Response to therapy of a type III hyperlipoproteinemic subject with the rare apolipoprotein E1 (Gly127 → Asp,Arg158 → Cys) variant

Summary In a preceding paper, we described the molecular biological defects in a patient with a severe form of the familial lipoprotein disorder type III hyperlipoproteinemia (HLP) and an unusual apolipoprotein (apo) El phenotype and 1/null genotype. The index case was a 60-year-old white male of German ancestry who suffered from a myocardial infarction at age 50 years. He had distinctly elevated levels of plasma lipids (triglycerides 551 mg/dl and cholesterol 747 mg/dl, respectively) and typical clinical signs of this inborn error of lipoprotein metabolism. His mutant apo E1 was shown to be identical to a rare (already described) apo E1 (Gly₁₂₇Asp, Arg₁₅₈Cys) variant. A second independent defect at the molecular level was a nucleotide deletion of a guanosine (G) in the codon for amino acid 31 of the proband's apo 3 allele. This single base deletion (not described before) changed his apo 3 allele to a nonfunctional null allele devoid of a stable gene product. Here we describe the response to combined dietary and medical treatment of the patient with this unusual form of type III HLP. His response to therapy was excellent, similar to patients with classical type III HLP and homozygosity for apo E2. However, the correct diagnosis of this familial lipoprotein disorder seems to be necessary, even in patients without the expected apo E2/2 phenotype, in terms of the prompt and beneficial response to therapeutic interventions.Abbreviations Apo Apolipoprotein - Chol cholesterol - HDL high density lipoproteins - HDL-C HDL-cholesterol - HLP hyperlipoproteinemia - IDL intermediate density lipoproteins - IEF isoelectric focusing - LDL low density lipoproteins - LDL-C LDL-cholesterol - TG triglycerides - VLDL very low density lipoproteins - VLDL-C VLDL-cholesterol Dedicated to Prof. Dr. G. Schettler on the occasion of his 75th birthday on April 13, 1992     

Serum-cholesterol-lowering effect of metronidazole and possible mechanisms of action

Summary In five patients with Crohn's disease long-term therapy with metronidazole (400 mg b.i.d.) was followed by a significant reduction of total serum cholesterol from 179 mg/dl to 156 mg/dl, 134 mg/dl, and 143 mg/dl, after 2–4 months, 6 months, and 9–12 months, respectively. Lipoprotein analysis before and after 3 weeks of administration of metronidazol (400 mg/day) to five normolipemic volunteers revealed that LDL-cholesterol was reduced by 21% (P<0.05), whereas HDL-cholesterol remained unchanged. Biliary secretion of cholesterol and bile acids were reduced by 13% and 20% (P<0.05), respectively, which might suggest a decreased sterol synthesis. The amount and percentage of intestinal cholesterol absorption were decreased by 33% and 22% (P<0.05). Thus, a possible decrease in sterol synthesis and a reduction of cholesterol absorption might be responsible for the serum-cholesterol-lowering effect of metronidazole. However, caution should be taken when considering metronidazole for long-term treatment of patients with hypercholesterolemia due to possible side effects.This project was supported by a grant from Sandoz Stiftung für therapeutische Forschung.The authors thank Mrs. P. Pitters, G. Westphal, H., Ahten und Mr. S. Weiner for their technical assistance     

Clinical features of type III hyperlipoproteinemia: analysis of 64 patients

Summary The clinical and biochemical characteristics of type III hyperlipoproteinemia are described in 64 patients (35 males and 29 females). Homozygosity for apolipoprotein E2, the presence of an abnormally cholesterol-rich very low density lipoprotein fraction (-VLDL) and an elevated ratio of very low density lipoprotein cholesterol to plasma triglycerides (>0.3; normal ratio about 0.2) were the basis for the diagnosis. Mean serum cholesterol and triglyceride concentrations at the first visit in the clinic were 426 ± 221 and 719 ±996 mg/dl, respectively. The mean age at diagnosis of the disorder was 49 years in males and 53 years in females. There was a high prevalence of obesity (72%), xanthomas (42%), and atherosclerosis (39%), especially peripheral vascular disease (31%). Early and correct diagnosis of this familial lipoprotein disorder seems necessary because of the prompt and beneficial response to therapeutic interventions.Abbreviations Apo apolipoprotein - BMI body mass index - CAD coronary artery disease - HDL high-density lipoproteins - HLP hyperlipoproteinemia - HMG CoA 3-hydroxy-3-methylglutaryl coenzyme A - LDL low-density lipoproteins - Lp(a) lipoprotein (a) - PVD peripheral vascular disease - TG triglycerides - VLDL very low density lipoproteins     

