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Biomedical subjects

K C Hayes

Publications and source records attributed to K C Hayes.

At least 73 records · Page 4Linked to original sources
PubMed1994

Dietary palmitic acid results in lower serum cholesterol than does a lauric-myristic acid combination in normolipemic humans.

In a double-blind crossover study, 17 normocholesterolemic male volunteers were fed carefully designed whole-food diets in which 5% of energy was exchanged between palmitic (16:0) and lauric + myristic acids (12:0 + 14:0) whereas all other fatty acids were held constant. Resident males received each diet during separate 4-wk periods. The test diets supplied approximately 30% of energy as fat and 200 mg cholesterol/d. Compared with the 12:0 + 14:0-rich diet, the 16:0-rich diet produced a 9% lower serum cholesterol concentration, reflected primarily by a lower (11%) low-density-lipoprotein-cholesterol concentration and, to a lesser extent, high-density-lipoprotein cholesterol. No diet-induced changes were noted in the cholesterol content of other lipoproteins, nor did exchange of saturated fatty acids affect the triglyceride concentration in serum or lipoprotein fractions. These data indicate that a dietary 12:0 + 14:0 combination produces a higher serum cholesterol concentration than does 16:0 in healthy normocholesterolemic young men fed a low-cholesterol diet.

Adult↗
PubMed1994

Dietary myristic, palmitic, and linoleic acids modulate cholesterolemia in gerbils.

Previous studies with cebus monkeys and review of published human data indicated that 85% to 90% of the variation in plasma cholesterol (TC) could be explained on the basis of dietary myristic (14:0) and linoleic (18:2) acid intake in the absence of cholesterol, and that 16:0 contributed to cholesterolemia as dietary cholesterol was increased. Because monkeys are a limited resource, a more convenient, sensitive model was sought for investigating these dietary fatty acid and plasma lipid relationships. Accordingly, this report describes the results of multiple regression analysis of the TC response to dietary fatty acids based on 319 young, male Mongolian gerbils fed a total of 59 purified diets supplying about 40% energy as fat from single or blended fat sources. Gerbils (6-16 animals per dietary group) were fed purified diets (21 with 0.01 to 0.08% cholesterol and 38 cholesterol-free) for 4-week periods. When cholesterol-free diets were fed, dietary 14:0 and 18:2 together accounted for 89% of the observed variation in TC. Although 14:0 consumption increased TC in a linear manner, the independent ability of 18:2 to lower cholesterol was nonlinear and exhibited a threshold effect at 5-6% dietary energy, above which further lowering of TC was less remarkable. In gerbils consuming cholesterol-supplemented diets, 87% of the observed variation in TC could be accounted for by a regression equation that included 14:0, palmitic acid (16:0), and a log function of 18:2 plus dietary cholesterol itself. These results demonstrate the applicability of gerbils for such studies and confirm previous observations in monkeys and humans that dietary 14:0 and 18:2 are the main fatty acids modulating plasma cholesterol under normocholesterolemic circumstances (i.e., when consuming low-cholesterol diets and lipoprotein metabolism is normal) whereas 16:0 also appears modestly hypercholesterolemic when LDL receptors are compromised (i.e., when dietary cholesterol or certain metabolic factors have encumbered lipoprotein metabolism).

Animals↗
PubMed1993

Dietary palmitic acid raises plasma LDL cholesterol relative to oleic acid only at a high intake of cholesterol.

Using a crossover design, the effects of exchanging up to 10% dietary energy (%en) between oleic (18:1) and palmitic acid (16:0) on plasma lipoprotein metabolism was investigated in 12 normocholesterolemic cebus monkeys, both in the absence and presence of dietary cholesterol (0.3%, w/w). In all the purified diets, which contained 33%en as fat blends, myristic acid (14:0) and linoleic acid (18:2) were held constant at 0.3%en and 3.7%en, respectively. Cholesterol-free diets containing either high 18:1 (19%en), roughly equivalent levels of 16:0 and 18:1 (12 and 15%en, respectively), or a high level of 16:0 (18%en), generated similar values for total plasma cholesterol (TC), HDL-C and LDL-C. Plasma triacylglycerol concentrations (TG) were significantly higher when monkeys were fed the 16: 0-rich diet than when fed the 18: 1-rich diet (75 +/- 6 vs. 52 +/- 8 mg/dl; P < 0.05). LDL and HDL kinetic parameters (assessed after simultaneous injection of homologous 131I-LDL and 125I-HDL) revealed no significant differences between the 18: 1-rich or 16: 0-rich diets. By contrast, with added dietary cholesterol (0.78 mg/kcal) the 16: 0-rich diet resulted in significantly higher TC (318 +/- 20 vs. 299 +/- 20 mg/dl; P < 0.05) and LDL-C (136 +/- 10 vs. 117 +/- 10 mg/dl; P < 0.05) in comparison to the 18: 1-rich diet. HDL-C was unaffected (159 +/- 8 vs. 156 +/- 5 mg/dl), but plasma TG concentrations also tended to be higher (70 +/- 8 vs. 60 +/- 6 mg/dl, P < 0.08). Kinetic studies revealed that the higher LDL-C concentration was associated with an elevated pool size of LDL apo B (40 +/- 2 vs. 34 +/- 2 mg/kg body weight; P < 0.005), the latter attributed to decreased FCR (1.06 +/- 0.07 vs. 1.27 +/- 0.12 pools/day; P < 0.04) with no effect on the transport rate of LDL apo B (41 +/- 2 vs. 42 +/- 3 mg/kg body weight per day). HDL kinetic parameters were comparable during the 16: 0 and 18: 1 dietary periods, but dietary cholesterol caused an increase in apo A-I pool size and transport rate without impacting FCR. In this study a palmitic acid-rich diet failed to alter plasma or LDL-C when compared to an oleic acid-rich diet, unless the diet also contained cholesterol. In the latter case, 16: 0 increased LDL-C, which reflected a decrease in the efficiency of LDL apo B removal.

