Purified black tea theaflavins and theaflavins/catechin supplements did not affect serum lipids in healthy individuals with mildly to moderately elevated cholesterol concentrations.

Background: Ingestion of tea flavonoids found in both green and black tea is linked to cardiovascular health benefits such as lowering serum lipids. Evidence for a cholesterol-lowering benefit of green or black tea consumption from human intervention studies is, however, conflicting and active components responsible for the effect have not yet been clearly identified.

Aim Of The Study: In a randomized, double-blind, placebo-controlled, parallel design study the effects of ingesting a purified black tea theaflavins (TFs) powder alone or in combination with catechin (TFs/catechins) on lowering serum total (TC) and LDL-cholesterol (LDL-c) were assessed.

Black tea consumption dose-dependently improves flow-mediated dilation in healthy males.

Objectives: Flavonoids may protect against cardiovascular disease. Tea is a major source of dietary flavonoids. Studies indicate black tea improves endothelial function but data on arterial haemodynamics, blood pressure (BP) and insulin resistance are equivocal.

Plant sterol-enriched milk tea decreases blood cholesterol concentrations in Chinese adults: a randomised controlled trial.

The cholesterol-lowering effects of plant sterols in a format suitable for use in China have not previously been investigated. We conducted the study to quantify in adult Chinese the effects on blood lipid concentrations of a plant sterol-enriched milk tea powder. The study was a double-blind, randomised trial in which 309 participants were randomised to receive daily 2.

Cholesterol ester transfer protein (CETP) Taq1B polymorphism influences the effect of a standardized cardiac rehabilitation program on lipid risk markers.

Cardiac rehabilitation programs (CR) are standard treatment for patients with coronary artery disease (CAD), yet a large variation in risk factor and lipoprotein changes exists. We investigated the role of three common genetic polymorphisms (CETP Taq1B, LIPC -514 and apo E) associated with alterations of lipoprotein metabolism, in patients before and after standardized CR. Three-hundred and seven patients were recruited for this study.

Lipopolysaccharide is transferred from high-density to low-density lipoproteins by lipopolysaccharide-binding protein and phospholipid transfer protein.

Lipopolysaccharide (LPS), the major outer membrane component of gram-negative bacteria, is a potent endotoxin that triggers cytokine-mediated systemic inflammatory responses in the host. Plasma lipoproteins are capable of LPS sequestration, thereby attenuating the host response to infection, but ensuing dyslipidemia severely compromises this host defense mechanism. We have recently reported that Escherichia coli J5 and Re595 LPS chemotypes that contain relatively short O-antigen polysaccharide side chains are efficiently redistributed from high-density lipoproteins (HDL) to other lipoprotein subclasses in normal human whole blood (ex vivo).

The cholesteryl ester transfer protein Taq1B gene polymorphism predicts clinical benefit of statin therapy in patients with significant coronary artery disease.

Background: Cholesteryl ester transfer protein (CETP) regulates plasma lipid distribution. A polymorphism in the CETP gene (Taq1B) is associated with CETP activity, HDL concentration, atherosclerosis progression, and response to statins, and may influence cardiovascular (CV) events. We studied CETP Taq1B genotype, plasma HDL, and clinical events among all patients and patients stratified by statin treatment.

A novel LCAT mutation (Phe382-->Val) in a kindred with familial LCAT deficiency and defective apolipoprotein B-100.

We studied a four-generation family (17 subjects) with familial lecithin:cholesterol acyltransferase (LCAT) deficiency. A 30-year-old Caucasian male with corneal clouding and HDL cholesterol <0.1 mmol/l was a compound heterozygote for a novel mutation (Phe(382)-->Val), a previously reported mutation (Thr321-->Met) and a common variant (Thr208-->Ser) of the gene.

Transcriptional regulation of the elafin gene in human keratinocytes.