Lipid lowering treatment with bezafibrate in patients on chronic haemodialysis: Pharmacokinetics and effects

Summary Hyperlipidaemia may contribute to the high rate of cardiovascular complications in patients on chronic haemodialysis (CHD). However, possibilities of lipid lowering therapy in CHD are still limited. The applicability of bezafibrate (BF), a recently developed clofibrate analogue, was investigated in patients on CHD with triglyceride and/or total cholesterol levels above 300 mg/dl.The lipid lowering effect was studied in a placebo-controlled trial over 6 months in 19 patients. Long-term effect was followed in six patients over a mean period of 29 months.Elimination half-life and mean therapeutic serum concentration were calculated by 72-h BF serum profiles, obtained after the first drug administration of a single 200-mg dose and during steady state after 12 weeks of treatment. Elimination half-lives were 17 h at start and 22 h after 12 weeks compared with 2 h in subjects with normal renal function. Dose reduction to 200 mg every 3rd day was necessary and resulted in a mean therapeutic serum concentration of 3.4 mg/l, which was similar to 3.0 mg/l of normal subjects, who received the dose optimal for lowering of lipids (200 mg 3 × /day). The protein-bound serum fraction of BF was decreased to 8% in CHD patients, compared with 95% found in normal subjects.BF therapy resulted in a marked reduction of serum triglycerides from 478 mg/dl by 31% and total cholesterol levels from 311 mg/dl by 19% as well as -Lp-cholesterol from 178 mg/dl by 17%, whereas the initially low -Lp-cholesterol increased significantly from 18,3 mg/dl by 58%. Under long-term therapy not only continuously low triglyceride and cholesterol levels could be maintained, moreover a further decline (–20% and –7%) could be achieved.Safety laboratory controls, comprising haemoglobin, bilirubin, liver enzymes, CK and albumin, showed no significant changes apart from a slight reversible increase in CK and a decrease in gamma-GT and alkaline phosphatase. Subjective side effects were not reported. Under this dosage schedule, BF therapy was thus effective and safe, improving potentially atherogenic disturbances of lipid metabolism.Abbreviations BF bezafibrate - CHD chronic haemodialysis - HDL high density lipoproteins - IDL intermediate density lipoproteins - LDL low density lipoproteins - VLDL very low density lipoproteins     

Simvastatin and Preparation of Polyunsaturated Phospholipids Produce Similar Changes in the Phospholipid Composition of High-Density Lipoproteins during Hypercholesterolemia

We studied the phospholipid composition of high-density lipoproteins in patients with coronary heart disease and hypercholesterolemia treated with simvastatin (Zocor, inhibitor of the key enzyme of cholesterol synthesis) and preparation of polyunsaturated phospholipids (lipostabil forte). Simvastatin produced a hypolipidemic effect and modulates the phospholipid composition of high-density lipoproteins (similarly to lipostabil forte). These changes contribute to functional activity of high-density lipoproteins in the reverse cholesterol transport.__________Translated from Byulleten Eksperimentalnoi Biologii i Meditsiny, Vol. 139, No. 2, pp. 178–180, February, 2005     

A test of the John Henryism hypothesis: Cholesterol and blood pressure

The personality predisposition John Henryism (JH) is a self-perception that one can meet demands of the environment through hard work and determination. The JH scale measures efficacy of mental and physical vigor, commitment to hard work, and determination to reach one's goals. Previous research found an increased prevalence of hypertension among African-Americans with high JH scores and low socioeconomic status (SES). Six hundred fifty-three adult African-Americans in a church-based cardiovascular risk factor screening program completed the JH questionnaire. The prevalence of cholesterol 240 mg/dl was highest (27%) among the high-JH/low-SES group when adjusted for age, sex, and body mass index. High JH/low SES was not associated with a greater prevalence of high blood pressure. Findings of this study suggest the need for additional research on John Henryism, socioeconomic factors, and cardiovascular risk among randomly selected samples of geographically and economically diverse African-Americans.This research was supported in part by NIH Biomedical Research Support Grant 1S07RR05975, Pfizer Pharmaceutical, and the Oklahoma City-County and State Health Departments.     