Analysis of Variance↗
PubMed1993

A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa.

OBJECTIVE: To determine whether supplements of vitamin A or vitamin E alone or in combination affect the course of retinitis pigmentosa. DESIGN: Randomized, controlled, double-masked trial with 2 x 2 factorial design and duration of 4 to 6 years. Electroretinograms, visual field area, and visual acuity were measured annually. SETTING: Clinical research facility. PATIENTS: 601 patients aged 18 through 49 years with retinitis pigmentosa meeting preset eligibility criteria. Ninety-five percent of the patients completed the study. There were no adverse reactions. INTERVENTION: Patients were assigned to one of four treatment groups receiving 15,000 IU/d of vitamin A, 15,000 IU/d of vitamin A plus 400 IU/d of vitamin E, trace amounts of both vitamins, or 400 IU/d of vitamin E. MAIN OUTCOME MEASURE: Cone electroretinogram amplitude. RESULTS: The two groups receiving 15,000 IU/d of vitamin A had on average a slower rate of decline of retinal function than the two groups not receiving this dosage (P = .01). Among 354 patients with higher initial amplitudes, the two groups receiving 15,000 IU/d of vitamin A were 32% less likely to have a decline in amplitude of 50% or more from baseline in a given year than those not receiving this dosage (P = .01), while the two groups receiving 400 IU/d of vitamin E were 42% more likely to have a decline in amplitude of 50% or more from baseline than those not receiving this dosage (P = .03). While not statistically significant, similar trends were observed for rates of decline of visual field area. Visual acuity declined about 1 letter per year in all groups. CONCLUSIONS: These results support a beneficial effect of 15,000 IU/d of vitamin A and suggest an adverse effect of 400 IU/d of vitamin E on the course of retinitis pigmentosa.

Adolescent↗
PubMed1993

Cholesterol gallstone induction in hamsters reflects strain differences in plasma lipoproteins and bile acid profiles.

Because different strains of hamsters vary in their susceptibility to gallstones, the relationship between plasma lipoproteins, hepatic cholesterol, bile lipids and bile acid profile was examined during gallstone induction in strains of male Syrian hamsters from Charles River Lakeview (CHR), Biobreeder F1B (BIO) and Harlan Sprague-Dawley (HAR). Gallstones were induced by feeding a purified diet containing 0.4 or 0.8% cholesterol for 5 wk. Basal plasma total cholesterol was similar, but the hypercholesterolemia induced by dietary challenge was significantly lower in CHR than in HAR and BIO hamsters. Cholesterol-fed CHR hamsters transported cholesterol mainly in HDL (47%), whereas VLDL-C + IDL-C predominated in BIO and HAR hamsters, and their HDL transported only 28 and 38%, respectively. HAR hamsters accumulated the most hepatic cholesterol, revealed the highest cholate/cheno ratio, the lowest glycine/taurine ratio and hydrophobicity index. HAR also developed the fewest cholesterol gallstones (23%), while 64% of CHR and 58% of BIO hamsters had cholesterol gallstones and 34% of BIO hamsters developed pigment stones. Doubling dietary cholesterol from 0.4 to 0.8% doubled the incidence of cholesterol gallstones but exerted minimal impact on other parameters compared to strain differences. Thus, different strains of hamsters vary considerably with respect to biliary cholesterol, bile acid profile and formation of cholesterol gallstones associated with differences in plasma lipoprotein profiles.

Animals↗
PubMed1993

Modeling plasma lipoprotein-bile lipid relationships: differential impact of psyllium and cholestyramine in hamsters fed a lithogenic diet.