Elafin (also known as skin-derived anti-leukoproteinase/trappin-2) is an epithelial host-defense protein that is absent in normal skin but highly induced in keratinocytes of inflamed skin (e.g., psoriasis), in epidermal skin tumors, and after wounding.

ATP binding cassette G5 C1950G polymorphism may affect blood cholesterol concentrations in humans.

ATP binding cassette protein G5 (ABCG5) and G8 (ABCG8) may be involved in the regulation of intestinal cholesterol absorption. Therefore, genetic variation at these loci may affect blood cholesterol concentrations by influencing dietary responsiveness. We studied the association between the ABCG5 C1950G (Gln640Glu) polymorphism and blood cholesterol concentrations in 486 subjects and responsiveness to dietary cholesterol in 99 participants in dietary trials.

Nevirapine-containing antiretroviral therapy in HIV-1 infected patients results in an anti-atherogenic lipid profile.

Background: Protease inhibitor-containing antiretroviral therapy for the treatment of HIV-1 infection is associated with elevated triglyceride and low-density lipoprotein (LDL)-cholesterol levels which may expose patients to an increased risk of coronary artery disease (CAD). We report the lipid and lipoprotein profiles of a representative subset of treatment-naive patients included in the Atlantic Study. This study compares patients treated with stavudine and didanosine plus the random addition of either the non-nucleoside reverse transcriptase inhibitor nevirapine (NVP), the protease inhibitor indinavir or the nucleoside reverse transcriptase inhibitor lamivudine.

Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease.

Background: Low plasma HDL cholesterol (HDL-C) is associated with an increased risk of coronary artery disease (CAD). We recently identified the ATP-binding cassette transporter 1 (ABCA1) as the major gene underlying the HDL deficiency associated with reduced cholesterol efflux. Mutations within the ABCA1 gene are associated with decreased HDL-C, increased triglycerides, and an increased risk of CAD.

Age and residual cholesterol efflux affect HDL cholesterol levels and coronary artery disease in ABCA1 heterozygotes.

We and others have recently identified mutations in the ABCA1 gene as the underlying cause of Tangier disease (TD) and of a dominantly inherited form of familial hypoalphalipoproteinemia (FHA) associated with reduced cholesterol efflux. We have now identified 13 ABCA1 mutations in 11 families (five TD, six FHA) and have examined the phenotypes of 77 individuals heterozygous for mutations in the ABCA1 gene. ABCA1 heterozygotes have decreased HDL cholesterol (HDL-C) and increased triglycerides.

Biochemical and compositional analyses of recombinant lecithin:cholesterol acyltransferase (LCAT) obtained from a hepatic source.

Lecithin:cholesterol acyltransferase (LCAT) is an important plasma glycoprotein which plays a central role in lipid metabolism. This protein is responsible for generation of cholesteryl esters in plasma and it has been proposed to play a pivotal role in the reverse cholesterol transport pathway. Structural and functional studies of LCAT have employed various expression systems for production of recombinant LCAT (rLCAT).

Mutations in the ABC1 gene in familial HDL deficiency with defective cholesterol efflux.

Background: A low concentration of HDL cholesterol is the most common lipoprotein abnormality in patients with premature atherosclerosis. We have shown that Tangier disease, a rare and severe form of HDL deficiency characterised by a biochemical defect in cellular cholesterol efflux, is caused by mutations in the ATP-binding-cassette (ABC1) gene. This gene codes for the cholesterol-efflux regulatory protein (CERP).

Mutations in ABC1 in Tangier disease and familial high-density lipoprotein deficiency.

Genes have a major role in the control of high-density lipoprotein (HDL) cholesterol (HDL-C) levels. Here we have identified two Tangier disease (TD) families, confirmed 9q31 linkage and refined the disease locus to a limited genomic region containing the gene encoding the ATP-binding cassette transporter (ABC1). Familial HDL deficiency (FHA) is a more frequent cause of low HDL levels.

Assignment of Tangier disease to chromosome 9q31 by a graphical linkage exclusion strategy.

