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Background and Purpose: Atherosclerotic remodeling of the aneurysm wall, which could be detected as aneurysm wall enhancement (AWE) by magnetic resonance–vessel wall imaging, is a part of degenerative change of unruptured intracranial aneurysms (UIAs). The purpose of this study was to determine whether the luminal concentrations of atherosclerotic proteins in the aneurysm sac were associated with increased wall enhancement of UIAs in vessel wall imaging. Methods: We performed a prospective study of subjects undergoing endovascular treatments for UIAs. All subjects underwent evaluation using 3T–magnetic resonance imaging, including pre/postcontrast vessel wall imaging of the UIAs. Blood samples were collected from the aneurysm sac and the parent artery during endovascular procedures. Presence/absence of AWE was correlated with the delta difference in concentration for each atherosclerotic protein between the lumen of UIA and in the parent artery. Results: A total of consecutive 17 patients with 19 UIAs were enrolled. The delta difference of lipoprotein(a) was significantly higher in UIAs with AWE compared with those without AWE (−6.9±16.0 versus −45.4±44.9 μg/mL, P =0.03). Conclusions: Higher luminal concentrations of lipoprotein(a) in the aneurysm sac were significantly associated with increased wall enhancement of UIAs. A larger study is needed to confirm these findings.

The present study aimed to review the literature regarding Coronavirus disease (COVID-19). Basic and clinical updates were reviewed. Coronaviruses are infections of both clinical and veterinary significance. Coronaviruses are single stranded RNA infections with a lipoprotein envelope and enter the host cells by a Class I combination protein, for example, one that doesn’t require some other viral surface proteins for combination. Clinical presentation of patients with Coronaviruses included cough, fever, headache. The age of patients in some cases was as early as 112 days. As a conclusion, although, the existence of widespread of Coronaviruses, vital information remains to be elucidated.

Background: Current lipid guidelines suggest measurement of Lp(a) (lipoprotein[a]) and ApoB (apolipoprotein B) for atherosclerotic cardiovascular disease risk assessment. Polygenic risk scores (PRSs) for Lp(a) and ApoB may identify individuals unlikely to have elevated Lp(a) or ApoB and thus reduce such suggested testing. Methods: PRSs were developed using least absolute shrinkage and selection operator regression among 273 222 and 356 958 UK Biobank participants of white British ancestry for Lp(a) and ApoB, respectively, and validated in separate sets of 60 771 UK Biobank and 15 050 European Prospective Investigation into Cancer and Nutrition-Norfolk participants. We then assessed the proportion of participants who, based on these PRSs, were unlikely to benefit from Lp(a) or ApoB measurements, according to current lipid guidelines. Results: In the UK Biobank and European Prospective Investigation into Cancer and Nutrition-Norfolk cohorts, the area under the receiver operating curve for the PRS-predicted Lp(a) and ApoB to identify individuals with elevated Lp(a) and ApoB was at least 0.91 (95% CI, 0.90–0.92) and 0.74 (95% CI, 0.73–0.75), respectively. The Lp(a) PRS and measured Lp(a) showed comparable association with atherosclerotic cardiovascular disease incidence, whereas the ApoB PRS was in general less predictive of atherosclerotic cardiovascular disease risk than measured ApoB. In the context of the European Society of Cardiology/European Atherosclerosis Society lipid guidelines, at a 95% sensitivity to identify individuals with elevated Lp(a) and ApoB levels, at least 54% of Lp(a) and 24% of ApoB testing could be reduced by prescreening with a PRS while maintaining a low false-negative rate. Conclusions: A substantial proportion of suggested testing for elevated Lp(a) and a modest proportion of testing for elevated ApoB could potentially be reduced by prescreening individuals with PRSs.

Genetic variation in apolipoprotein E (APOE) influences Alzheimer's disease (AD) risk. APOE e4 alleles are the strongest genetic risk factor for late onset sporadic AD. The AD risk is dose dependent, as those carrying one APOE e4 allele have a 2–3-fold increased risk, while those carrying two e4 alleles have a 10–15-fold increased risk. Individuals carrying APOE e2 alleles have lower AD risk and those carrying APOE e3 alleles have neutral risk. APOE is a lipoprotein which functions in lipid transport, metabolism, and inflammatory modulation. Isoform specific effects of APOE within the brain include alterations to Aβ, tau, neuroinflammation, and metabolism. Here we review the association of APOE with AD, the APOE isoform specific effects within brain and periphery, and potential therapeutics.

