Search PubMed⌕ Search

Biomedical subjects

E Herrera

Publications and source records attributed to E Herrera.

At least 91 records · Page 5Linked to original sources
PubMed1994

Cutaneous leishmaniasis in subtropical Ecuador: popular perceptions, knowledge, and treatment.

Popular perceptions and knowledge about cutaneous leishmaniasis and its treatment were studied in an endemic area of subtropical Northwest Ecuador. Although most of the adults surveyed were familiar with the disease, the vector, and traditional treatments, many showed a lack of knowledge about transmission of the disease, ulcer healing, and conventional treatment. Gender was found to have a significant impact on disease risk, perceptions, and treatment knowledge. Males experienced a risk of contracting cutaneous leishmaniasis that was almost triple that of women. Men were also more likely to perceive that the disease seriously diminished the victim's capacity to work. Women, on the other hand, were more prone to perceive that cutaneous leishmaniasis was a serious disease that significantly decreased self-esteem. Although 80% of the subjects knew at least one method of treating the disease, women tended to know more methods than men. Most of 150 different therapies reported involved the use of indigenous plants, chemicals, acids, antibiotics, heat treatments, or petroleum by-products. Some of these treatments could have clinical value. However, only 7% of the subjects knew about pentavalent antimonials. Almost 70% of the subjects with a past or present infection history were treated solely by traditional methods; only 12% received a full course of Glucantime, while 7.5% got an incomplete course. The findings indicate that it will be important to consider the identified gaps in knowledge and gender perceptions regarding the disease and its treatment when planning future control programs.

Adolescent↗
PubMed1993

Cholesteryl ester transfer activity in lipoprotein lipase deficiency and other primary hypertriglyceridemias.

Cholesteryl ester transfer protein (CETP) activity was measured in d > 1.21 g/ml plasma from hypertriglyceridemic patients and compared with normolipidemic subjects. The assay consisted in measuring the specific transfer of [3H]cholesteryl oleate from a prelabelled, apo E-poor HDL fraction to VLDL after incubation at 37 degrees C in the presence of the d > 1.21 g/ml plasma sample: the lipoproteins were then separated by precipitation with dextran sulfate/Mg2+ solution. Increasing the volume of d > 1.21 g/ml plasma or purified human CETP in the assay produced linear responses in measured activity, whereas, either during incubation at 4 degrees C or in the presence of rat plasma instead of human plasma, the transfer of [3H]cholesteryl oleate to VLDL was not stimulated. Thus, the assay reflects changes in CETP in the sample and appears to be suitable for measuring CETP activity in d > 1.21 g/ml plasma. CETP activity was very similar in the two groups of normolipidemic subjects considered: adolescents (203 +/- 11 nmol esterified cholesterol transferred per 8 h/ml plasma) and adults (215 +/- 5). Patients were grouped into lipoprotein-lipase (LPL)-deficient and non-LPL-deficient according to their enzyme activity in postheparin plasma. CETP activity was highly increased in LPL-deficient, severe hyperchylomicronemic patients (430 +/- 42) and was directly correlated with VLDL levels in the non-LPL-deficient individuals. Marked differences were observed in the lipid composition of HDL and apolipoprotein A-I levels among patients and controls. In the control group, CETP activity was correlated only with HDL-triglyceride and HDL-triglyceride/apo A-I mass ratio, which is compatible with the physiological role of CETP in transferring triglyceride to HDL from other lipoprotein particles. When all hypertriglyceridemic patients were considered together, CETP activity was inversely correlated with apo A-I and HDL-cholesterol, whereas it was directly correlated with HDL-triglyceride/HDL-cholesterol and HDL-triglyceride/apo A-I mass ratios. The results indicate that the enhanced CETP activity associated with hypertriglyceridemia contributes to the compositional change of HDL, which in turn may be responsible for the reduction of HDL levels in this condition.

Adolescent↗
PubMed1993

Studies with etofibrate in the rat. Part II: A comparison of the effects of prolonged and acute administration on plasma lipids, liver enzymes and adipose tissue lipolysis.

