SYM oral administration [once daily]). SYM treatment significantly reduced the HFr diet-induced increase expression of peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α/ß, peroxisome proliferator-activated receptor (PPAR)-α, forkhead box protein O1 (FOXO1), sterol regulatory element binding protein (SREBP)-1c, liver X receptor (LXR)-ß, fatty acid synthase (FAS) and PPARγ genes in rat liver. SYM also reduced HFr diet mediated increase in plasma triglycerides (TG), non-esterified fatty acids (NEFA), uric acid, malondialdehyde (MDA), total nitrite and pro-inflammatory cytokines (C-reactive protein [CRP], interleukin-6 [IL-6], interferon-gamma [IFN-γ] and tumor necrosis factor [TNF]) levels. Moreover, SYM ameliorated HFr diet induced reduction in glucose utilization and endothelial dysfunction. Additionally, SYM significantly reduced platelet activation (adhesion and aggregation), prolonged ferric chloride-induced blood vessel occlusion time and protected against exacerbated myocardial ischemia reperfusion (MI-RP) injury. SYM treatment prevented HFr induced mRNA expression of hepatic PGC-1α/ß and also its target transcription factors which was accompanied with recovery in insulin sensitivity and reduced propensity towards thrombotic complications and aggravated MI-RP injury.