Background: Lp(a) (lipoprotein [a]) levels are higher in individuals of African ancestry (AA) than in individuals of European ancestry (EA). We examined associations of genetically predicted Lp(a) levels with (1) atherosclerotic cardiovascular disease subtypes: coronary heart disease, cerebrovascular disease, peripheral artery disease, and abdominal aortic aneurysm and (2) nonatherosclerotic cardiovascular disease phenotypes, stratified by ancestry. Methods: We performed (1) Mendelian randomization analyses for previously reported cardiovascular associations and (2) Mendelian randomization–phenome-wide association analyses for novel associations. Analyses were stratified by ancestry in electronic Medical Records and Genomics, United Kingdom Biobank, and Million Veteran Program cohorts separately and in a combined cohort of 804 507 EA and 103 580 AA participants. Results: In Mendelian randomization analyses using the combined cohort, a 1-SD genetic increase in Lp(a) level was associated with atherosclerotic cardiovascular disease subtypes in EA—odds ratio and 95% CI for coronary heart disease 1.28 (1.16–1.41); cerebrovascular disease 1.14 (1.07–1.21); peripheral artery disease 1.22 (1.11–1.34); abdominal aortic aneurysm 1.28 (1.17–1.40); in AA, the effect estimate was lower than in EA and nonsignificant for coronary heart disease 1.11 (0.99–1.24) and cerebrovascular disease 1.06 (0.99–1.14) but similar for peripheral artery disease 1.16 (1.01–1.33) and abdominal aortic aneurysm 1.34 (1.11–1.62). In EA, a 1-SD genetic increase in Lp(a) level was associated with aortic valve disorders 1.34 (1.10–1.62), mitral valve disorders 1.18 (1.09–1.27), congestive heart failure 1.12 (1.05–1.19), and chronic kidney disease 1.07 (1.01–1.14). In AA, no significant associations were noted for aortic valve disorders 1.08 (0.94–1.25), mitral valve disorders 1.02 (0.89–1.16), congestive heart failure 1.02 (0.95–1.10), or chronic kidney disease 1.05 (0.99–1.12). Mendelian randomization–phenome-wide association analyses identified novel associations in EA with arterial thromboembolic disease, nonaortic aneurysmal disease, atrial fibrillation, cardiac conduction disorders, and hypertension. Conclusions: Many cardiovascular associations of genetically increased Lp(a) that were significant in EA were not significant in AA. Lp(a) was associated with atherosclerotic cardiovascular disease in four major arterial beds in EA but only with peripheral artery disease and abdominal aortic aneurysm in AA. Additionally, novel cardiovascular associations were detected in EA.

Altres ajuts: Fondo Europeo de Desarrollo Regional (FEDER). Some lipoprotein disorders related to the residual risk of premature cardiovascular disease (PCVD) are not detected by the conventional lipid profile. In this case-control study, the predictive power of PCVD of serum sdLDL-C, measured using a lipoprotein precipitation method, and of the physicochemical properties of serum lipoproteins, analyzed by nuclear magnetic resonance (NMR) techniques, were evaluated. We studied a group of patients with a first PCVD event (n = 125) and a group of control subjects (n = 190). Conventional lipid profile, the size and number of Very Low Density Lipoproteins (VLDL), Low Density Lipoproteins (LDL), High Density Lipopro-teins (HDL) particles, and the number of particles of their subclasses (large, medium, and small) were measured. Compared to controls, PCVD patients had lower concentrations of all LDL parti-cles, and smaller and larger diameter of LDL and HDL particles, respectively. PCVD patients also showed higher concentrations of small dense LDL-cholesterol (sdLDL), and triglycerides (Tg) in LDL and HDL particles (HDL-Tg), and higher concentrations of large VLDL particles. Multivariate logistic regression showed that sdLDL-C, HDL-Tg, and large concentrations of LDL particles were the most powerful predictors of PCVD. A strong relationship was observed between increased HDL-Tg concentrations and PCVD. This study demonstrates that beyond the conventional lipid profile, PCVD patients have other atherogenic lipoprotein alterations that are detected by magnetic resonance imaging (MRI) analysis.

Low Density Lipoprotein (LDL) cholesterol is a lipoprotein compound that has low-density. Smoking activity can increase LDL cholesterol levels. The nicotine compound in cigarettes can increase the oxidation of LDL cholesterol that will cause atherosclerosis. This research used descriptive study. The purposed of this study was to known about the level of LDL cholesterol in active smoker serum at areas Banjar Taman, Darmasaba Village, Abiansemal, Badung. Sampels in this research are males active smoker aged 18 years old and over which amount to 30 sampels. That sampling using accidental sampling. Examination of LDL cholesterol using Calculated method. The result of LDL concentration on this research based on the characteristics of the respondens such as: normal concentration of LDL on the group of 18-40 years (60%), with time period of smoked less than 5 years (53.4%) and the light smokers category (36 , 7%). Concentration of LDL exceeded the normal limits found on the group of 18-40 years (23.3%), smoked with 6 until 10 years period have 16.7% and category of light smokers (26.7 %). The conclusion of this research , were: 66.7% have normal levels and 33.3% with over normal limits. Active smokers were expected to reduce or stop smoked habits for the better health quality.

