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Biomedical subjects

K E Anderson

Publications and source records attributed to K E Anderson.

At least 127 records · Page 7Linked to original sources
PubMed1994

Inositol 1,4,5-trisphosphate receptor function in neonatal cardiomyocytes.

We have previously reported that the metabolism of inositol(1,4,5)trisphosphate (Ins(1,4,5)P3) is altered when rat neonatal ventricular cardiomyocytes are isolated and cultured. In the current study we show that the mass content of Ins(1,4,5)P3 is lower in the isolated cells than in the intact tissue. However, the properties of the Ins(1,4,5)P3 receptors were not different in the two preparations and the isolated cells remained insensitive to Ins(1,4,5)P3 in terms of 45Ca2+ release. Thus, despite the altered pattern of metabolism of Ins(1,4,5)P3 in isolated neonatal cells, the properties of the receptors were similar to those reported in other myocardial preparations.

Animals↗
PubMed1994

Acute peripheral neuropathy due to hereditary coproporphyria.

A 23-year-old man with epilepsy and a past history of abdominal pain and ileus, developed hypertension and arm and bulbar weakness when valproic acid and carbamazepine were reinitiated. Electrophysiologic studies demonstrated a peripheral neuropathy with features of axonal degeneration and demyelination. Axonal degeneration was documented by sural nerve biopsy. Markedly elevated urinary delta-aminolevulinic acid and porphobilinogen indicated a diagnosis of acute porphyria. Other laboratory studies were most consistent with hereditary coproporphyria. Motor function improved considerably but incompletely over 1 year. An acute, primarily motor neuropathy can occur in several forms of porphyria, including acute intermittent porphyria, variegate porphyria, and hereditary coproporphyria, sometimes even in the absence of concomitant gastrointestinal symptoms.

Acute Disease↗
PubMed1994

Some pre- and postjunctional effects of castration in rabbit isolated corpus cavernosum and urethra.

Pre- and postjunctional effects of castration were investigated in isolated corpus cavernosum (CC) and prostatic and preprostatic urethral preparations obtained from rabbits that had been castrated surgically 14 days before investigation. Preparations obtained from untreated animals were used as controls. Castration did not change the relaxing effects of SIN-1 (NO donor) or papaverine in CC preparations contracted by noradrenaline (NA). Electrical field stimulation of CC preparations contracted by NA or endothelin-1 produced frequency-dependent and tetrodotoxin-sensitive relaxations. As compared with controls, the electrically induced relaxations were increased in preparations from castrated animals. Pretreatment with prazosin increased the electrically induced relaxations in CC from untreated rabbits, but had no effect on preparations from castrated animals. In CC preparations incubated with 3H-NA, castration significantly reduced the electrically evoked release of 3H. L-NOARG, an inhibitor of NO synthase, had no effect on 3H-efflux. In prostatic, but not preprostatic, urethral preparations contracted by NA, the relaxant effects of SIN-1 and vasoactive intestinal polypeptide were significantly smaller following castration. Furthermore, castration significantly reduced electrically evoked relaxations in prostatic urethral preparations contracted by NA, while in preprostatic urethra, no such effect was seen. Castration or L-NOARG had no effect on the electrically induced release of 3H-NA in either of the urethral tissues. The results suggest that the hormonal changes caused by castration may modulate the functional effects in vitro of some parts of the urogenital tract. In penile erectile tissue, the relaxations induced by electrical field stimulation are increased, probably for the most part through a decrease in the neuronal release of NA. In prostatic urethra, on the other hand, electrically evoked relaxations are decreased, possibly as a result of an impaired ability of the smooth muscle itself to respond to relaxant agents. In preprostatic urethra, castration has no obvious functional effects. The physiological consequences of these findings in the in vivo situation remain to be established.

Animals↗
PubMed1994

Reperfusion following myocardial ischaemia enhances inositol phosphate release in the isolated perfused rat heart.

1. Global myocardial ischaemia (MI) for periods greater than 5 min caused an inhibition of phosphatidylinositol specific phospholipase C (PtdIns-PLC) activity. 2. Two min reperfusion following a 20 min MI period, a time point associated with reperfusion-induced arrhythmias, resulted in an activation of PtdIns-PLC activity, dependent on endogenous noradrenaline and mediated via alpha 1-adrenoceptors. 3. This 2 min reperfusion response, in contrast to healthy myocardium, resulted in: (i) enhanced PtdIns-PLC activity; (ii) increased sensitivity to endogenous noradrenaline; (iii) rapid increases in inositol(1,4,5)trisphosphate (Ins(1,4,5)P3); and (iv) PLC hydrolysis primarily of PtdIns(4,5)P2, such that the majority of InsP isomers derive from Ins(1,4,5)P3. 4. Together, these data suggest a functional role for Ins(1,4,5)P3 under post-ischaemic reperfusion conditions, and provide a possible link between alpha 1-adrenoceptor stimulation of the PtdIns turnover pathway and reperfusion injury.

