A historical chronology of teaching physiological sciences to medical students in Hungary.

Starting from the second half of the 18th century, a brief chronology of teaching medical physiology and pathophysiology in Hungary is given in this article. Even when the major milestones of this history are only identified, one can recognize several significant achivements that may inspire the present and coming generations to develope and enrich this inheritance of high values. These achivements involve--inter alia--influential scientific "schools" founded by eminent professors, outstanding institutions of basic medicine, recognition of the relevance of the integrative approach in medical education, close relationship between teaching and scientific research, high-standard theoretical and practical training, teaching based on excellent domestic and foreign textbooks, extensive international relationships and experience.

Value of carcinoembryonic antigen (CEA) and cholesterol assays of ascitic fluid in cases of inconclusive cytology.

AIM: To determine whether assays of carcinoembryonic antigen (CEA) and cholesterol in ascites add diagnostic value to cytology. METHODS: The additional diagnostic efficacy of the biochemical assays was studied in the ascitic fluid from 130 patients, of whom 57 had peritoneal carcinomatosis. All diagnoses were verified by subsequent necropsy and/or histology. RESULTS: CEA concentrations over 5 ng/ml indicated carcinomas, occasionally without peritoneal involvement of the tumour. However, increased values were significantly more common in cancer with peritoneal involvement (p < 0.01), giving a sensitivity of 51% and specificity of 97% for carcinomatosis. A cholesterol value exceeding 1.21 mmol/litre was found in 93% of cancers with peritoneal involvement, but it was not entirely specific (96%) for carcinomatosis. Simultaneous increases in CEA and cholesterol concentrations were specific for carcinomatosis and this combination increased the sensitivity for diagnosing carcinomatosis from 77% with cytology alone to 88%. The correct diagnosis could thus be made in five of 12 cases with inconclusive cytology. CONCLUSIONS: The measurements of both CEA and cholesterol concentrations in ascites give additional specific information about peritoneal carcinomatosis and can therefore be a useful adjunct to cytology-in particular, in inconclusive cases.

Flow-induced constriction in arterioles of hyperhomocysteinemic rats is due to impaired nitric oxide and enhanced thromboxane A(2) mediation.

Hyperhomocysteinemia (HHcy) is thought to promote arteriosclerosis and peripheral arterial disease, in part by impairing the function of endothelium. Because flow-induced dilation is mediated by the endothelium, we hypothesized that HHcy alters this response by interfering with the synthesis/action of NO and prostaglandins. Thus, changes in the diameter of isolated, pressurized (at 80 mm Hg) gracilis skeletal muscle arterioles (diameter approximately 170 microm) from control and methionine diet-induced HHcy rats were investigated with videomicroscopy. Increases in intraluminal flow (from 0 to 25 microL/min) resulted in dilations of control arterioles (maximum, 34+/-4 microm). In contrast, increases in flow elicited constrictions of HHcy arterioles (-36+/-3 microm). In control arterioles, the NO synthase inhibitor N:(omega)-nitro-L-arginine-methyl ester significantly attenuated (approximately 50%) dilation, whereas the additional administration of indomethacin, an inhibitor of cyclooxygenase, eliminated flow-induced dilation. In the arterioles of HHcy rats, flow-induced constriction was not affected by N:(omega)-nitro-L-arginine-methyl ester, whereas it was abolished by indomethacin or the prostaglandin H(2)/thromboxane A(2) (TXA(2)) receptor antagonist SQ 29,548 or the TXA(2) synthase inhibitor CGS 13,080. Thus, in HHcy, increases in intraluminal flow elicit constrictions of skeletal muscle arterioles due to the impaired NO and enhanced TXA(2) mediation of the response, alterations that likely contribute to the development of peripheral arterial disease.

Simultaneously increased TxA(2) activity in isolated arterioles and platelets of rats with hyperhomocysteinemia.