A low level of high density lipoprotein (HDL) cholesterol is a strong predictor of ischaemic heart disease (IHD) and myocardial infarction. One cause of low HDL-cholesterol is Tangier disease (TD), an autosomal codominant inherited condition first described in 1961 in two siblings on Tangier Island in the United States of America. Apart from low HDL-cholesterol levels and an increased incidence of atherosclerosis, TD is characterized by reduced total cholesterol, raised triglycerides, peripheral neuropathy and accumulation of cholesteryl esters in macrophages, which causes enlargement of the liver, spleen and tonsils.

SKALP/elafin gene polymorphisms are not associated with pustular forms of psoriasis.

Psoriasis is a multifactorial skin disease characterised by epidermal abnormalities and infiltration by lymphocytes and polymorphonuclear leukocytes (PMN). Skin-derived antileukoproteinase (SKALP), also known as elafin, is a potent inhibitor of human leukocyte elastase and proteinase 3, two PMN-derived proteinases implicated in tissue destruction and leukocyte migration. We have shown that, at least at the protein level, SKALP is significantly decreased in lesional skin of patients with pustular psoriasis compared with plaque-type psoriasis.

Simultaneous detection and strain differentiation of Mycobacterium tuberculosis for diagnosis and epidemiology.

Widespread use of DNA restriction fragment length polymorphism (RFLP) to differentiate strains of Mycobacterium tuberculosis to monitor the transmission of tuberculosis has been hampered by the need to culture this slow-growing organism and by the level of technical sophistication needed for RFLP typing. We have developed a simple method which allows simultaneous detection and typing of M. tuberculosis in clinical specimens and reduces the time between suspicion of the disease and typing from 1 or several months to 1 or 3 days.

Structural, biochemical, and cell biological aspects of the serine proteinase inhibitor SKALP/elafin/ESI.

Skin-derived antileukoproteinase, also described as elafin or as elastase specific inhibitor, is a serine proteinase inhibitor which is thought to play a regulatory role in inflammation. Research in the last few years has increased our knowledge on the structural, biochemical, and cell biological aspects of this molecule. Here we will review the most relevant literature presently available on this proteinase inhibitor.

SKALP/elafin is an inducible proteinase inhibitor in human epidermal keratinocytes.

Skin-derived antileukoproteinase (SKALP), otherwise known as elafin, is a recently discovered epidermal proteinase inhibitor with specificity for polymorphonuclear leukocyte (PMN)-derived elastase and proteinase-3; in addition to the proteinase-inhibiting domain, SKALP contains several transglutaminase substrate motifs. SKALP is virtually absent in normal human epidermis but is found in a number of inflammatory skin diseases, including psoriasis. Here we report the induction and processing of SKALP in vivo and in vitro.

Assignment of the human gene encoding the epidermal serine proteinase inhibitor SKALP (PI3) to chromosome region 20q12-->q13.

Recently we isolated a cDNA clone corresponding to an epidermal serine proteinase inhibitor named SKALP (skin-derived antileukoproteinase). Here we report the chromosomal localization of the human gene encoding SKALP by Southern blot analysis of a panel of human x hamster hybrid cell lines and by nonradioactive in situ hybridization on R-banded human lymphocyte chromosome spreads. The SKALP-encoding gene has been assigned the approved symbol PI3 by the Human Gene Mapping nomenclature committee.

Differential expression of SKALP/Elafin in human epidermal tumors.

Recently we described a new epidermal serine proteinase inhibitor, skin-derived antileukoproteinase (SKALP), also known as elafin. SKALP/elafin was found to be absent in normal human epidermis, but can be induced in vitro and in vivo under hyperproliferative conditions. Here we studied the expression of SKALP/elafin in several types of epidermal tumors (basal cell carcinoma, squamous cell carcinoma, Bowen's disease, actinic keratosis, and keratoacanthoma).