Animals↗
PubMed1994

Inositol-1,4,5-trisphosphate [ins(1,4,5)P3] and ins(1,4,5)P3 receptor concentrations in heart tissues.

1. The isolation and culture of neonatal cardiomyocytes causes changes in the metabolism of inositol(1,4,5) trisphosphate (Ins(1,4,5)P3) from primarily dephosphorylation in the intact tissue to a combination of phosphorylation and dephosphorylation in the cultured cells (Woodcock et al. 1992). 2. The content of Ins(1,4,5)P3 was found to be higher in intact heart tissue than in the isolated neonatal cells (10.9 +/- 1.3 and 0.5 +/- 0.1 pmol/mg tissue, mean +/- s.e.m., n = 4, P < 0.002, respectively). 3. Despite this difference, Ins(1,4,5)P3 receptors in intact tissue and in isolated cells were not different in terms of affinity (8.0 +/- 1.7 and 10.9 +/- 1.6 nmol/L, n = 3, respectively) or concentration (143.3 +/- 20.5 and 91.2 +/- 16.0 fmol/mg protein, n = 3, respectively). 4. Thus, while there appears to be a relationship between the tissue content of Ins(1,4,5)P3 and its metabolism, no relationship to the properties of Ins(1,4,5)P3 receptors could be demonstrated.

Animals↗
PubMed1994

Acute intermittent porphyria: identification and expression of exonic mutations in the hydroxymethylbilane synthase gene. An initiation codon missense mutation in the housekeeping transcript causes "variant acute intermittent porphyria" with normal expression of the erythroid-specific enzyme.

Acute intermittent porphyria (AIP), an autosomal dominant inborn error, results from the half-normal activity of the heme biosynthetic enzyme, hydroxymethylbilane synthase (EC 4.3.1.8). Diagnosis of AIP heterozygotes is essential to prevent acute, life-threatening neurologic attacks by avoiding various precipitating factors. Since biochemical diagnosis is problematic, the identification of hydroxymethylbilane synthase mutations has facilitated the detection of AIP heterozygotes. Molecular analyses of unrelated AIP patients revealed six exonic mutations: an initiating methionine to isoleucine substitution (M1I) in a patient with variant AIP, which precluded translation of the housekeeping, but not the erythroid-specific isozyme; four missense mutations in classical AIP patients, V93F, R116W, R201W, C247F; and a nonsense mutation W283X in a classical AIP patient, which truncated the housekeeping and erythroid-specific isozymes. Each mutation was confirmed in genomic DNA from family members. The W283X lesion was found in another unrelated AIP family. Expression of each mutation in Escherichia coli revealed that R201W, C247F, and W283X had residual activity. In vitro transcription/translation studies indicated that the M1I allele produced only the erythroid-specific enzyme, while the other mutant alleles encoded both isozymes. These mutations provide insight into the molecular pathology of classic and variant AIP and facilitate molecular diagnosis in AIP families.

Base Sequence↗
PubMed1994

Positive changes and worksite health education.

44 of 70 employees attended 7 biweekly sessions during the lunch hour. Assessments of health risk and biometric measurements showed improvement at posttest on exercise, stress awareness, and systolic blood pressure.

Adult↗
PubMed1994

Effects of floor versus cage rearing and feeder space on growth, long bone development, and duration of tonic immobility in single comb White Leghorn pullets.

The effects of feeder space on growth of commercial layer pullets reared in cages or floor pens were examined by allocating 1-d-old chicks to either cages (14 chicks) or floor (119 chicks). Feeder spaces were 5.4, 4.0, and 2.7 cm per pullet and were held constant throughout the growing period, resulting in a 2 x 3 factorial arrangement. Measurements of pullet body weight, feed consumption, skeletal development, and fearfulness were taken through the rearing period to 18 wk. Pullets allowed 5.4 cm of feeder space were heavier (P < .001) (1,329 g at 18 wk of age) than birds allowed either 4.0 or 2.7 cm of feeder space (1,289 and 1,272 g, respectively). Floor-reared pullets weighed significantly more at 12, 16, and 18 wk of age than cage-reared pullets. Feed consumption was not affected by the feeder space, but the floor-reared birds consumed more (P < .001) feed than those in cages (61.2 vs 52.8 g per pullet per d). Mortality, skeletal development, and bone strength were not affected by either feeder space or floor vs cage rearing. Floor-reared pullets had longer (P < .05) duration of tonic immobility (TI) than those reared in cages (519.7 and 471.4 s, respectively, as measured at 18 wk). Feeder space per pullet had no effect on the duration of TI of the pullets. Cage and floor rearing environments are comparable for rearing pullets provided feeder space is not restricted to such an extent as to inhibit BW.