Hamsters fed a lithogenic diet become hyperlipemic with elevated very-low-density lipoprotein (VLDL) and high-density lipoprotein 2 (HDL2) cholesterol pools and develop lithogenic bile in which chenodeoxycholate (cheno) typically predominates. The relationship between these distorted lipoprotein and bile lipid profiles and gallstone induction was investigated in male Syrian hamsters fed for 5 weeks a gallstone-inducing purified diet (5% butter, 0.4% cholesterol) or the same diet supplemented with 5% psyllium or 1% cholestyramine, agents known to alter bile acid metabolism. The gallstone diet essentially doubled plasma cholesterol level, whereas psyllium decreased it to near normal, and cholestyramine to a subnormal level, while correcting the distorted distribution of cholesterol among lipoproteins. Both the gallstone diet and psyllium produced cholesterol-laden livers, in contrast to subnormal values produced by cholestyramine. Fecal bile acid excretion was increased eightfold with cholestyramine and fourfold with psyllium relative to the value produced by the gallstone diet and a literature control value. Supersaturated bile developed with the gallstone diet (lithogenic index [LI], 2.3 +/- 0.6), whereas the LI was decreased by psyllium (1.2 +/- 0.4) and cholestyramine (0.7 +/- 0.3). The gallstone diet decreased the concentration of bile acids in gallbladder bile, but greatly increased the percentage of taurochenodeoxycholic acid, whereas psyllium preferentially decreased all taurine-conjugated bile acid levels and expanded glycocholate output. Cholestyramine greatly decreased the secretion of biliary cholesterol and cheno independent of its conjugation. Accordingly, psyllium increased the glycine to taurine ratio of gallbladder bile fivefold, whereas cholestyramine did not affect this ratio, but increased the cholate to cheno ratio dramatically (25-fold) as compared with a threefold increase with psyllium. This combination of biliary lipid and bile acid alterations induced coordinated responses in the LI and the hydrophobicity index (HI) such that cholesterol gallstones developed in 11 of 12 hamsters fed the gallstone diet, whereas only one of 11 of the psyllium-fed and none of 12 cholestyramine-fed hamsters had cholesterol stones. Thus, psyllium and cholestyramine differentially increased bile acid excretion, which improved the lipoprotein profile and inhibited cholesterol gallstone formation. Both agents operated by different means to decrease biliary cholesterol secretion and the percentage of cheno, which decreased the LI and HI, respectively.

Analysis of Variance↗
PubMed1993

Plasma lipoproteins, biliary lipids and bile acid profile differ in various strains of Syrian hamsters Mesocricetus auratus.

1. Plasma and biliary lipids were assessed in four strains of Syrian hamsters [Charles River Lakeview, (CHR), Biobreeder F1B (BIO), Harlan Sprague-Dawley (HAR) and Sasco (SAS)] fed a cholesterol-free diet. 2. Plasma cholesterol differed with SAS > CHR > HAR > BIO. 3. BIO Hamsters had the lowest HDL and highest VLDL + LDL/HDL ratio, but their biliary secretion of bile acids, phospholipids and cholesterol was 50% lower than other hamsters. 4. Chenodeoxycholate was highest in CHR and the cholate:cheno ratio depressed in CHR hamsters. 5. CHR hamsters had the highest lithogenic index and cholesterol-saturated bile.

Adipose Tissue↗
PubMed1993

Effects of induced hypothermia on somatosensory evoked potentials in patients with chronic spinal cord injury.

We have investigated the effects of mild whole body hypothermia on the amplitude and latency of somatosensory evoked potentials (SEPs) in control subjects (n = 12) and patients (n = 15) with chronic compressive or contusive spinal cord injury (SCI). Mild hypothermia (-1 degree C) was induced by controlled circulation of propylene glycol through a 'microclimate' head and vest garment while reductions in oral and limb temperatures were monitored. Cooling induced a delayed onset and reduced amplitude of tibial nerve SEPs in control subjects. All SCI patients with recordable SEPs (n = 11) showed similarly delayed onset of the cortical response. In contrast to the controls, nine of the 11 SCI patients showed an increase in amplitude of cortical SEPs. In three of these patients the increase in amplitude exceeded 100% of the precooling values. The cooling-induced changes in SEP amplitude and latency reversed on rewarming for both groups. The cooling-induced increases in cortical SEP amplitude support the a priori hypothesis that cooling would enhance central conduction in some SCI patients with conduction deficits due to focal demyelination.

Adult↗
PubMed1993

Preclinical trial of 4-aminopyridine in patients with chronic spinal cord injury.

