lipase/뇌졸중

Cholesteryl ester transfer protein (CETP) and lipoprotein lipase (LPL) are both key players in plasma lipoprotein homeostasis and, as such, genetically induced alterations in their respective activities may affect susceptibility to cerebrovascular diseases. In this study, we examined the

The present study aimed to investigate the interaction between the Ser447Term polymorphism in the lipoprotein lipase (LPL) gene and some common risk factors for stroke. A total of 704 unrelated patients with ischemic stroke were recruited for genetic analysis; they were all of Han Chinese origin.

BACKGROUND Previous studies suggested lipoprotein lipase (LPL) Ser447Ter and Asn291Ser polymorphisms were associated with the risk of ischemic heart disease, however, their effects on ischemic stroke were controversial. A meta-analysis was performed to assess the associations between these two LPL

BACKGROUND Lipoprotein lipase (LPL) polymorphisms were suggested to be the risk factor for ischemic stroke (IS). However, controversial results were obtained. Our objective was to investigate the association of LPL polymorphisms at Ser447Ter, HindIII (+/-), and PvuII (+/-) with IS

OBJECTIVE Ischemic stroke is prevalent in type 2 diabetes and may be due to metabolic, vascular and inflammatory factors. Genetic variants implicated in these pathways may have joint effects on stroke risk. In this proof-of-concept study, we examined gene-gene interactions on risk of incident

BACKGROUND Lipoprotein lipase (LPL) plays an important role in plasma lipoprotein metabolism. The Ser447Ter mutation of LPL may be associated with ischemic cerebrovascular diseases. We investigated whether the LPL variants were related to risk of strokes in Chinese Hans. METHODS We recruited 160

OBJECTIVE To investigate the relevance between lipoprotein lipase (LPL) Hind III gene polymorphism and cerebral hemorrhage. METHODS A case-control study was performed utilizing PCR-RFLP method and sequencing of amplified products to detect LPL Hind III gene polymorphism in 350 cases of hemorrhagic

BACKGROUND MicroRNAs have emerged as important epigenetic regulators in cardiovascular diseases (CVDs). Using an observational meta-analysis design, we previously characterized a gain-of-function microRNA-410 target site polymorphism (rs13702T>C) in the 3'untranslated region of the lipoprotein

Ischaemic stroke is pathogenetically heterogeneous, but there is strong evidence that genetic as well as environment factors contribute to the risk of the individual. Here we report the similar distribution of polymorphic markers of the lipoprotein lipase (LPL) gene in 128 patients with ischaemic

Lipoprotein Lipase (LPL) is known to be a key enzyme for lipid metabolism specifically in an enzymatic glycoprotein which provide tissues without fatty-acids and eliminates triglycerides (TG) by the circulation. Mutations in LPL were proven to cause alteration in fractions within lipoprotein,

BACKGROUND Several studies have studied the relationship between lipoprotein lipase (LPL) HindIII gene polymorphism and stroke susceptibility. However, the conclusions remain controversial. To clarify the association of LPL gene HindIII polymorphism and stroke susceptibility, we therefore conducted

UNASSIGNED Stroke is the most common neurological disorder and genetic susceptibility has an important role in its etiology. Polymorphism in several genes such as lipoprotein lipase (LPL) is propounded as a risk for stroke. This meta-analysis investigated the association of rs285 and rs320 LPL

MAGL (monoacylglycerol lipase) is an enzyme that hydrolyzes the endocannabinoid 2-arachidonoylglycerol and regulates the production of arachidonic acid and prostaglandins-substances that mediate tissue inflammatory response. Here, we have studied the effects of the selective MAGL inhibitors JZL184

BACKGROUND Because apolipoprotein E (apoE) and lipopoprotein lipase (LPL) polymorphisms interact with each other and with other factors to affect lipid metabolism, we sought to determine their separate and combined effects in association with ischemic vascular disease. METHODS We performed a

There is evidence that most forms of ischaemic stroke (IS) result from synergistic effects of the modifiable predisposing factors and multiple genes. In the present work, we report results of case-control study of IS association with apolipoprotein E gene (APOE) (promoter and coding polymorphisms)