Objective— Lp(a) [lipoprotein(a)] levels vary by race/ethnicity and were recently found to be associated with risk of heart failure (HF). We aimed to determine whether Lp(a)-related risk of HF is similar across different races and whether Lp(a) may further be related to HF with reduced ejection fraction or HF with preserved ejection fraction (HFpEF). Approach and Results— In 6809 participants of the MESA (Multi-Ethnic Study of Atherosclerosis), aged 45 to 84 years and free of cardiovascular disease, 308 incident HF events occurred during a median 13-year follow-up. Baseline Lp(a) concentrations were determined by immunoassay. Incident HF was adjudicated, distinguishing HF with reduced ejection fraction (ejection fraction, P =0.02); Lp(a) ≥30 mg/dL (HR, 1.69; P =0.01), Lp(a) ≥50 mg/dL (HR, 1.87; P =0.006). No significant relations were found in black, Hispanic, or Chinese participants, and significant race interactions were observed. Lp(a) was additionally related to greater risk of HFpEF in white participants: per log unit Lp(a) (HR, 1.48; P =0.001), Lp(a) ≥30 mg/dL (HR, 2.15; P =0.01), Lp(a) ≥50 mg/dL (HR, 2.60; P =0.004). Lp(a)-related risk of HF and HFpEF in whites was independent of aortic valve disease. Conclusions— In a multiethnic sample, Lp(a)-related risks of HF and HFpEF were only evident in white participants. If confirmed, these findings have implications in further Lp(a) research and clinical practice.

Lipoprotein (a) [Lp(a)] is a lipoprotein defined by presenting a specific apolipoprotein, ApoA, linked to the ApoB-100 by different types of chemical bonds, including a disulfide bridge. Despite their atherogenic mechanism is not fully understood, its importance has been demonstrated in the development of premature aterosclerosis. Multiple studies have shown its role as a cardiovascular risk factor associated with heart disease and stroke. We report the case of a patient with a diagnosis of Takayasu arteritis in which a massive elevation of Lp(a) was detected. We emphasize its diagnostic and therapeutic implications.

The β-barrel assembly machinery, the Bam complex, consists of five components, BamA to -E, among which BamA and BamD are highly conserved and essential. The nonessential components are believed to play redundant roles simply by improving the rate of β-barrel folding. Here we show that BamE contributes a specific and nonoverlapping function to the Bam complex. BamE coordinates BamA and BamD to form a complex between the lipoprotein RcsF and its partner outer membrane β-barrel protein, allowing RcsF to reach the cell surface. In the absence of BamE, RcsF accumulates on BamA, thus blocking the activity of the Bam complex. As the Bam complex is a major antibiotic target in Gram-negative bacteria, the discovery that a lipoprotein can act as a jamming substrate may open the door for development of novel Bam complex inhibitors., The β-barrel assembly machinery, the Bam complex, is central to the biogenesis of integral outer membrane proteins (OMPs) as well as OMP-dependent surface-exposed lipoproteins, such as regulator of capsule synthesis protein F (RcsF). Previous genetic analysis established the model that nonessential components BamE and BamB have overlapping, redundant functions to enhance the kinetics of the highly conserved BamA/BamD core. Here we report that BamE plays a specialized nonredundant role in the Bam complex required for surface exposure of RcsF. We show that the lack of bamE, but not bamB, completely abolishes assembly of RcsF/OMP complexes and establish that the inability to assemble RcsF/OMP complexes is a molecular reason underlying all synthetic lethal interactions of ΔbamE. Our genetic analysis and biochemical cross-linking suggest that RcsF accumulates on BamA when BamA cannot engage with BamD because of its limited availability or the incompatible conformation. The role of BamE is to promote proper coordination of RcsF-bound BamA with BamD to complete OMP assembly around RcsF. We show that in the absence of BamE, RcsF is stalled on BamA, thus blocking its function, and we identify the lipoprotein RcsF as a bona fide jamming substrate of the Bam complex.

Biotechnological pharmaceuticals is a key course offered to third-year undergraduates majoring in biotechnology in our university. However, students often experience difficulties in understanding the principles of related technologies. In this study, we developed and implemented an elective course on preliminary structural biology for biotechnology undergraduates, aiming at reinforcing the principles of these technologies by experimental practice. The course was composed of three phases and lasted for 15 weeks, 18 students were randomly divided into six teams and were encouraged to design, prepare, carry out, and conclude a project on their own. The main contents of their project were cloning, expression, purification, and crystal screening of HpaA, a lipoprotein from the gastric pathogen Helicobacter pylori. Examination scores of biotechnology pharmaceuticals were used to assess learning outcomes. The results showed that students who participated in this course gained higher scores in the final examination, and they performed better on the questions specifically related to the elective course. These results demonstrated that the course enhanced students' understanding of the technologies involved in this course by practical applications. Thus, this elective course was effective in helping biotechnology undergraduates to learn the theory and application of biological technologies, and the experience gained in this course may be useful for other technology-based courses.