Lipid changes in the nephrotic syndrome: New insights into pathomechanisms and treatment

Summary The abnormalities of lipid metabolism in nephrotic syndrome consist in an increase in total and low-density lipoprotein (LDL) cholesterol, apoliproteins B (ApoB), C-II and C-III, associated in patients with heavier or marked hypoalbuminemia with an increase in triglycerides and very low-density lipoprotein (VLDL) cholesterol, while the high-density lipoproteins (HDL) are distributed abnormally (increased HDL3 fraction and decreased HDL2 fraction) and the Apo A-I to Apo B ratio is reduced. Both increased hepatic lipoprotein synthesis and reduced removal capacity contribute to this hyperlipidemia. Proteinuria may lead to the lipoprotein abnormalities through stimulation of VLDL synthesis by the liver induced by hypoalbuminemia, although it has been more recently suggested that urinary protein loss is associated with the urinary loss of some important cofactor for the regulation of lipid synthesis or catabolism.Treatment of lipid abnormalities in patients with long-lasting heavy proteinuria is mandatory, because they may cause or contribute to accelerated atherosclerosis, but also because they appear to accelerate progression of renal disease by favouring mesangial sclerosis. Four groups of lipidlowering drugs have been tested: 1) bile acid-binding resins; 2) fibric acid; 3) probucol; 4) inhibitors of HMG CoA reductase. The drugs of the last group appear to be effective and safe in short-term experiments, but long-term studies are necessary to confirm their validity. A dietary approach, consisting in a strictly vegetarian soy diet, very rich in polyand monounsaturates fatty acids, has been recently tested by the author, with very promising results.Abbreviations LDL low density lipoproteins - VLDL very low density lipoproteins - HDL high density lipoproteins - Apo Apolipoprotein - LCAT Lecithin cholesterol acyltransferase - HMGCoA Hydroxymethylglutaryl coenzyme A Preprint of a lecture to be read at the 22nd Congress of the Gesellschaft für Nephrologie, Heidelberg, September 15–18, 1991 (Editor: Prof. Dr. E. Ritz, Heidelberg)     

Evaluation of the classical methods for the diagnosis of type III hyperlipoproteinemia

Summary Familial type III hyperlipoproteinemia is characterized by the presence of elevated plasma levels of very low density lipoproteins (VLDL) which contain an increased amount of cholesterol and by the presence of a significant amount of lipoproteins with an intermediate density between that of VLDL and low density lipoproteins (LDL); the intermediate density lipoproteins, designated IDL or Lp III, have a slower electrophoretic migration rate than VLDL, and are found in the ultracentrifugal top fraction as a contaminant. Classically, the diagnosis of type III is based on the demonstration of beta-migrating lipoproteins in the ultracentrifugal top fraction (density <1.006), thus floating beta-lipoprotein. More recently, it has been proposed that an elevated VLDL-cholesterol to triglyceride ratio is diagnostic of the disorder. In the present report, we have compared the two methods for their diagnostic value and have concluded that the chemical index definition is the more reliable method for the diagnosis of type III hyperlipoproteinemia.     

Familial disorders of plasma apolipoproteins

Summary Numerous molecular variants of the protein moiety of human circulating lipoproteins (apolipoproteins or apoproteins) have been described in recent years. Molccular alterations of apolipoproteins may lead to an impaired lipid binding and/or to an accelerated or delayed lipoprotein catabolism. Many variants, particularly those of the E apoprotein system, are associated with premature atherosclerosis. In the case of the Apo AI variants, the concomitant deficiency of Apo AI and Apo CIII leads to severe clinical atherosclerosis. Conversely, molecular variants of Apo AI (several of which come from FRG, i.e. AI-Marburg, -Giessen, -Münster) do not go together with significant clinical abnormalities. The case is different for Tangier disease, characterized by the complete absence of high density lipoproteins, where a dramatic tissue lipid deposition may occur. One molecular variant, Apo AI-Milano, while leading to a significant reduction of HDL, does not seem to be associated with clinical atherosclerosis, but rather with a protection from the disease. The presence of major apolipoprotein abnormalities in familial groups of variable size, provides a molecular explanation for some significant alterations of lipid metabolism. Moreover, it offers, to clinical and basic studies, a useful model for the understanding of the function and metabolism of human apolipoproteins.Abbreviations ABL abetalipoproteinemia - Apo apoprotein - CAD coronary artery disease - HBL hypobetalipoproteinemia - HDL high density lipoproteins - HL hepatic lipase - IEF isoelectric focusing - LCAT lecithin-cholesterol acyltransferase - LDL low density lipoproteins - LPL lipoprotein lipase - Proapo proapoprotein - VLDL very low density lipoproteins     