We aimed to elucidate the effect of hyperhomocysteinemia (HHcy) on the synthesis of prostaglandins in rat skeletal muscle arterioles and platelets. Male Wistar rats were divided into 2 groups: (1) control rats, with plasma Hcy levels of 6.5+/-0.5 micromol/L (n=50) and (2) rats with HHcy, induced by daily intake of 1 g/kg body weight methionine in the drinking water for 4 weeks (plasma Hcy levels were 20.6+/-3.0 micromol/L, P<0.01 versus controls; n=50). Arterioles (diameter approximately 130 micrometer) were isolated from the gracilis muscle, cannulated, and pressurized (at 80 mm Hg), and changes in their diameters were followed by video microscopy. Constrictions to bradykinin (BK; 10(-10) to 10(-7) mol/L) were significantly greater in HHcy than in control rat arterioles (at 10(-9) mol/L BK, changes were 11+/-3% in control and 41+/-9% in HHcy rats). The cyclooxygenase inhibitor indomethacin (10(-5) mol/L), the prostaglandin H(2)/thromboxane A(2) (PGH(2)/TxA(2)) receptor antagonist SQ 29,548 (10(-6) mol/L), or the TxA(2) synthase inhibitor furegrelate (5x10(-6) mol/L) significantly decreased constrictions to BK in both groups but more so in HHcy arterioles, thus eliminating the difference between responses of HHcy and control arterioles. Constrictions to U46619 (a TxA(2) analogue) were significantly greater in HHcy than in control arterioles (at 10(-8) mol/L U46619, values for controls were 33+/-2% and 54+/-3% for HHcy). Endothelium removal or indomethacin treatment attenuated constrictions to U46619 in HHcy arterioles and eliminated the difference in responses. Also, aggregation of platelets from HHcy rats to collagen and ADP was significantly enhanced compared with controls (with 5 microgram/mL collagen: controls, 23+/-5%; HHcy, 49+/-5%; with 10(-7) mol/L ADP: controls, 25+/-3%; HHcy, 35+/-3%). Indomethacin or SQ 29,548 caused greater inhibition of aggregation of HHcy platelets compared with controls, thereby eliminating the differences between the 2 groups. Thus, HHcy enhances TxA(2) synthesis both in the arteriolar endothelium and platelets. By promoting vascular constriction and platelet aggregation simultaneously, these alterations are likely to contribute to the atherothrombotic vascular diseases described in HHcy.

Effects of early nutrition on free radical formation in VLBW infants with respiratory distress.

OBJECTIVE: We studied the development of essential fatty acid deficiency (EFAD) and its effects together with those of vitamin E deficiency on the free radical formation of very low birth weight (VLBW) infants with respiratory distress. METHODS: Infants were divided into three groups based on the way each was supplied with daily total energy intake: (1) by fat free parenteral nutrition only or by nutrition composed of (2) less than or (3) higher than 25% of total daily energy intake given in oral feeding. We measured plasma lipid parameters and autoxidative susceptibility (AOS) of red blood cells (RBCs). RESULTS: Plasma concentrations of linoleic acid were low in all the groups. After at least 14 days of feeding, eicosatrienoic acid (EA) was not detected. One week after the introduction of oral feeding, the abnormal triene/tetraene ratio of the groups had decreased, but was not normalized. Vitamin E deficiency was associated with significantly increased AOS, but EFAD was not. The two factors together caused an increase of AOS, that was additive. CONCLUSIONS: Our data confirm that EFAD increases AOS of RBCs in VLBW infants. We assume that prevention of EFAD in VLBW infants could decrease the prevalence of complications associated with free radical formation.

Metabolism of activated complement component C3 is mediated by the low density lipoprotein receptor-related protein/alpha(2)-macroglobulin receptor.