To contribute to the understanding of the hypolipidemic action of etofibrate, which is the 1,2-ethandiol ester of clofibric acid and nicotinic acid, 300 mg of this drug/kg body weight or of the medium were administered daily by a stomach tube to normolipidemic rats. Some animals were decapitated at the 10th day of daily treatment (prolonged treatment), whereas others were studied at different times after one single administration (acute treatment). In animals on prolonged treatment etofibrate decreased plasma levels of cholesterol, triacylglycerols, free fatty acids (FFA) and glycerol, as well as the total and unesterified cholesterol concentrations, in liver microsomes. In these rats, etofibrate increased the activity of liver cytosolic glycerol-3-P dehydrogenase, whereas it decreased the activity of both microsomal HMG-CoA reductase and cholesterol 7 alpha-hydroxylase and did not affect acyl-CoA: cholesterol acyltransferase (ACAT). At 3, 5 and 7 h after acute treatment, etofibrate decreased plasma levels of triacylglycerols, glycerol and FFA, and this effect disappeared at 24 h, whereas plasma cholesterol did not change 3 h after etofibrate but decreased at 5 and 7 h and remained low after 24 h, and a similar change was found in the liver microsomes free cholesterol concentration. However, with the exception of a significant reduction in cytosolic glycerol-3-P dehydrogenase at 7 h and in ACAT at 5 h, acute etofibrate treatment did not affect the activity of the liver enzymes studied. At low concentrations (10(-5) M) in the incubation medium, etofibrate decreased the release of both FFA and glycerol by epididymal fat pad pieces incubated in vitro. These findings together with those previously reported by us in rats using a similar etofibrate treatment protocol [6] indicate that etofibrate decreases the availability of lipolytic products in the liver by acting on their release from adipose tissue and on their intrinsic hepatic metabolism. Consequently, this drug would decrease liver VLDL triacylglycerol synthesis and secretion, which together with facilitating the clearance of circulating triacylglycerols causes its hypotriglyceridemic effect. The hypocholesterolemic effect of etofibrate after acute treatment may be a secondary consequence of the reduced liver VLDL production caused by decreased adipose tissue lipolysis, but after prolonged treatment, this effect also seems to be influenced by the inhibition of HMG-CoA reductase activity which would reduce cholesterol synthesis.

Adipose Tissue↗
PubMed1993

Different hydrolytic efficiencies of adipose tissue lipoprotein lipase on very-low-density lipoprotein subfractions separated by heparin-Sepharose chromatography.

Human very-low-density lipoproteins (VLDL) were subfractionated by heparin-Sepharose chromatography into an unbound (A) and three bound (B, C and D) populations at increasing ionic strengths. Subfractions were characterized regarding their chemical composition and efficiency of triacylglycerol hydrolysis by rat adipose tissue LPL. The triacylglycerol content decreased, whereas the cholesterol and protein contents increased from subfractions A and B to subfraction D. VLDL-D showed the highest apo E/apo C ratio, though all the subfractions contained appreciable apo E. Appearance of VLDL-A resulted from exceeding the binding capacity of the column, since practically all its particles eluted at positions of bound VLDL under re-chromatography. Subfractions B, C and D stimulated LPL activity on emulsified tri[14C]oleoylglycerol to a similar extent, indicating that their apo C-II content was equally effective activating LPL. Incubation of tri[14C]oleoylglycerol labeled VLDL subfractions with fat pad pieces in the presence or absence of heparin resulted in greater hydrolysis and fatty acid uptake for VLDL-B and -C than for VLDL-D, a pattern observed over a wide range of LPL activities in the media. We conclude: (1) any VLDL particle can interact with heparin, which is consistent with the presence of apo E in all the subfractions, and (2) triacylglycerols in apo E-rich VLDL are less efficiently hydrolyzed by LPL than those in apo E-poor particles. We propose that richness in apo E impairs LPL action upon VLDL and decreases the rate of delivery of fatty acids to peripheral tissues.

Adipose Tissue↗
PubMed1993

Interindividual variation in the partition of lipoprotein(a) into lipoprotein subfractions.