The origin and physiological significance of lipid droplets (LDs) in the nucleus is not clear. Here we show that nuclear LDs in hepatocytes are derived from apolipoprotein B (ApoB)-free lumenal LDs, a precursor to very low-density lipoproprotein (VLDL) generated in the ER lumen by microsomal triglyceride transfer protein. ApoB-free lumenal LDs accumulate under ER stress, grow within the lumen of the type I nucleoplasmic reticulum, and turn into nucleoplasmic LDs by disintegration of the surrounding inner nuclear membrane. Oleic acid with or without tunicamycin significantly increases the formation of nucleoplasmic LDs, to which CDP-choline diacylglycerol phosphotransferase α (CCTα) is recruited, resulting in activation of phosphatidylcholine (PC) synthesis. Perilipin-3 competes with CCTα in binding to nucleoplasmic LDs, and thus, knockdown and overexpression of perilipin-3 increases and decreases PC synthesis, respectively. The results indicate that nucleoplasmic LDs in hepatocytes constitute a feedback mechanism to regulate PC synthesis in accordance with ER stress., The origin and physiological significance of lipid droplets (LDs) in the nucleus is not clear. Here authors show that nucleoplasmic LDs in hepatocytes are derived from apolipoprotein B (ApoB)-free lumenal LDs and constitute a feedback mechanism to regulate PC synthesis in accordance with ER stress.

Lipoprotein apheresis involves the extracorporeal removal of low-density lipoprotein cholesterol and other atherogenic lipoproteins from the blood. It is a lifesaving treatment for patients with very high low-density lipoprotein levels which cannot be sufficiently lowered by lipid-lowering drugs and diet. However, it is an invasive, repetitive and chronic treatment under taken at fortnightly intervals on an outpatient basis, meaning that patients need considerable commitment to undertake the treatment. The Lipoprotein Apheresis Unit at University Hospital Llandough is one of only eight centres in the UK, and has undertaken patient research to evaluate the service, so that changes can be implemented to ensure the service meets the needs and expectations of patients. The survey showed that patients consider apheresis treatment to be an important and beneficial part of their health care. The majority of patients (68%) reported that their general health had improved since starting lipoprotein apheresis treatment and the other 32% reported that their general health remained the same.

Hyperlipidemia is a lipoprotein metabolic disorder characterized by high serum Low density Lipoprotein and blood cholesterol. It is a major risk factors in the development and progression of atherosclerosis that eventually lead to cardiovascular diseases. This poses a major problem to majority of society because of the close correlation between cardiovascular diseases and lipid abnormalities. There are various features which are associated directly or indirectly as etiological factors viz. heredity, age, obesity, sex, diet, physical inactivity, hypertension, lifestyle disorders and various stress factors. For alleviation and treatment there are many ways such as allopathic medications, alternative systems like Ayurvedic, Diet control, lifestyle discipline etc. Recently Spice therapies are seen useful and effective. In India, Ayurveda and other Indian literature mentions the use of various plants and spices. Spices in diet are useful as they play effective role in the functioning of various body systems such as gastrointestinal, cardiovascular and nervous system. Along with proper food habits, diet which contains variety of spices which have been proved as hypolipidemic, can be effective in controlling hyperlipidemia. Spices used in day-to-day life as food, can also be used in the treatment of various human ailments. Along with the taste, flavor, colour and preservative property, spices also possess hypolipidemic effects. This review is focused mainly on the beneficial hypolipidemic effect of five spices (Dill, Garlic, Fenugreek, Ginger, Coriander) in the management of hyperlipidemia. This article is based on the traditional knowledge, mechanism of action for hypolipidemic activity and some experimental scientific studies done to support the use of these spices in the management of hyperlipidemia.

BPSL1445 is a lipoprotein produced by the Gram-negative bacterium Burkholderia pseudomallei (B. pseudomallei), the etiological agent of melioidosis. Immunodetection assays against sera patients using protein microarray suggest BPSL1445 involvement in melioidosis. Herein we report backbone, side chain NMR assignment and secondary structure for the recombinant protein.

Background: Lipoprotein particle sizes and concentrations are characteristically altered in patients with insulin resistance (IR) or type 2 diabetes mellitus (T2DM). This study assessed the ability of an IR score, based on nuclear magnetic resonance (NMR)-derived lipoprotein information, to detect IR in otherwise healthy individuals.Lipoprotein subclass and size information were evaluated for strength of association with IR, as measured by homeostasis model assessment of insulin resistance (HOMA-IR) in the Multi-Ethnic Study of Atherosclerosis (MESA). To increase the likelihood of identifying subjects with IR, six lipoprotein measures were combined into a single algorithm. The resulting assay [Lipoprotein Insulin Resistance Index (LP-IR)] was developed using HOMA-IR in 4972 nondiabetic subjects from MESA and verified independently using glucose disposal rates (GDRs) measured during hyperinsulinemic-euglycemic clamps in 56 insulin-sensitive, 46 insulin-resistant, and 46 untreated subjects with T2DM.LP-IR exhibited stronger associations with HOMA-IR (r=0.51) and GDR (r=-0.53) than each of the individual lipoprotein parameters as well as the triglycerides/high-density lipoprotein cholesterol (TGs/HDL-C) ratio (r=0.41 and -0.44, respectively). In MESA, associations between the LP-IR score and HOMA-IR were strong in men (r=0.51), women (r=0.52), European Americans (r=0.58), African Americans (r=0.48), Chinese Americans (r=0.49), and Hispanic Americans (r=0.45). When LP-IR was categorized by HOMA-IR and either body mass index (BMI) or fasting plasma glucose (FPG), subgroups were revealed whose LP-IR scores were high (≥ 50), despite having normal BMIs (24 kg/m(2)) or FPG (100 mg/dL).LP-IR scores had strong associations with multiple measures, HOMA-IR, and GDR, the former being more reflective of hepatic and the latter of peripheral insulin sensitivity, and may represent a simple means to identify individuals with IR.