Complement component 3 (C3) and alpha(2)-macroglobulin evolved from a common, evolutionarily old, ancestor gene. Low density lipoprotein-receptor-related protein/alpha(2)-macroglobulin receptor (LRP/alpha(2)MR), a member of the low density lipoprotein receptor family, is responsible for the clearance of alpha(2)-macroglobulin-protease complexes. In this study, we examined whether C3 has conserved affinity for LRP/alpha(2)MR. Ligand blot experiments with human (125)I-C3 on endosomal proteins show binding to a 600-kDa protein, indistinguishable from LRP/alpha(2)MR by the following criteria: it is competed by receptor-associated protein (the 39-kDa receptor-associated protein that impairs binding of all ligands to LRP/alpha(2)MR) and by lactoferrin and Pseudomonas exotoxin, other well known ligands of the multifunctional receptor. Binding of C3 is sensitive to reduction of the receptor and is Ca(2+)-dependent. All these features are typical for cysteine-rich binding repeats of the low density lipoprotein receptor family. In LRP/alpha(2)MR, they are found in four cassettes (2, 8, 10, and 11 repeats). Ligand blotting to chicken LR8 demonstrates that a single 8-fold repeat is sufficient for binding. Confocal microscopy visualizes initial surface labeling of human fibroblasts incubated with fluorescent labeled C3, which changes after 5 min to an intracellular vesicular staining pattern that is abolished in the presence of receptor-associated protein. Cell uptake is abolished in mouse fibroblasts deficient in LRP/alpha(2)MR. Native plasma C3 is not internalized. We demonstrate that the capacity to internalize C3 is saturable and exhibits a K(D) value of 17 nM. After intravenous injection, rat hepatocytes accumulate C3 in sedimentable vesicles with a density typical for endosomes. In conclusion, our ligand blot and uptake studies demonstrate the competence of the LRP/alpha(2)MR to bind and endocytose C3 and provide evidence for an LRP/alpha(2)MR-mediated system participating in C3 metabolism.

Dysfunction of nitric oxide mediation in isolated rat arterioles with methionine diet-induced hyperhomocysteinemia.

In humans, increased plasma homocysteine (Hcy) has been shown to be correlated with occlusive arterial diseases and atherosclerosis. Studies of isolated conductance vessels of experimental animals suggest that Hcy may interfere with local vasoregulatory mechanisms, yet the effect of hyperhomocysteinemia (HHcy) on the function of microvessels, such as skeletal muscle arterioles, has not been investigated. Male Wistar rats were divided into 2 groups: control rats (C; plasma Hcy, 7.1+/-0.3 micromol/L; n=25), and rats made HHcy by 1 g/kg body weight daily intake of methionine in the drinking water for 4 weeks (plasma Hcy, 23.6+/-2.9 micromol/L; P<0.01 versus C; n=25). First-order arterioles ( approximately 130 micrometer in diameter) were isolated from gracilis muscle, cannulated, and pressurized (80 mm Hg, no-flow conditions). Changes in diameter were observed by videomicroscopy. Arteriolar constrictions to norepinephrine (NE; 3x10(-7) mol/L) were significantly (P<0.01) greater in HHcy compared with C rats (C, 37.7+/-4.9%; HHcy, 59.5+/-5. 2%). Removal of the endothelium (-E) augmented NE-induced constrictions only in arterioles from C rats, whereas it had no effect on responses of arterioles from HHcy rats (C-E, 55.9+/-6.9%; HHcy-E, 56.5+/-7.0%). Dilations to cumulative doses of acetylcholine (ACh; 10(-8) mol/L) were significantly reduced in arterioles from HHcy rats (C, 64.0+/-5.2%; HHcy, 24.1+/-6.8%). Inhibition of nitric oxide (NO) synthesis with N(omega)-nitro-L-arginine (L-NNA; 10(-4) mol/L) significantly decreased ACh-induced dilations of C arterioles, whereas it did not affect HHcy arterioles. Similar alterations were found in arteriolar dilations to histamine, another known NO-dependent agonist. Endothelium-independent dilations to the NO donor sodium nitroprusside were not different in arterioles from C and HHcy rats, either in the presence or absence of L-NNA. Presence of superoxide dismutase and catalase (scavenger of reactive oxygen metabolites) did not affect HHcy-induced alterations in the ACh response. We conclude that hyperhomocysteinemia reduces rat skeletal muscle arteriolar dilations in response to ACh and histamine, and enhances constrictions to NE, alterations that are likely to be caused by the reduced mediation of these responses by NO. The reduced activity of NO in arterioles may contribute to the microvascular impairment described in HHcy.