In order to evaluate cardiovascular risk, we analyzed the lipid composition of HDL and the presence of lipoprotein(a) [Lp(a)] by both agarose gel electrophoresis and enzyme-linked immunoassay (ELISA). In 681 plasmas we found a close correspondence between the existence of a visible sinking pre-beta lipoprotein band and a concentration of Lp(a) higher than 300 mg/L. In the sinking pre-beta(+) samples, the HDL-cholesterol level obtained by differential ultracentrifugation was significantly higher than that obtained by precipitation with the MgCl2-phosphotungstic acid reagent; and the difference between these HDL-cholesterol values was linearly correlated with plasma Lp(a) concentration. Moreover, the other HDL lipid components and the lipid mass ratios of HDL isolated by ultracentrifugation were significantly different from those of HDL isolated by precipitation, and these changes were also correlated with plasma Lp(a). These differences are attributed to Lp(a) because it was detected in the 1.063-1.21 kg/L plasma fractions, whereas it was absent in the plasma supernates after precipitation with MgCl2-phosphotungstic acid. Although to a lesser extent, Lp(a) was also present in the LDL and VLDL density ranges and it directly depended on both the Lp(a) and the triglyceride plasma concentrations. The proportion of Lp(a) in HDL as related to that in LDL density fractions decreased as Lp(a) plasma levels increased, reflecting an interindividual variation of Lp(a) density species. Since 90% of our study population had detectable Lp(a) in plasma, the results reinforce the concept that the ultracentrifugation method is not equivalent to precipitation in most samples, and the contaminant effect of Lp(a) cannot be predicted because of Lp(a) partition into the different lipoprotein fractions.

Cholesterol, HDL↗
PubMed1992

[Serum lipoprotein (a) levels during treatment with LDL apheresis for homozygous familial hypercholesterolemia].

BACKGROUND: Due to the double atherogenic and antifibrinolytic action of lipoprotein (a) (Lp [a]) and its predictive value of cardiovascular disease in hypercholesterolemic patients, we document in the present work the changes in Lp (a) levels of a patient with homozygous familial hypercholesterolemia after one year of LDL-apheresis treatment. METHODS: A child with LDL-receptor deficiency under weekly LDL-apheresis treatment with dextran-sulfate columns. Serum samples were taken in basal conditions (pre-apheresis) and post-apheresis, as well as from the perfusion system to evaluate the lipoprotein retention capacity of the columns. Samples were processed for Lp (a) determination by ELISA with polyclonal antibodies. RESULTS: When the treatment was initiated, the patient's Lp (a) serum levels were very high (997 mg/l), and they reduced progressively with the apheresis sessions. After one year of treatment, maximum Lp (a) concentration is only slightly higher than 400 mg/l, whereas minimum Lp (a) concentration is lower than 50 mg/l. Dextran-sulfate columns in the apheresis system retain every lipoprotein containing apo B, including LDL and Lp (a), with high affinity and high capacity in such a way that the treatment of three-fold the plasma volume of the patient results in an 85% decrease of Lp (a) levels. After each LDL-apheresis treatment, there is a progressive increase in Lp (a) concentration. The analysis of these data allowed the estimation of the fractional catabolic rate of Lp (a) in the patient, which was 0.08 pools/day. Simultaneous treatment with lovastatin (20 mg/day) did not alter this parameter or Lp (a) serum concentration. CONCLUSIONS: After one year of weekly LDL-apheresis treatment, the patient's average Lp (a) serum concentration is lower than 300 mg/l, which is below the risk threshold level. Therefore, apheresis with dextran-sulfate columns is a very effective treatment for the reduction of both LDL and Lp (a) serum concentrations in homozygous familial hypercholesterolemia.

Blood Component Removal↗
PubMed1992

Longitudinal study of plasma lipoproteins and hormones during pregnancy in normal and diabetic women.