Density heterogeneities of hepatitis C virus in human sera due to the binding of β-lipoproteins and immunoglobulins

Heterogeneities in the density of hepatitis C virus RNA-carrying material (HCV-RNA-CM) found in human sera (1.03–1.20 g/cm³) are attributed to the binding of low-density lipoproteins and/or of IgG. In some sera HCV-RNA-CM seems to be nearly totally bound to -lipoproteins and cannot be precipitated by anti-IgG (); in others more than 95% of HCV-RNA-CM is bound to IgG and cannot be precipitated by anti--lipoprotein. Furthermore, there are sera from which HCV-RNA-CM can be completely be precipitated by either anti--lipoprotein or anti-IgG (), pointing to a binding of the two serum proteins to the same HCV-RNA-CM. There are other sera from which HCV-RNA-CM can be partially precipitated by the one or the other antiserum, leaving behind fractions, which are bound to -lipoprotein or to IgG. HCV-RNA-CM cannot be precipitated from some sera either by anti--lipoprotein or by anti-IgG ().     

Lipoprotein lipase activity in patients with combined hyperlipidaemia

The aetiology of familial combined hyperlipidaemia remains obscure, with both genetic and environmental factors contributing to the phenotype, which is frequently associated with premature coronary heart disease. We have studied lipoprotein lipase (LPL) activity and hepatic lipase (HL) activity in patients with coronary heart disease to determine whether variation in lipase activities contributes to this phenotype. Forty-one patients (mean age 50 years; 30 male) were selected on the basis of cholesterol levels above 6.5 mmol/l and triglyceride levels above 2.2 mmol/1, with apoprotein B values over the 90th percentile. There was a family history of premature coronary heart disease in 78% and a personal history in 64%, at mean age 44, the patient group therefore predominantly corresponded to the common definition of familial combined hyperlipidaemia, appropriate in the absence of molecular markers. None of the patients was diabetic; hypertension and smoking were not over represented. Blood samples were taken following intravenous administration of heparin (100IU/kg body wt), and LPL and HL activities were measured. Mean post-heparin LPL was significantly lower in patients than controls 10 min after heparin administration (2.98 ± 1.04 and 3.86 ± 0.93 mol ml^-1 h^-1, respectively, P = 0.001), and 37% patients had values below the 10th percentile of controls. Both male and female patients had significantly higher HL activities than their respective controls at 5, 10, 20 and 30 minutes postheparin. As expected, both female patients and controls had lower HL activities than males, although this sex difference did not reach statistical significance in the patient group. Mean lipid and lipoprotein results were: cholesterol 8.2 mmol/1; triglycerides 4.2 mmol/l; high-density lipoprotein cholesterol 0.90 mmol/1; apoprotein Al 122 mg/dl; apoprotein B 171 mg/dl; lipoprotein (a) 23 mg/dl (median 10 mg/dl). High-density lipoprotein cholesterol and triglycerides were negatively correlated (r = -0.26, P = 0.05). HL was significantly related to body mass index at all time points whereas the negative correlation between post-heparin LPL and body mass index was significant only 30 min after heparin administration. Post-heparin LPL was only weakly correlated with triglycerides 10 and 20 min after heparin administration. These lipid and lipoprotein results are clearly potentially atherogenic as indicated by the extent of premature coronary heart disease in the group described. A decrease in LPL activity may contribute to this pattern.Abbreviations FCHL familial combined hyperlipidaemia - CHD coronary heart disease - LPL lipoprotein lipase - HL hepatic lipase - HDL high-density lipoprotein - VLDL very low density lipoprotein; - apo apoprotein - TG triglyceride - BMI body mass index Correspondence to: M. Seed     

Statin treatment and a disease-specific pattern of β-amyloid peptides in Alzheimer’s disease

According to the amyloid cascade hypothesis, sporadic Alzheimers disease (AD) is caused by the production and aggregation of -amyloid (A), and the production of A has recently been linked to the metabolism of cholesterol. We have previously published clinical studies where the effect of statin treatment on A production has been investigated. No effect on A was found, which is in disagreement with cell and animal studies. In the present study we investigated the effect of statin treatment on a disease-specific pattern consisting of a C-terminally-truncated quintet of A peptides. Nineteen patients with AD were treated with simvastatin for 12 months and the quintet of A peptides were analysed in cerebrospinal fluid before and after treatment. Also included was a group of 15 untreated patients with AD. We found that the A peptide pattern at baseline was in agreement with earlier findings; however, we did not find any change in the A peptide pattern after statin treatment. We suggest that clinical studies with extended treatment periods are performed where higher dosages of statins are used. We also believe that the pleiotropic effects of statins should be investigated further in order to elucidate the connection between Alzheimers disease and statin treatment.     