Animal Husbandry↗
PubMed1994

Effects of cage versus floor rearing environments and cage floor mesh size on bone strength, fearfulness, and production of single comb White Leghorn hens.

Fourteen hundred pullets were reared at densities of 304 and 735 cm2 in cages and floor pens with litter, respectively. Feeder spaces of 2.7, 4.0, and 5.4 cm per bird were held constant during the brooding growing period. At 18 wk of age, the birds were housed four birds per cage (348 cm2 per bird) in a force-ventilated, light-controlled house with two rows of stair-step cages. In two rows, the standard 2.5 x 5.0 cm welded wire flooring was replaced randomly with 2.5 x 2.5 cm welded wire in eight-cage sections. Egg production, egg quality, feed conversion, and mortality were measured over a 48-wk production cycle. At 68 wk of age, a sample of hens was selected and euthanatized, and the right leg was excised for further evaluation. Rearing environment, rearing feeder space, or type of layer floor mesh had no significant effects on hen-day production or feed conversion. Hens reared in cages produced heavier (P < .001) eggs with a higher percentage of Grade A eggs and had fewer body checks than floor-reared birds. Femur, tibia, and shank lengths were not affected by the rearing treatments or the type of flooring in the layer cage. Tibia breaking strength was not different for the rearing systems or hens maintained on 2.5 x 2.5 vs 2.5 x 5.0 cm welded wire mesh flooring. Hens reared in floor pens on litter displayed a higher level of fearfulness at the end of the production cycle. The reduced (P < .05) body weights associated with cage rearing and reduced feeder space did not negatively affect the production variables. Alteration of the mesh size of layer cage floor had no effect on the production levels of the hens.

Animal Husbandry↗
PubMed1994

Duodenal calcium uptake, femur ash, and eggshell quality decline with age and increase following molt.

An experiment was conducted to test the hypothesis that the decline in eggshell quality over time during egg production, and its improvement after molting, paralleled the rate of calcium uptake by the duodenum of the laying hen. In vitro duodenal calcium uptake rate and femur ash (percentage of femur weight) were determined at 37, 45, 51, 58, 68, and 72 wk of age. Percentage shell and shell thickness (millimeters) were determined at 22, 29, 36, 44, 50, 57, and 71 wk of age. Molt was induced at 63 wk of age. Three commercial strains DeKalb XL-Link, ISA/Babcock B-300V, and Hy-Line W-36 were compared. There were no differences in duodenal calcium uptake rate among strains. There was a significant decline (P < .01) in duodenal calcium uptake from 408 pmol/mg tissue per min at 37 wk of age to 329 pmol/mg per min at 58 wk of age. Femur ash decreased (P < .01) from 50.8% at 37 wk of age to 47.6% at 58 wk of age. Percentage shell and shell thickness declined (P < .01) from 9.79% and .403 mm at 22 wk of age to 8.88% and .373 mm at 57 wk of age, respectively. After the induced molt, duodenal calcium uptake increased (P < .01) to 402 pmol/mg tissue per min, and percentage shell and shell thickness increased (P < .01) to 10.23% and .389 mm, respectively. Duodenal calcium uptake increased immediately postmolt, whereas femur ash did not increase until 72 wk of age (P < .01).

Age Factors↗
PubMed1993

Lyophilization can generate artifacts in chromatographic profiles of inositol phosphates.

Lyophilized extracts of [3H]inositol-labelled rat heart or renal tubule preparations were found to contain unidentified 3H-labelled compounds in addition to the inositol phosphates. The appearance of these labelled substances was caused by the presence in the extracts of compounds which bound [3H]inositol when lyophilized together with it. These studies demonstrate a previously undescribed source of [3H]inositol-labelled compounds which can complicate chromatographic profiles of inositol phosphates. These problems can be overcome either by not lyophilizing the samples or by lyophilizing in the presence of 0.3 M urea, which prevents the association with [3H]inositol and does not interfere with the chromatography.

Animals↗
PubMed1993

Inositol phosphates in rat atria and the importance of the extraction procedure.