Plasma lipoproteins were studied longitudinally at the 1st, 2nd, and 3rd trimester of gestation and at postpartum and postlactation in 12 age-matched PGDM women, 9 GDM women, and 12 healthy control subjects. FPG and HbA1c were higher in every case in PGDM women than in control subjects, whereas in GDM patients, glucose was augmented only after parturition. FFA and beta-hydroxybutyrate levels were higher in both PGDM and GDM patients than in control subjects during gestation but not after parturition. Total TGs and VLDL, LDL, and HDL TGs increased with gestational time in the three groups and declined at postpartum, and although total cholesterol and VLDL, LDL, and HDL cholesterol followed a similar trend, their rise was less pronounced, and the decline after parturition was slower than that of the TGs in the three groups, with no difference among them. The VLDL TG/cholesterol ratio declined in the three groups at the 3rd gestational trimester, whereas in both LDL and HDL, the TG/cholesterol ratio, but not the cholesterol/phospholipid ratio, increased during gestation in the three groups, indicating a specific enrichment of TGs in these particles. The increase in apoA-I and apoB with gestation was parallel to the respective changes in HDL and LDL cholesterol and, again, no difference was observed between the three groups. Plasma levels of beta-estradiol, progesterone, and prolactin increased sharply with gestation and declined at postpartum in the three groups, but absolute values of beta-estradiol and prolactin, at the three trimesters of gestation, were lower in PGDM patients, but progesterone levels were lower than controls in GDM women only at the 3rd trimester. (ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1992

A rapid and sensitive method for HPLC cholesterol determination in bile.

A relatively little time consuming simple method based on the treatment of bile with cholesterol oxidase and subsequent high performance liquid chromatography measurement of the 3-ketocholesterol produced in order to determine the level of the cholesterol concentration is described. The method avoids bilirubin interferences, has high reproducibility and recovery assays give 100% values. It is highly sensitive and suitable for use in the determination of cholesterol concentrations in bile and other bilirubin containing biological fluids.

Animals↗
PubMed1992

Glucose tolerance tests during gestation in the unanesthetized rat.

To establish the temporal stages at which changes in insulin/glucose interactions may appear during gestation in the rat, unanesthetized animals were subjected to oral glucose tolerance tests (2 g glucose/kg) at days 15 and 21 of gestation and were compared to virgin female controls. On day 15 glucose tolerance is enhanced in the pregnant rat whereas plasma insulin levels are like those in control animals. On day 21 glucose tolerance does not differ between the two groups although insulin is higher in the pregnant animals. Results show 2 differentiated stages of insulin/glucose relationships throughout gestation in the rat with enhanced insulin sensitivity on day 15 and enhanced insulin resistance during late gestation. It is suggested that these changes contribute to the anabolic tendencies of the mother during mid gestation and her catabolic condition during late gestation.

Animals↗
PubMed1992

Combination of an enzymatic method and HPLC for the quantitation of cholesterol in cultured cells.

The study of the cellular events that lead to the foam cell formation requires the development of fast, accurate, and sensitive methods to quantify cholesterol in cultured cells. Here we describe a procedure that allows the rapid determination of free and total cholesterol in a reduced number of cells, which makes it very suitable for cholesterol determination in cell cultures. The method consists of the enzymatic conversion of cholesterol to cholest-4-ene-3-one by cholesterol oxidase followed by the analysis of the sample by high performance liquid chromatography (HPLC) to detect this oxidized product. Due to the relatively high wavelength at which cholest-4-ene-3-one has its maximum absorption (240 nm), other cellular components do not interfere with the chromatographic procedure and prior lipid extraction is not required. Moreover, the duration of each chromatogram is about 3 min, contributing to the celerity of the method. All the cholesteryl esters used (oleate, palmitate, stearate and linoleate) were quantitatively hydrolyzed by incubation with cholesterol esterase; this was observed to occur with both pure standards and in cell homogenates. Sensitivity is enough to allow the determination of free and total cholesterol in less than 5 x 10(3) cells. We have applied this method to human monocyte-derived macrophages and the values obtained for free and total cholesterol are in close agreement with published data.

Cells, Cultured↗
PubMed1992

Dextran sulfate complexes with potassium phosphate to interfere in determinations of high-density lipoprotein cholesterol.