Increased myogenic tone in skeletal muscle arterioles of diabetic rats. Possible role of increased activity of smooth muscle Ca2+ channels and protein kinase C.

OBJECTIVE: The diabetes mellitus-induced microangiopathy is still not clearly characterized. In this study we aimed to elucidate the effect of streptozotocin (STZ)-induced diabetes on myogenic response of isolated rat skeletal muscle arterioles and the mechanisms responsible for its alterations. METHODS: Male rats were divided into two groups: (1) control rats (C, plasma glucose: 6.4 +/- 0.5 mmol/l, n = 40) (2) diabetic rats (DM, 65 mg/kg STZ i.v., plasma glucose: 25.7 +/- 0.7 mmol/l, n = 40). Changes in diameter of isolated, cannulated gracilis skeletal muscle arterioles (approximately 130 microns in diameter) were measured by video-microscopy. RESULTS: Step increases in perfusion pressure (PP; from 10 to 140 mmHg) elicited significantly greater constrictions in DM than in C gracilis arterioles, in the presence of the endothelium (E). Also, a step increase in PP (from 40 to 100 mmHg) elicited greater and faster constrictions in DM vs. C arterioles. There were no significant differences in the pressure-passive diameter (in Ca2+ free solution) curves of arterioles. Dilations to acetylcholine were impaired in arterioles of DM as compared to those of C rats (EC50, C: 4.0 +/- 0.9 x 10(-9) mol/l, DM: 4.8 +/- 2.0 x 10(-8) mol/l (p < 0.01), and unaffected by inhibition of nitric oxide synthesis with L-NNA (10(-4) mol/l). Arteriolar constrictions to norepinephrine (NE) were significantly greater in DM compared to those of C rats (EC50, C: 6.2 +/- 0.6 x 10(-7) mol/l, DM: 8.0 +/- 2.0 x 10(-8) mol/l, p < 0.01) both in the presence and absence of E. In the absence of the E, constrictions to increases in pressure, or Ca2+ (0.25-7.5 mmol/l), or the voltage-dependent Ca(2+)-channel agonist Bay K 8644 (EC50; DM: 4.2 +/- 1.5 x 10(-10) mol/l, C: 1.7 +/- 0.8 x 10(-9) mol/l, p < 0.05) or the protein kinase C activator phorbol 12-myristate 13-acetate (PMA, EC50; DM: 6 +/- 2 x 10(-9) mol/l, C: 2 +/- 1 x 10(-8) mol/l, p < 0.05) were significantly greater in arterioles of DM compared to those of C rats. CONCLUSION: The novel findings of our study are that in diabetes mellitus the myogenic response of rat skeletal muscle arterioles is enhanced, which seems to be independent from the impaired endothelial function present simultaneously, and likely due to the increased activity of voltage-dependent Ca2+ channels and/or upregulation of protein kinase C in arteriolar smooth muscle.

[Oncologic diagnosis of serous effusions in body cavities (cytologic study and evaluation of cholesterol and carcinoembryonic antigen levels)]. / A testüregi folyadékgyülemek daganatdiagnosztikája (A cytologia, a koleszterin és a carcinoembryonalis antigén vizsgálat együttes értékelése).

Conventional cytological evaluation of serous effusions often yields border line result: apart from positive (malignant) or negative (benign) diagnoses, a relatively large part of the findings are "suspicious for malignancy" (P3). In the present paper the authors have analysed to what extent contributes the determination of cholesterol and CEA levels of ascites and pleural effusion to the diagnostic accuracy of cytologically "suspicious" (P3) cases. In 155 histologically controlled cases, specificity, sensitivity and diagnostic efficiency were assessed on the basis of cytology as well as the determination of CEA and cholesterol levels. Statistical parameters were determined for each method separately and for their combined application. According to the findings, cholesterol and CEA levels over 1.16 mmol/l and 2.5 ng/ml, respectively, indicate malignancy. In 19 out of 29 cytologically "suspicious" cases (66%), which histologically proved to be positive, cholesterol and/or CEA levels were elevated. In all of the 12 non-neoplastic "suspicious" cases the two parameters were under the cutoff values. The application of an easy and inexpensive cholesterol test proves to be a sensitive technique for indicating carcinomatosis and it completes adequately the specific cytological evaluation. If clinical symptoms speak for tumor, but the cytology is negative, the evaluation of CEA level may prove to be useful as far as it can indicate cancer not yet accompanied by carcinomatosis.