In high-risk patients who are already on a maximal lipid-lowering therapy, a lipoprotein apheresis is an important therapeutic option in preventing further progress of vascular complications as it may decrease both LDL-cholesterol (LDL-C) and lipoprotein(a) (Lp(a)) levels. We looked at the occurrence of cardiovascular events before apheresis and during apheresis in three groups defined by their lipid patterns at the start of an apheresis treatment: Group 1 (LDL-C ≥ 3.4 mmol/l and Lp(a) ≤ 600 mg/l; n = 35), Group 2 (LDL-C ≤ 3.4 mmol/l and Lp(a) ≥ 600 mg/l n = 37) and Group 3 (LDL-C ≥ 3.4 mmol/l and Lp(a) ≥ 600 mg/l; n = 15). Group 2 shows a time period of about 10 years from the first event until the start of apheresis treatment (compared to 2–6 years in the other two groups). Before the start of apheresis treatment 2.1 events per patient had occurred in Group 1, 3.4 events per patient in Group 2 and 1.8 events per patient in Group 3. Under apheresis therapy just 0.9 events per patient occurred in Group 1, 0.5 in Group 2 and 0.5 in Group 3. When comparing the two years before the start of apheresis treatment with the first two years under apheresis we saw the following reduction rates of cardiovascular events: Group 1–54%; Group 2–83%; Group 3–83.5%. Our results show that the reduction of cardiovascular events due to lipoprotein apheresis is especially high in patients with elevated levels of Lp(a) compared to patients with elevated LDL-C only indicating that physicians should be more focused on the risk factor elevated Lp(a).

Accurate detection of carbapenemase-producing Gram-negative bacilli is of utmost importance for the control of nosocomial spread and the initiation of appropriate antimicrobial therapy. The modified Hodge test (MHT), a carbapenem inactivation assay, has shown poor sensitivity in detecting the worldwide spread of New Delhi metallo--lactamase (NDM). Recent studies demonstrated that NDM is a lipoprotein anchored to the outer membrane in Gram-negative bacteria, unlike all other known carbapenemases. Here we report that membrane anchoring of -lactamases precludes detection of carbapenemase activity by the MHT. We also show that this limitation can be overcome by the addition of Triton X-100 during the test, which allows detection of NDM. We propose an improved version of the assay, called the Triton Hodge test (THT), which allows detection of membrane- bound carbapenemases with the addition of this nonionic surfactant. This test was challenged with a panel of 185 clinical isolates (145 carrying known carbapenemase-encoding genes and 40 carbapenemase nonproducers). The THT displayed test sensitivity of>90% against NDM-producing clinical isolates, while improving performance against other carbapenemases. Ertapenem provided the highest sensitivity (97 to 100%, depending on the type of carbapenemase), followed by meropenem (92.5 to 100%). Test specificity was not affected by the addition of Triton (87.5% and 92.5% with ertapenem and meropenem, respectively). This simple inexpensive test confers a large improvement to the sensitivity of the MHT for the detection of NDM and other carbapenemases. Fil: Pasteran, Fernando. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”; Argentina Fil: Gonzalez, Lisandro Javier. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Albornoz, Ezequiel Pablo. Dirección Nacional de Institutos de Investigación. Administración Nacional de Laboratorios e Institutos de Salud. Instituto Nacional de Enfermedades Infecciosas. Área de Antimicrobianos; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Bahr, Guillermo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Vila, Alejandro Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Corso, Alejandra. Dirección Nacional de Institutos de Investigación. Administración Nacional de Laboratorios e Institutos de Salud. Instituto Nacional de Enfermedades Infecciosas. Área de Antimicrobianos; Argentina

Despite vitellins being essential yolk proteins, their presence in spiders remains almost unknown. Two vitellins from the spider Polybetes pythagoricus, named LV1 and LV2, were isolated and their size, shape, lipids, fatty acids, proteins and carbohydrates moieties were determined. LV1 has a density similar to that of HDL with 49.3% lipids, and LV2 has a density similar to that of VHDL with 9.7% lipids. The major neutral lipid present in both vitellins was found to be esterified cholesterol, 16% for LV1 and 24% for LV2. The major fatty acid was 18:1n-9 in LV1 and LV2. Results from native PAGE showed a lipoprotein of 550 kDa for LV1 and three lipoproteins of 571, 400 and 257 kDa for LV2. SDS-PAGE evidenced two major apolipoproteins of 64 and 25 kDa in LV1. The three lipoproteins of LV2 were electroeluted and analyzed by SDS-PAGE, showing different proportions of the same apolipoproteins (181, 67 and 60 kDa). LVs were analyzed by spectrophotometry, immunochemical and electron microscopy, showing that the respiratory pigment hemocyanin was not present as apolipoprotein. This fact evidenced that these LVs were not related to hemolymphatic lipoproteins.