The interference of dextran sulfate with the colorimetric determination of free cholesterol causes an increase in the absorbance that is proportional to the dextran sulfate concentration in the sample. This makes estimation of the free cholesterol concentration unreliable in high-density lipoprotein-containing supernates obtained after plasma precipitation with dextran sulfate/MgCl2. Analysis of the absorption spectrum demonstrated that the absorbance increase was due to turbidity. We observed this effect with colorimetric reagents based on potassium phosphate buffer but not with those based on sodium phosphate or Tris buffers. This effect is ascribed to dextran sulfate because neither the omission of Mg2+ ions nor their chelation with EDTA prevented turbidity, whereas precipitation of dextran sulfate with Ba2+ counteracted this effect. Therefore, potassium phosphate-buffered reagents appear unsuitable for colorimetric lipid determinations in samples containing dextran sulfate.

Barium↗
PubMed1991

[Treatment of homozygotic familial hypercholesterolemia with continuous apheresis of low density lipoproteins].

A boy of 8 years 4 months of age was diagnosed as having homozygotic familial hypercholesterolemia and commenced treatment with an apheresis technique of low density lipoproteins. This procedure consists in the extracorporeal elimination of low density lipoproteins by fixing the same in a cellulose column with dextran-sulphate. Each session lasts between 90-150 minutes and is carried out weekly. Prior to initiation of the treatment, the total plasmatic concentration of cholesterol was 24 mml/l (930 mg/dl), low density lipoprotein ligated cholesterol 22.6 mmol/l (876 mg/dl) and high density lipoprotein ligated cholesterol 0.98 mmol/l (38 mg/dl). Following 8 weeks of treatment total cholesterol and low density lipoprotein ligated cholesterol were 10 mmol/l (394 mg/dl) and 8.6 mmol/l (335 mg/dl) respectively upon commencing the treatment and 4.7 mmol/l (184 mg/dl) and 3 mmol/l (118 mg/dl) upon completion of the same. This is the first time in Spain that treatment with this technique has been used in homozygotic familial hypercholesterolemia.

Blood Component Removal↗
PubMed1991

Circulating metabolite utilization by periuterine adipose tissue in situ in the pregnant rat.

To study the use of glucose for lipid synthesis by the periuterine adipose tissue in situ, 14C-glucose was infused through the left uterine artery of anesthetized, fed pregnant and virgin control rats. A greater amount of 14C-lipid always appeared in the adipose tissue from the left uterine horn than in the tissue from the right uterine horn, indicating direct utilization of the infused 14C-glucose by the tissue. Glucose utilization for both glycerol and fatty acid synthesis increased from day 0 (virgin rats) to day 20 of gestation and then decreased dramatically on day 21. In virgin and 12-day pregnant rats, glucose was incorporated into either lipidic moiety at similar rates, whereas in late pregnant rats glucose utilization for glyceride glycerol synthesis was four to five times greater than for fatty acids. The utilization of circulating fatty acids and the lipoprotein triglyceride-derived fatty acids was studied by infusing 14C-palmitate or 14C-triolein-labeled very-low-density lipoprotein (VLDL) through the left uterine artery in both virgin and 20-day pregnant rats. Incorporation of fatty acids from either one of these plasma sources was significantly higher in the pregnant than in virgin rats. This high amount of fatty acid acquisition did not account for the very active glyceride glycerol synthesis observed in pregnant rats and can only be explained by the intracellular reesterification of some lipolytic fatty acids. The results suggest a highly accelerated triacylglycerol/fatty acid substrate cycle in adipose tissue during late pregnancy, which would allow active esterification (contributing to fat accumulation) and responsive lipolysis (permitting rapid fat mobilization) by the mother.

Adipose Tissue↗
PubMed1991

Carcass and tissue fat content in the pregnant rat.