Noncovalent interactions in maintaining the native structure of low density lipoprotein.

The integrity and the surface charge distribution of native low density lipoprotein (LDL) are prerequisites of its binding to the LDL receptor. Oxidation is one of the most important physiological effects resulting in an altered structure and metabolism of LDL. To reveal forces responsible for maintaining the intact structure of LDL in the absence of cells we have determined the kinetics of lipid peroxidation, changes in electrophoretic mobilities and size distributions of LDL samples as a function of Cu++ induced oxidative modification in a cell-free system at two different (50 mM and 150 mM) ionic strengths by electrophoretic and dynamic light scattering. Our data show that the lipid peroxidation is almost complete before LDL is degraded at 50 mM while a slight extent of lipid peroxidation is enough to result in the same effect at 150 mM. These suggest that both ionic and hydrophobic interactions are necessary to maintain the integrity of the LDL molecule.

Effects of administration of different intravenous lipid emulsions on plasma LP-X concentrations in the rat.

BACKGROUND: Prolonged parenteral nutrition with lipid emulsions is essential to provide sufficient energy supply and to avoid essential fatty acid deficiency in preterm infants. However, chronic administration of lipid emulsions may lead to the development of pathological plasma lipid and LP-X concentrations. The aim of this study was to evaluate the relative importance of the phospholipid-triglyceride (PL-TG) ratio and the source of phospholipid in lipid emulsions, with respect to plasma lipid and LP-X levels. METHODS: Rats were infused for 9 days with IV lipid emulsion containing 10% (IL-10) or 20% (IL-20) egg lecithin or Lipofundin containing 20% soya lecithin (LF), with PL-TG ratios of .12, .06, and 0.75, respectively. RESULTS: LF significantly increased plasma triglyceride concentration (p < .01), whereas the rise in cholesterol levels observed with all emulsions was primarily caused by the increase in low-density lipoprotein cholesterol concentrations. The plasma phospholipid concentration was increased most by IL-10 (p < .005). There was a strong correlation between the PL-TG ratio of emulsions and the developing plasma phospholipid and LP-X concentrations (r2 = .91 and .96, respectively), despite the different origin of phospholipids in the emulsions, suggesting that it is the PL-TG ratio, rather than the source of phospholipids in lipid emulsions that primarily influences developing plasma lipid and LP-X concentrations. CONCLUSION: These results indicate that the administration of lipid emulsions with lower PL-TG ratios should be considered, to avoid the development of pathological plasma lipoprotein concentrations.

Erythrocyte lipids in triose-phosphate isomerase deficiency.

Marked hypoalphalipoproteinemia was found together with relatively low serum cholesterol, triacylglycerol, and LDL levels in a triose-phosphate isomerase (TPI; D-glyceraldehyde-3-phosphate ketol-isomerase, EC 5.3.1.1)-deficient Hungarian family, especially in the two compound-heterozygote brothers. Apart from a slight increase in palmitic and stearic acids together with a slight decrease in oleic and linoleic acids, no other changes were found in the fatty acid composition of the erythrocyte phospholipids. Anisotropy measurements with n-(9-anthroyloxy) stearic and -palmitic acid fluorophores revealed increased motional freedom of the fatty acid chains in the external lipid layers of the intact erythrocytes from all members of the TPI-deficient family as compared with normal age-matched controls. This asymmetric increase in membrane fluidity was found to be significantly higher in the propositus than in his compound-heterozygote brother without any neurological disorders. The change in membrane fluidity may result from as-yet-unresolved aspects of the lipid composition of the plasma membrane. Our findings that the differences between the TPI-deficient individuals and normal controls and the differences between the two compound-heterozygote brothers were all absent in the phospholipid extracts of the same erythrocytes favor the assumption that the increased motional freedom of the fatty acid chains in the external surface of the bilayer is caused by the binding of the mutant TPI molecule to the N-terminal sequence of band 3 protein.