Chronic hyperprolactinemia and plasma lipids in women

Summary Plasma total cholesterol (TC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C) were studied in 15 hyperprolactinemic women who had a prolactin (PRL) adenoma, in comparison to 15 age-matched control women. In the hyperprolactinemic group, plasma lipids were also correlated to age, excess body weight (EBW), plasma PRL, and estradiol-17 (E2). Plasma TC, TG, and LDL-C were similar in both hyperprolactinemic and control women, while plasma HDL-C was significantly lower (P<0.01) in the hyperprolactinemic group. The correlation study showed a significant negative correlation between HDL-C and EBW (r=–0.64;P<0.02) and a slightly significant positive correlation between TG and PRL (r=0.54;P<0.05). The direct effect of PRL on plasma lipids is difficult to establish since many factors influencing lipid metabolism are altered during hyperprolactinemia.Abbreviations EBW excess body weight - E2 estradiol-17 - GH growth hormone - HDL-C high-density lipoprotein-cholesterol - LDL-C low-density lipoprotein-cholesterol - LPL lipoprotein lipase - PRL prolactin - RIA radioimmunoassay - TC total cholesterol - TG triglycerides     

On muscle strength and the threshold of anaerobic work

Summary 1.When subjects are exercised on a bicycle ergometer at 80% of aerobic power, there is a progressive increase of arterial lactate for 5–15 min, and in subjects of poor cardio-respiratory fitness the terminal level may approach that found in maximal exercise. 2. 5 min of sub-maximal exercise at 70 or 80% of aerobic power leads to a substantial accumulation of arterial lactate (38.3±8.9, 47.6±8.9 mg/100 ml) respectively. 3. The arterial lactate levels following 5 min of sub-maximal exercise are negatively correlated with the strength of hand-grip and knee extension. 4. Evidence is presented that lactate accumulation represents an effect of muscle contraction on oxygen supply rather than an overloading of intracellular biochemical mechanisms. 5. Perceived exertion in sub-maximal exercise is related to pulse rate as previously described byBorg. However, it is not related to arterial lactate or sensitivity to thermal stress.     

Uric acid levels in southern Germany in 1989

Summary Since 1962 our group has performed four studies on uric acid values in blood donors in southern Germany (Bavaria). Uric acid levels in men have increased over the years, from 4.86 mg/dl in 1962 to 6.00 mg/dl in 1971, 5.60 mg/dl in 1984, and 5.90 mg/dl in 1989. Levels in women have increased slightly, from 4.05 mg/dl in 1962 to 4.35 mg/dl in 1971, 4.10 mg/dl in 1984, and 4.16 mg/dl in 1989. Women aged 51 to 60 years had significantly higher uric acid levels than those in the fourth decade. In women treated with oral contraceptives uric acid levels were significantly lower than in other women of the same age.Hypouricemia (uric acid levels 2.0 mg/dl) was observed in three women, none of whom had a history of medication.Hyperuricemia exists when uric acid levels are 6.5 mg/dl. In 1989 2.6% of the female blood donors and 28.6% of the males were hyperuricemic, with an increased risk of gout, nephrolithiasis, and nephropathy.Dedicated to Prof. Walter Seitz on the occasion of his 85th birthday     

Molecular analysis of <Emphasis Type="Italic">Fiji disease virus</Emphasis> genome segments 5, 6, 8 and 10

Summary. The complete sequences of Fiji disease virus (FDV) genome segments 5 (S5), S6, S8 and S10 were obtained and comprised 3150nt, 2831nt, 1959nt and 1819nt, respectively. Each segment contained a single ORF which encoded putative proteins of 115kDa, 97kDa, 69kDa and 63.0kDa, respectively. The putative amino acid sequences encoded by S5 and S6 contained putative leucine zipper motifs while FDV S5 and S8 each contained an ATP-GTP-binding motif. At the amino acid level, FDV S5, S6, S8 and S10 showed most similarity to the corresponding segments of Rice black-streaked dwarf virus. Based on sequence similarities, it is predicted that FDV S8 encodes a minor core protein, while FDV S10 encodes an outer capsid protein. The evolutionary relationships of FDV to other reoviruses are discussed.The nucleotide sequence data for FDV S5, S6, S8 and S10 are available in the DDBJ/EMBL/GenBank databases under the accession numbers AY029521, AF356083, AY297693 and AY297694, respectively.     