The present study in rats was aimed at determining the specific day of pregnancy on which maternal body fat accumulation starts and which tissues are involved. Most of the body weight increase at day 12 of gestation corresponded to conceptus-free maternal weight which progressively increased until the 19th day of gestation after which maternal weight stabilized and the rate of conceptus weight gain became maximal. Maternal carcass fat content progressively increased until day 18 of gestation, increased very markedly on day 19, stabilized between day 19 and 20 and then decreased on day 21. These changes were the opposite of the course of the specific-gravity values. The fresh weight of lumbar fat-pads and mesenteric adipose tissue reflected the changes in carcass fat content throughout gestation. Periuterine adipose-tissue mass declined on day 12 of gestation to be recuperated later, subcutaneous adipose tissue increased on day 12 to decline progressively thereafter and interscapular brown adipose tissue remained stable until day 20 and increased on day 21. With only a few exceptions, the lipid concentration in all these adipose tissues remained stable throughout gestation. Mammary glands and liver weights increased intensely from day 12 and, whereas the lipid concentration in the former was stable, in the latter it decreased on day 12 and increased on days 18 and 19. These results show that in the rat (a) maternal carcass fat accumulation during gestation is not paralleled by the size of the different fat-storing tissues and (b) mammary-gland fat accumulation also contributes to maternal fat storage.

Adipose Tissue↗
PubMed1991

Maternal hypothyroidism during the first half of gestation compromises normal catabolic adaptations of late gestation in the rat.

Female rats were mated and thyroidectomized on the same day. Some animals were kept without treatment and killed on day 12 or 21 of gestation (T). Others were subsequently treated daily with 1.8 micrograms L-T4/100 g BW for either the first 12 days and then not treated from that time until day 21 [T+T4(I+0)] or else not treated for the first 12 days and then treated from days 12-21 [T+T4(0+II)]. A final group received treatment during the entire 21-day study [T+T4(I+II)] and was used as the control. The net maternal body weight increased until day 12 of gestation in T+T4(I+II) rats, but not in T animals. On day 21 net maternal body weight was significantly lower in T and T+T4(0+II) than in T+T4(I+II) rats. Lipoprotein lipase activity in the lumbar fat pads increased from days 0 to 12 of gestation and decreased on day 21, whereas in the heart the change was in the opposite direction, and these changes were greater in T+T4(I+II) rats than in T rats. Incorporation of [U-14C]glucose administered in vivo into liver [14C]fatty acids or [14C]glycogen was significantly lower in T rats than in T+T4(I+II) on either the 12th or 21st day of gestation. The response of plasma triglyceride, glycerol, or beta-hydroxybutyrate levels to 24 h of starvation was similar in 12-day pregnant rats regardless of whether they were treated with T4, whereas on day 21 the change was greater in T+T4(I+II) or T+T4(I+0) animals than in T or T+T4(0+II) animals. Results show that maternal hypothyroidism during the first half of gestation impaired the anabolic events occurring during this phase and compromised the normal catabolic response during late gestation even when T4 treatment was restored. However, once maternal metabolic stores were built up normally during the first half of gestation, maternal hypothyroidism during late gestation did not affect the mother's normal metabolic adaptation, including the accelerated response to starvation.

Adipose Tissue↗
PubMed1991

Intermediary metabolism in pregnancy. First theme of the Freinkel era.

During the first half of gestation in the rat, maternal net body weight increases rapidly, whereas in the second half of gestation, the mass of maternal structures declines, coincident with the rate of maternal fat accumulation. Enhanced maternal food intake, extrahepatic tissue lipoprotein lipase (LPL) activity, and adipose tissue lipogenesis are responsible for the progressive accumulation of maternal fat. However, during late gestation, decreased fat synthesis in maternal adipose tissue, enhanced lipolytic activity, and decreased LPL activity deplete maternal fat depots. These changes, plus enhanced endogenous production of triglyceride-rich lipoproteins, are also responsible for maternal hypertriglyceridemia. This condition benefits the offspring in two ways: 1) enhanced LPL activity in maternal liver when fasting increases triglyceride consumption for ketone body synthesis, giving the basis for accelerated starvation; and 2) induction of LPL activity in the mammary gland before parturition diverts maternal circulating triglycerides to milk synthesis in preparation for lactation. The magnitude of the maternal-fetal glucose transfer was higher than that of any of the other substrates studied, including alanine, and despite actions to spare glucose, this transfer causes maternal hypoglycemia, which is especially intense in the fasting condition. This increases sympathoadrenal activity in the mother, which may contribute to her active gluconeogenesis. Glycerol was a more efficient glucose precursor than alanine and pyruvate, and whereas glycerol placental transfer is very small, it is proposed that the fetus benefits from this product of adipose tissue lipolysis when it is previously converted into glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