Long-term effects of unsaturated fatty acid dominance on the release of free radicals in the rat.

The aim of this study was to investigate the effects of an abundance of unsaturated fatty acids, hyperoxia, and vitamin E on free radical formation in vitamin E-deficient rats. The excess of unsaturated fatty acids was achieved by i.v. administration of a lipid emulsion (Intralipid). To assess free radical formation, we measured the autooxidative susceptibility of red blood cells (AOS) and the thiobarbituric acid reacting substrates (TBARS) in LDL and HDL. Intralipid significantly increased all the measured parameters compared with controls (AOS: 1385 +/- 73 versus 1056 +/- 55; LDL-TBARS: 4955 +/- 422 versus 1050 +/- 33; HDL-TBARS: 6855 +/- 573 versus 1033 +/- 26 nmol TBARS/mmol). Hyperoxia alone increased AOS more than Intralipid alone, whereas LDL- and HDL-TBARS concentrations were affected less by hyperoxia than lipid emulsion. The combination of hyperoxia and Intralipid was most effective in raising all measured parameters (AOS: 2285 +/- 141; LDL-TBARS: 6716 +/- 318; HDL-TBARS: 14614 +/- 1000 nmol TBARS/mmol). Vitamin E completely prevented the increase in AOS, LDL-TBARS, and HDL-TBARS without fully reversing the increase in free radical formation caused either by Intralipid or by the combination of hyperoxia and Intralipid. These findings suggest that vitamin E supplementation is beneficial to counter increased free radical formation, such as that in response to hyperoxic attacks or lipid-containing parenteral nutrition, which is frequently encountered in the treatment of premature infants.

Effect of metoprolol and pindolol monotherapy on plasma lipid- and lipoprotein-cholesterol levels (including the HDL subclasses) in mild hypertensive males and females.

Forty-five patients with mild hypertension were treated for 2 months with either metoprolol or pindolol in a randomized, blind, crossover study. The effects of metoprolol (100-300 mg/day) and pindolol (5-15 mg/day) on triglyceride (TG), cholesterol (C), high-density lipoprotein cholesterol (HDL-C), and HDL subfraction (HDL2-C and HDL3-C) levels were compared in males and females separately. Pindolol and metoprolol significantly elevated (10% above baseline level) the plasma TG level in both males and females. After metoprolol treatment, the HDL-C level remained unchanged in both sexes; however, a shift was found between HDL2-C and HDL3-C:HDL2-C decreased and a concomitant elevation in HDL3-C was observed. Pindolol significantly decreased total C, HDL-C, and HDL2-C levels in males. A similar trend (although the changes were not significant) was found in females. The results demonstrate the role of beta blockers in the inhibition of TG-rich lipoprotein elimination. These findings suggest that during long-term administration of metoprolol and pindolol, risks and benefits from beta-blocker therapy must be carefully considered. Continuous monitoring of lipid profiles is suggested during this treatment in order to avoid the potential worsening effect of beta blockers on risk factors of ischemic heart disease.

Binding of fibronectin to human lipoproteins.

