<b>Context:</b> Spinal cord injury or disease (SCI/D) leads to unchanged low-density lipoprotein and cholesterol, very low high-density lipoprotein a form of dyslipidemia and physical inactivity which combine to increase risk of morbidity and mortality from cardiometabolic disease.
<i>In vivo</i> ceramide reduction by inhibition of <i>de novo</i> ceramide synthesis reduced PLIN2 and hepatic steatosis in alcohol-fed mice, but only <i>de novo</i> synthesis inhibition, not sphingomyelin hydrolysis, improved glucose tolerance and dyslipidemia.
(1) Background: We analyzed, using PET-SCAN and cognitive tests, how growth hormone (GH) could act in the brain of an older woman, not deficient in GH, who showed mild cognitive alterations (MCI) and had a genotype of ApoE 4/3 and familial dyslipidemia.
5A5A and 5A6A genotypes of MMP-3 (odds ratio (OR) 1.5; P = 0.021), II and ID genotypes of ACE (OR 1.7; P = 0.006) along with traditional ischaemic heart disease risk factors such as smoking (OR 4.9; P = 0.001), hypertension (OR 2.0; P = 0.001), diabetes mellitus (OR 2.9; P = 0.001) and dyslipidaemia (OR 2.1; P = 0.001) increased the risk of STEMI.
5A5A and 5A6A genotypes of MMP-3 (odds ratio (OR) 1.5; P = 0.021), II and ID genotypes of ACE (OR 1.7; P = 0.006) along with traditional ischaemic heart disease risk factors such as smoking (OR 4.9; P = 0.001), hypertension (OR 2.0; P = 0.001), diabetes mellitus (OR 2.9; P = 0.001) and dyslipidaemia (OR 2.1; P = 0.001) increased the risk of STEMI.
Dyslipidemia and TAFIThr325Ile polymorphism were the main variables associated with recanalization resistance by the end of t-PA infusion: odds ratio (OR) 4.1 [95% confidence interval (95% CI) 1.6-10.8, P = 0.003] and OR 5.6 (95% CI 1.2-20, P = 0.031), respectively.
Dyslipidemia and TAFI Thr325Ile polymorphism were the main variables associated with recanalization resistance by the end of t-PA infusion: odds ratio (OR) 4.1 [95% confidence interval (95% CI) 1.6-10.8, P = 0.003] and OR 5.6 (95% CI 1.2-20, P = 0.031), respectively.
Dyslipidemia and apolipoprotein E4 (APOE ϵ4) allele are risk factors for age-related cognitive decline, but how these risks are modified by human immunodeficiency virus (HIV) infection is unclear.
Dyslipidaemia is key to colorectal carcinogenesis, and the prediction of baseline triglycerides (TG), total cholesterol (TC), high- and low-density lipoprotein cholesterol (HDLC and LDLC) for postsurgical colorectal cancer mortality has not been researched.
Dyslipidemia is the leading cause of atherosclerotic cardiovascular diseases (ASCVD) in T2D patients. hsa-miR-33 (miR-33) serves as a regulator in lipid metabolism.
Dyslipidemia caused significant (p < 0.05) increase in OS (lipid peroxidation, nitric oxide, and protein carbonyl), pro-inflammatory cytokine (CRP, IL-1β, MCP-1, and TNF-α), and eicosanoid (PGE<sub>2</sub>, LTB<sub>4</sub>, and LTC<sub>4</sub>) level in serum of both young and aged rats.
Dyslipidemia caused significant (p < 0.05) increase in OS (lipid peroxidation, nitric oxide, and protein carbonyl), pro-inflammatory cytokine (CRP, IL-1β, MCP-1, and TNF-α), and eicosanoid (PGE<sub>2</sub>, LTB<sub>4</sub>, and LTC<sub>4</sub>) level in serum of both young and aged rats.
Dyslipidemia caused significant (p < 0.05) increase in OS (lipid peroxidation, nitric oxide, and protein carbonyl), pro-inflammatory cytokine (CRP, IL-1β, MCP-1, and TNF-α), and eicosanoid (PGE<sub>2</sub>, LTB<sub>4</sub>, and LTC<sub>4</sub>) level in serum of both young and aged rats.
Dyslipidemia caused significant (p < 0.05) increase in OS (lipid peroxidation, nitric oxide, and protein carbonyl), pro-inflammatory cytokine (CRP, IL-1β, MCP-1, and TNF-α), and eicosanoid (PGE<sub>2</sub>, LTB<sub>4</sub>, and LTC<sub>4</sub>) level in serum of both young and aged rats.
Dyslipidemia is a common and persistent complication in children with CKD and it worsens in proportion to declining GFR, worsening proteinuria, and increasing BMI.