A very strong association between phenotype Lp(a +) and presence of pre-β1-lipoprotein has been observed in two series of healthy young adults. The data are in agreement with the view that pre-β1-lipoprotein is identical to the lipoprotein carrying the Lp(a) antigen: the Lp(a) lipoprotein. Lp(a) antigen/pre-β1-lipoprotein occurred more frequently in persons with a positive than with a negative family history of coronary heart disease, though this trend was not statistically significant. Occurrence of Lp(a) antigen/pre-β1-rlipoprotein was not correlated with smoking or with the use of contraceptive pills.

Previous studies have shown that a slow-moving pre-beta-lipoprotein fraction, named the pre-beta1-lipoprotein, occurred significantly more frequently among subjects with coronary heart disease (CHD) than among healthy individuals. This lipoprotein is closely related to, and probably identical with, the Lp(a) lipoprotein. Immunological tests likewise showed that Lp(a) lipoprotein was significantly more common among patients with CHD than among controls. Mean cholesterol and triglyceride levels were higher in pre-beta1-lipoprotein positive than in pre-beta1-lipoprotein negative individuals. Lp(a+) individuals tended to have higher serum cholesterol values than did Lp(a-) persons but there was no difference in the mean triglyceride value. This apparent discrepancy seems to be due to the presence in occasional sera of lipoprotein fractions with pre-beta1-mobility, usually of a VLDL nature. These lipoproteins are not associated with the Lp(a) lipoprotein.

Summary This paper presents evidence of five isoimmune sera, which identified five antigens of cattle blood serum. These antigens were examined by means of staining, immuno-electrophoresis and Sephadex G 200 column chromatography. It was established that the BA-2, BA-3, BA-4 and BA-4′ antigens were proteins, whilst the BA-1 antigen was a lipoprotein. The BA-3 antigen migrated in the γ-globulin position; the remaining four antigens migrated in the α-globulin region. The antigens under examination were already present in the blood serum during the first few days of life and appeared to be of a stable character. The results of genetic analysis suggest that these antigens were transmitted according to Mendelism.

A small number of recent studies have reportedly failed to detect the well-established association between a high Lp(a) lipoprotein level and coronary heart disease (CHD). This has made some workers question the importance of a high Lp(a) lipoprotein level as a CHD risk factor. However, serious problems with some of the commercially available test kits, inadequate test techniques or failure to consider the lability of the Lp(a) lipoprotein particle are more plausible explanations of the confounding results. The problems with some of the commercially available test kits include lack of standardization and validation; risk of cross-reactivity with plasminogen or other serum proteins; failure to consider potential problems when measuring samples with varying length of the Lp(a) polypeptide chain (i.e. failure to cope with the isoform variation); non-divulgence of contents of test reagents; and pretreatments of samples that drastically change the Lp(a) lipoprotein particles from their native state. Any test system should be validated at the scientific level before it is assumed to provide correct measurements of Lp(a) lipoprotein level in serum. New test kits should be safely anchored in validation in one of the research laboratories active in the area, before they are put on the market. As new batches are produced, the quality of every new batch of test kits should be monitored on a long-term basis in collaboration with a research laboratory.

the mixture of lipids and proteins that comprises pulmonary surfactant is both complex and multifunctional. Although surfactant was originally identified as a lipoprotein complex that reduces surface tension at the air-liquid interface of the lung ([4][1], [20][2]), both in vitro and in vivo studies

To the Editor: Previous reports have demonstrated that lipoprotein-associated phospholipase A2 (Lp-PLA2), an enzymatic inflammatory biomarker, is associated with increased risk of cardiovascular events [(1)][1]. Lp-PLA2 mediates formation of bioactive mediators (lysophosphatidyl choline and

The effects of cholesterol on droplet size distribution and rheological properties of cholesterol-reduced egg yolk-stabilized emulsions were determined. Oil-in-water emulsions were prepared by using spray-dried eggs submitted to different levels of cholesterol reduction (14–81 wt% of cholesterol removed). Cholesterol was extracted in a modified Jennings apparatus with subcritical CO2 (9°C and 4.66·106 Pa). Oscillatory and steady flow tests, as well as droplet size distribution measurements, were carried out on the cholesterol-reduced egg yolk-stabilized emulsions. The rheological parameters increased with the level of cholesterol reduction up to 40–80 wt% for emulsions having the same total amount of egg yolk. Opposite results, however, were obtined with some emulsions stabilized by a highly cholesterol-reduced (≈80 wt%) egg yolk. These results were explained by taking into account two opposite phenomena: an increase in the concentration of surface-active agents as cholesterol content decreased, and a lipoprotein structural rearrangement induced by cholesterol removal.