High molecular mass adhesive glycoprotein plasma fibronectin binds to isolated HDL and LDL lipoprotein fractions in a solid phase radioimmunoassay. Mean dissociation constants of interaction of fibronectin and immobilized HDL and LDL lipoproteins isolated from eight patients with type IIa and type IV hyperlipoproteinemia are 7.8 +/- 3.2 X 10(-7) mol/l and 6.8 +/- 2.6 X 10(-7) mol/l, respectively. Fibronectin can also bind to HDL and LDL isolated from six healthy subjects with mean dissociation constants of 2.07 +/- 0.45 X 10(-6) mol/l and 2.25 +/- 0.48 X 10(-6) mol/l, respectively. The binding is not dependent on the presence of divalent cations. Fibronectin-lipoprotein interaction is inhibited by soluble lipoproteins. There is no observable interaction between fibronectin and VLDL fraction. Binding of fibronectin to HDL and LDL lipoproteins can have an in vivo significance, since the interaction may play a role in the metabolism, deposition of lipoproteins into the vessel wall and in atherogenesis.

Oxytocin regulates Ca2+ level in myometrium by influencing phosphoinositide metabolism.

The effect of oxytocin on phosphoinositide metabolism as well as on membrane protein phosphorylation in myometrial tissue was studied. Oxytocin enhanced the 32P incorporation into phospholipids in myometrial tissue. The effect of oxytocin on phosphoinositide metabolism was also detected in plasma membrane of 20 days pregnant rats. Phosphorylated membrane lipids have been analysed and phosphatidylinositol 4, 5-bisphosphate proved to be the main reaction product. Oxytocin enhanced the 32P incorporation into phospholipids measured in the first 30 sec then the labeling decreased more rapidly then in case of the control. The effect of oxytocin proved to be concentration dependent. The protein phosphorylation was also influenced by oxytocin. However the amount of alkylphosphate formed depended on the presence or absence of Ca2+, Ca2+-calmodulin and cyclic AMP, oxytocin influenced the protein phosphorylation in the presence of Ca2+-calmodulin only.

Lipid and lipoprotein measurements in a normal, adult Cuban population.

An attempt was made to determine the normal reference values of lipid- and lipoprotein levels (cholesterol), triglycerides, cholesterol in high- and low-density lipoproteins) in a selected, apparently healthy, Cuban population. Results were expressed as mean, and various percentiles of measured values; two ratios: Risk 1 (LDL-C/HDL-C) and Risk 2 (TC/HDL-C) were also calculated. Approximately 40% of the subjects aged 20 to 30 years had cholesterol values above 200 mg/dl. Females had significantly higher cholesterol HDL-C values than males, whereas the concentrations of LDL-C and LDL were higher in males. Risk 2 ratios were elevated in males. A correlation was shown between lipid levels and age. There was a strong negative correlation between HDL-C and relative body weight. It is suggested that obesity might be an individual risk factor in the population studied.

Lipid and lipoprotein profiles in Cuban children of three age groups.

We determined the lipid and lipoprotein levels in a selected group of apparently healthy adult Cuban subjects in a previous paper /27/. In this paper the basic lipid variables (TC, TG, HDL-C) in 271 healthy children are published. LDL-C levels were also calculated. A small, but continuous, rise was found in the TC level between 0 and 14 years in both sexes. The rise of TG was accompanied by HDL increase in girls but by LDL increase in boys. This phenomenon might explain the augmented susceptibility of men to ischaemic heart disease. Children at "high risk" should be identified (in case of positive family history of ischaemic heart disease) by cholesterol determinations, the borderline of the pathologic cholesterol levels seems to be very similar to that found in the USA, 170-190 mg/dl in the age group between 0 and 14 years.

Colloidal gold-labeled lipoprotein binding and internalization in adrenocortical cells in vitro.

Human (normal and adenomatous) and rat (normal) adrenocortical cells were incubated in vitro with colloidal gold labeled low-density (LDL-Au) and high-density (HDL-Au) lipoproteins, respectively, in order to visualize lipoprotein binding and internalization at an electron microscopic level. Both normal and adenomatous human adrenocortical cells accumulated LDL-Au by receptor-mediated endocytosis via coated pits, coated vesicles, noncoated vesicles, and lysosomes. HDL-Au was not internalized. In rat adrenocortical cells, both HDL-Au and to a lesser extent LDL-Au were internalized. It is concluded that LDL-Au and HDL-Au conjugates can be used to identify lipoprotein receptors and to follow lipoprotein internalization in adrenocortical cells.