4-Aminopyridine (4-AP) is a K+ channel blocking agent that enhances nerve conduction through areas of demyelination by prolonging the duration of the action potential and increasing the safety factor for conduction. We have investigated the effects of 4-AP (24 mg total dose-intravenous) in 6 patients with spinal cord injury (3 complete, 3 incomplete) with the intent of overcoming central conduction block, or slowing, due to demyelination. Vital signs remained stable and only mild side effects were noted. The 3 patients with incomplete injuries all demonstrated enhanced volitional EMG interference patterns and one patient exhibited restored toe movements. The changes were reversed on drug washout. There were no changes in segmental reflex activities. These results are consistent with those obtained from 4-AP trials with animal models of spinal cord injury, showing modest therapeutic benefit attributable to enhanced central conduction.

4-Aminopyridine↗
PubMed1993

Bacterial biofilm formation on the bladder epithelium of spinal cord injured patients. II. Toxic outcome on cell viability.

As a follow up to our first study of 10 spinal cord injured patients, a further 8 patients were investigated over 2 months for biofilm formation on their bladder epithelial cells and for evidence that these uropathogens damage the host bladder. All the patients were found to be colonized with uropathogens, regardless of whether or not they were receiving antibiotics. Using vital staining, it was discovered that there was a significant reduction (33%) in bladder cell viability in the presence of bacterial biofilms compared to controls. This was not associated with cell turnover rates. In vitro tests showed a similar reduction in cell viability when uropathogens were incubated with bladder cells. In addition, white cell counts were significantly elevated in the patients' urine, indicative of an infectious and/or inflamed state. There was no difference between symptomatic and asymptomatic patients in their mean bacterial adhesion counts. Patients were just as likely to be symptomatic as asymptomatic when on antibiotics. In summary, the presence of virulent organisms in the bladder does adversely affect the host, even when the patient has insignificant signs and symptoms of infection, thereby raising concerns over the decision not to treat the patient. Unless specific antibiotics are used which eradicate adherent biofilms from the bladder, the treatment of symptomatic patients will only impact upon the signs and symptoms in some patients, and not alter their susceptibility to reinfection.

Adult↗
PubMed1993

Differences in the plasma transport and tissue concentrations of tocopherols and tocotrienols: observations in humans and hamsters.

Certain aspects of tocopherol and tocotrienol absorption, plasma transport, and tissue distribution were examined in humans and hamsters. Plasma transport differed in that tocopherols were found primarily in low density lipoprotein and high density lipoprotein in association with plasma surface components, whereas tocotrienols disappeared from plasma with chylomicron clearance. In keeping with transport by triglyceride-rich lipoproteins, tocotrienols were deposited in conjunction with triglycerides in the adipose tissue of hamsters. In hamsters, tocopherols were the only tocol readily detected in all tissues, except adipose during tocotrienol supplementation. In fasting humans, the plasma tocotrienol concentration was not significantly increased after tocotrienol supplementation, whereas the platelet concentration of delta-tocotrienol doubled. Furthermore, tocotrienol intake did not appear to modulate the plasma cholesterol concentration in normolipemic hamsters. Thus, the transport, tissue concentration, and relative biologic function of tocopherol and tocotrienol appear somewhat disparate and possibly unrelated.

Animals↗
PubMed1993

Comparison of taurine, alpha-tocopherol, retinol, selenium, and total triglycerides and cholesterol concentrations in cats with cardiac disease and in healthy cats.

Epidemiologic relations were evaluated between plasma concentrations of nutrients and cardiovascular diseases. A total of 220 cats were assessed: 144 cats with noninduced acquired heart disease and 76 clinically normal cats. Plasma was assayed for taurine, alpha-tocopherol, selenium, retinol, and total cholesterol and triglycerides concentrations. Cardiovascular disease groups included dilated cardiomyopathy (n = 53), left ventricular hypertrophy (n = 28), hyperthyroidism (n = 11), and uncertain classification (n = 52). In cats with dilated cardiomyopathy, mean plasma taurine concentration was the lowest of that in cats of any group, being only 38% of the value in healthy cats; females had less than half the mean value of males. Tocopherol concentration was 20% lower than normal, and retinol concentration was 40% higher than normal. Total cholesterol concentration was 36% lower than normal. Triglycerides concentration was higher in these cats than in any other group--twice the value recorded in healthy cats and 67% higher than that in hyperthyroid cats. In cats with hypertrophic cardiomyopathy, almost 15% had mean plasma taurine concentration < 30 mumol/L. Retinol concentration was 15% higher, and triglycerides concentration was 54% higher than normal. Approximately 27% of hyperthyroid cats had mildly decreased plasma taurine concentration. Hyperthyroid cats had the lowest tocopherol and cholesterol values; both were at least 30% lower than normal. Retinol concentration was 30% higher than normal. Approximately 14% of cats with uncertain classification had mildly decreased plasma taurine concentration. Plasma retinol and triglycerides concentrations were higher than normal in 25 and 38% of these cats, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