Stereochemical aspects of the interaction of myosin and actomyosin with nucleotides

Summary The five possible analogues of ATP and the three possible analogues of ADP which contain single non-bridging sulphur atoms instead of oxygen in the polyphosphate structure have been used as probes of the interaction of nucleotides with myosin and actomyosin. Evidence is presented for the requirement of an , , -tridentate complex of magnesium and ATP as the substrate for myosin. Of the four possible tridentate MgATP diastereomers, the exo isomer (nomenclature of Cornelius & Cleland, 1978) appears to be the actual substrate.Abbreviations ATP Adenosine-5-O-triphosphate - ATP(-S) Adenosine-5-O-(1-thiotriphosphate) - ATP(-S) Adenosine-5-O-(2-thiotriphosphate) - ATP(-S) Adenosine-5-O-(3-thiotriphosphate) - ADP Adenosine-5-O-diphosphate - ADP(-S) Adenosine-5-O-(1-thiodiphosphate) - ADP(-S) Adenosine-5-O-(2-thiodiphosphate) - Enzyme Myosin ATPase (EC 3.6.1.3)     

Partitioning of Cortical and Deep Cytoskeleton Responses from Transient Magnetic Bead Twisting

We attempted to estimate in living adherent epithelial alveolar cells, the degree of structural and mechanical heterogeneity by considering two individualized cytoskeleton components, i.e., a submembranous cortical cytoskeleton and a deep cytoskeleton (CSK). F-actin structure characterizing each CSK component was visualized from spatial reconstructions at low and high density, respectively, especially in a 10-m-cubic neighborhood including the bead. Specific mechanical properties (Young elastic and viscous modulus E and ) were revealed after partitioning the magnetic twisting cytometry response using a double viscoelastic solid model with asymmetric plastic relaxation. Results show that the cortical CSK response is a faster ( ₁ 0.7s), softer (E₁: 63-109 Pa), moderately viscous (₁: 7-18 Pa s), slightly tensed, and easily damaged structure compared to the deep CSK structure which appears slower (₂ min), stiffer (E₂: 95-204 Pa), highly viscous (₂: 760-1967 Pa s), more tensed, and fully elastic, while exhibiting a larger stress hardening behavior. Adding drug depolymerizing actin filaments decreased predominantly the deep CSK stiffness. By contrast, an agent altering cell–matrix interactions affected essentially the cortical CSK stiffness. We concluded that partitioning the CSK within cortical and deep structures is largely consistent with their respective functional activities. © 2003 Biomedical Engineering Society. PAC2003: 8716Ka, 8716Ac, 8380Lz     

Factors influencing serum neopterin and β2-microglobulin levels in a healthy diverse population

Sera and questionnaire data from a population-based random sample of healthy adults was used to evaluate factors influencing neopterin and 2-microglobulin (2m) values. Both neopterin and 2m levels increased with age and were higher among white than blacks (mean values for whites and blacks: neopterin, 5.06 vs 4.49 nmol/L; 2m, 1.36 vs 1.28 mg/L). Gender differences were noted for 2m but not neopterin values (2m males vs females: 1.37 vs 1.29 mg/L). Neopterin values were lower among current smokers than among nonsmokers (4.32 vs 5.16 nmol/L) and were higher among users of antihistamines (5.46 among users vs 4.65 nmol/L among nonusers). Neopterin and 2m were correlated in this healthy adult population (adjustedr=0.53,P=0.001), yet no other interrelationships with numerous biologic markers except between 2m and serum-soluble interleukin-2 receptor levels (adjustedr=.41,P=0.05) were observed. These findings provide important baseline information to consider before planning or evaluating studies utilizing neopterin or 2m levels.     

Changes in blood cholesterol,protein fractions,and lipoproteins in functional disturbances of the central nervous system

Summary In experiments on 8 rabbits a study was made of the effect produced by nervous disorders on the protein-lipid composition of the blood. The method of electrophoresis of proteins and lipoproteins was used. In neurosis there is a drop of the total blood chlesterol, in the majority of the cases following a brief rise of its concentration in the blood; the percentage content of albumins fall with a corresponding rise of the -and, in individual cases, of the -and -globulin fractions. The -/-lipoproteins ratio increases. Observations carried out testify to an important role played by the CNS in the control of cholesterol, lipid, and protein metabolism.Presented by Active Member AMN SSSR, A. V. Lebedinskii Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 57, No. 1, pp. 30–32, January, 1964