Polyunsaturated fatty acids (PUFAs) are critical to nervous system function and structure, but their rates of incorporation from plasma into brain have not been evaluated. In the adult rat, calculations based on our model show that at least 3;-5% of esterified brain arachidonic acid (AA) and 2;-8% of esterified brain docosahexaenoic acid (DHA) are replaced daily by unesterified PUFAs in plasma. These rates, when related to unlabeled brain PUFA composition, give half-lives of 1-2 weeks for plasma-brain exchange of AA and DHA. In the human brain, the arachidonate replacement rate is 0.3% per day. Although unesterified plasma PUFA concentrations are low, their rates of incorporation into brain are sufficient to compensate for metabolic and efflux losses, so that PUFA transport from plasma into brain as a component of a lipoprotein is unnecessary. Dietary supplementation, by altering plasma unesterified PUFA concentrations, can regulate brain PUFA content and may help to treat brain diseases involving PUFA imbalance.

Background: The conformation and assembly of lipoproteins, proteins containing large amounts of noncovalently bound lipid, is poorly understood. Lipoproteins present an unusual challenge as they often contain varying loads of lipid and are not readily crystallized. Lipovitellin is a large crystallizable oocyte protein of approximately 1300 residues that contains about 16% w/w lipid. Lipovitellin contains two large domains that appear to be conserved in both microsomal triglyceride transfer protein and apolipoprotein B-100. To gain insight into the conformation of a lipoprotein and the potential modes of binding of both neutral and phospholipid, the crystal structure of lamprey lipovitellin has been determined. Results: We report here the refined crystal structure of lipovitellin at 2.8 a resolution. The structure contains 1129 amino acid residues located on five peptide chains, one 40-atom phosphatidylcholine, and one 13-atom hydrocarbon chain. The protein contains a funnel-shaped cavity formed primarily by two β sheets and lined predominantly by hydrophobic residues. Conclusions: Using the crystal structure as a template, a model for the bound lipid is proposed. The lipid-binding cavity is formed primarily by a single-thickness β -sheet structure which is stabilized by bound lipid. This cavity appears to be flexible, allowing lipid to be loaded or unloaded.

Lipoprotein (a) [Lp(a)] is a lipoprotein which has a plasma concentration that is highly correlated with cardiovascular disease. In this study, the new Lp(a) assay for the Vitek Immuno-Diagnostic Assay System (VIDAS) developed by bioMerieux was evaluated. This method uses an enzyme linked fluorescent immunoassay (ELFIA) technique. Within-run and between-run reproducibility of the Vidass Lp(a) assay are characterized by coefficients of variation (CV) of 3 to 5.9% and 3.9 to 5.9%, respectively. Using analysis of variance, no statistical difference was shown between ELFIA and immunonephelometric assay (INA). When comparing results of the Vidas Lp(a) test with the INA, a highly significant correlation of r = 0.9708 and regression line equation y = 0.963x-0.037 was found. Interference of lipemia was studied: no influence was observed up to 12.3 mmol l(-1) triglycerides. No interference of haemoglobin was noted for Lp(a) > 0.20 g l(-1). Hyperbilirubinemia ( > 120 micromol l(-1)) led to results being underestimated for concentrations of Lp(a) which were < 0.20 g l(-1). No pre-analytical interference of citrate was measured but pre-analytical interference of EDTA was found. In conclusion, this new fully automated immunofluorimetric Lp(a) assay enables to the rapid, accurate and reliable determination of Lp(a) in blood samples.

Among various taste stimuli, bitter substances are most abundant and their chemical structures are greatly diverse from each other. It has been known that there are multiple receptor sites and transduction mechanisms. Already in neonates, bitter stimuli elicit rejection responses, indicating strong negative hedonic tone. Bitter taste is decidedly unpleasant when the sensation is strong. The development of a method to mask bitterness has widely been required in pharmaceutical sciences and food sciences. To mask bitterness, a specific bitterness inhibitor would be most useful. Such an inhibitor would also be useful in elucidating the receptor mechanisms of bitter substances. No inhibitor has, however, been available. Recently we found that a lipoprotein, PA-LG made of phosphatidic acid (PA) and beta-lactoglobulin (beta-LG), selectively suppresses the taste responses to bitter substances. In this paper we describe the protocol used for inhibition of the frog taste (glossopharyngeal) nerve responses to bitter stimuli by the lipoprotein. The frog taste system is used because it is sensitive to various bitter substances and surgery of the animal for the electrophysiological recording is rather easy. We also describe the protocol used for inhibition of human taste sensation to bitter stimuli.

Summary The genetically determined Lp(a) lipoprotein whose specific apoprotein evolved from plasminogen exhibits association with atherosclerotic/thrombotic diseases including coronary heart disease (CHD). People with an Lp(a) lipoprotein concentration corresponding to the top quartile in the healthy population have a significantly increased CHD risk compared with those with a lower value, and the risk in the top decile appears to be particularly high. However, a very low Lp(a) lipoprotein level may also cause disadvantage with respect to CHD and longevity. Lp(a) lipoprotein may compromise thrombolytic processes through molecular mimicry and in vitro it stimulates vascular cells to cell division. The normal function of Lp(a) lipoprotein is unknown. It could be related to repair processes. Preliminary evidence suggests that Lp(a) lipoprotein may be involved in vascular processes in the placenta. It has been reported that Lp(a) lipoprotein increases following myocardial infarction in a way suggesting that it could possess characteristics of an acute phase reactant. In view of the strikingly high heritability of Lp(a) lipoprotein, this would a priori be unlikely. We have not been able to confirm a significant increase in Lp(a) lipoprotein following myocardial infarction. Several commercially available test kits are of a doudtful quality. At present, a highly needed, international effort at standardizing Lp(a) lipoprotein measurements is taking place.

High density lipoprotein (HDL) is a lipoprotein containing apo A-1, associated with other apolipoproteins. One of the HDL functions is as the reversed transporter of cholesterol in order to reduce cholesterol level in peripheral tissues. Low HDL cholesterol level is often related to obesity. High cholesterol level, obesity, and low HDL level are known as risk factors of coronary heart diseases. Overweight subjects have higher probabality for suffering from heart diseases and stroke. This study aimed to elaborate high density lipoprotein (HDL) levels in males aged 40-59 years with body mass index higher than 23 kg/m2. This study used consecutive sampling method. Total subjects involved in this study were 20 males who lived in Malalayang. The results showed that there were 11 subjects with normal HDL levels and nine subjects (45%) with low HDL levels (60 mg/dL). Terdapat 19 subjek (95%) dengan obesitas dan hanya satu subjek (5%) yang mengalami overweight. Simpulan: Sebagian besar laki-laki berusia 40-59 tahun yang berdomisili di Kecamatan Malalayang Manado dengan indeks massa tubuh ≥23 kg/m2 mempunyai kadar HDL normal. Kata kunci: laki-laki, high density lipoprotein, indeks massa tubuh

We administered testosterone, with or without the aromatase inhibitor testolactone, to determine the effects of testosterone and its aromatization to estradiol on Lp(a) levels in normal men. Average Lp (a) values decreased by 37% during testosterone alone and by 28% when testosterone and testolactone were combined, suggesting that testosterone reduces Lp(a) in men primarily by an androgenic effect and not by its conversion to estradiol.

Two hundred and ninety four pairs of Swedish twins reared apart and twins reared together were used to evaluate the importance of genetic and environmental influences on lipoprotein(a) (Lp(a)) levels. Lp(a) levels ranged from10 mg/l to 926 mg/l with 7.9% of the sample having undetectable Lp(a) levels (i.e.10 mg/l). A substantial genetic component in Lp(a) variation was indicated by a heritability estimate of approximately 90%. No difference in heritability was found across age groups. Quantitative genetic analyses also suggest correlated environmental effects most likely composed of maternal, neonatal and postnatal environmental influences. However, these effects did not reach statistical significance, partly due to a lack of power. Results from analyses of co-twin differences in Lp(a) levels for monozygotic twins indicate that sex hormone use may be of importance for Lp(a) variation in women. There was no evidence of potential influences of alcohol consumption, beta-blocker and diuretic administration on Lp(a) levels in either men or women.

In order to evaluate whether Lp(a), a lipoprotein that is potentially thrombogenic and atherogenic, is a potential risk factor for CAD in non-insulin-dependent diabetes (NIDDM), we compared the Lp(a) and its distribution in 145 NIDDM patients with that in 94 healthy control subjects. Furthermore, we studied the effect of insulin treatment on serum Lp(a) in 108 patients with NIDDM. Male and female NIDDM patients had similar Lp(a) concentrations to healthy controls (median value 167 mg L-1, range 15-1550 mg L-1 vs. 157 mg L-1, range 15-919 mg L-1, NS and 92, range 15-1190 mg L-1 vs. 103 mg L-1, range 15-842 mg L-1, NS). Also, the cumulative distribution of Lp(a) did not differ between the NIDDM patients and healthy subjects. Insulin treatment increased Lp(a) in diabetics with a Lp(a) concentration of less than 300 mg L-1, but this effect was not related to the concomitant improvement in metabolic control (mean change (+/- SEM) of HbA1c from 9.80 +/- 0.15 to 8.00 +/- 0.12; P0.001). In subjects with elevated Lp(a) concentrations (300 mg L-1) the Lp(a) concentration was unaffected by insulin, despite a similar improvement in glycaemic control. These results suggest that insulin may modulate the concentration of Lp(a).