The nature of the inositol phosphates present in adult rat left atria have been examined. Trichloroacetic acid extracts of [3H] inositol-labelled left atria contained the 1 (or 3)-, 2- and 4-isomers of inositol monophosphate, inositol-1,4-bisphosphate, and inositol-1,4,5-trisphosphate. Addition of noradrenaline increased all of these isomers. However, even in the presence of noradrenaline, there was no evidence for the presence of inositol-1,3,4,5-tetrakisphosphate or its dephosphorylation products including inositol-1,3,4-trisphosphate and the 1,3- and 3,4-isomers of inositol bisphosphate. Total accumulation of inositol phosphates in the presence of LiCl was 98% accounted for by dephosphorylation of inositol-1,4,5-trisphosphate and its cyclic isomer. These data indicate that, in intact left atria, metabolism of inositol-1,4,5-trisphosphate is by dephosphorylation and that significant activity of the phosphorylation pathway is not present. When extractions were performed using either acidified chloroform-methanol or perchloric acid, other [3H] inositol-labelled compounds were detected in atrial extracts. One of these chromatographed with ATP and might be mistaken for inositol-1,3,4-trisphosphate if co-chromatography with ATP was used to identify that compound. Another compound had a similar, but not identical chromatographic profile to inositol-1,3,4,5-tetrakisphosphate and is thus likely to be mistaken for that compound. In addition, perchloric acid extraction caused phosphate group migration generating extra isomers of the inositol phosphates and other unidentified [3H]-labelled compounds. Such extraction artifacts are likely especially problematic in studies of intact heart tissue because of the time required to effectively homogenize the tissue. These findings demonstrate the need for caution in interpreting data relating to estimations of inositol phosphates in intact heart tissue.

Animals↗
PubMed1993

The isolation of adult rat cardiomyocytes activates inositol(1,4,5) trisphosphate 3'kinase activity.

Addition of norepinephrine to [3H]inositol-labeled rat hearts or isolated left atria caused the release of inositol(1,4,5)trisphosphate which was metabolized by dephosphorylation to inositol(4)monophosphate. Products of the inositol(1,4,5)trisphosphate 3'-kinase pathway were not present at detectable levels. When norepinephrine was added to [3H]inositol-labeled isolated adult cardiomyocytes the released inositol(1,4,5)trisphosphate was metabolized partially by phosphorylation as evidenced by the presence of the immediate phosphorylation product inositol(1,3,4,5)-tetrakis-phosphate and its dephosphorylation products inositol (1,3,4)trisphosphate and inositol(1,3)-bisphosphate. Direct measurement of inositol trisphosphate 3'-kinase activity in cytosols prepared from intact hearts and isolated myocytes demonstrated activation of the enzyme during cell isolation from 20 +/- 0.5 p mol/min/mg protein to 124 +/- 14 (mean +/- S.E.M., n = 3, P < 0.001). These data show that the kinase pathway is suppressed in healthy heart tissue and show that it can be activated under conditions such as those required for cell isolation.

Animals↗
PubMed1993

Stimulation of phosphatidylinositol turnover in adult rat left atria does not involve release of inositol(1,4,5)trisphosphate.

1. The turnover rate of inositol(1,4,5)trisphosphate (Ins(1,4,5)P3) in noradrenaline-stimulated adult rat left atria was calculated from changes in specific activity and was found to equal 110 ct/min per mg tissue. In contrast, the isomers of inositol mono- and bisphosphates accumulated at a rate of 508 ct/min per mg. 2. Neomycin, which inhibits release of Ins(1,4,5)P3, inhibited the accumulation of inositol phosphates in noradrenaline-stimulated isolated neonatal cardiomyocytes but did not inhibit accumulation in left atria. 3. These data demonstrate that most of the inositol phosphates which accumulate in adult rat left atria do not derive from Ins(1,4,5)P3. 4. These data are best explained by a model in which noradrenaline stimulation results mainly in the breakdown of phosphatidylinositol(4)monophosphate (PtIns(4)P1) to inositol(1,4)bisphosphate (Ins(1,4)P2). Thus, heart tissue avoids the generation of Ins(1,4,5)P3.

Animals↗
PubMed1993

Angiosarcoma, porphyria cutanea tarda, and probable chloracne in a worker exposed to waste oil contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin.

A worker developed angiosarcoma, porphyria cutanea tarda, and skin lesions characteristic of mild chloracne. About 10 years earlier he had been employed at a truck terminal in Saint Louis, Missouri, at a time when it was sprayed with waste oil contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The occurrence of these three rare conditions in a single exposed worker supports the aetiological relation between environmental exposure to TCDD and the subsequent development of soft tissue sarcoma and porphyria cutanea tarda.

Acne Vulgaris↗
PubMed1993

Coronary blood flow in senescent rats with late-onset hypertension.

We tested the hypothesis that the imposition of hypertension late in life would markedly limit maximal myocardial perfusion (MP). Young adult (8 mo) and senescent (24 mo) Fischer 344 rats were studied 3 mo after one-kidney, figure-8 renal wrap hypertension (RH) was induced. Sham-operated rats served as controls (Con). Regional MP was determined with radioactive microspheres in conscious rats before and during maximal coronary vasodilation with infusion of dipyridamole. Systolic arterial pressure (SAP) was significantly elevated in both RH age groups during weeks 2-6 following surgery and then fell to normotensive levels. After 3 mo SAP (mmHg) was significantly lower in the senescent RH rats (125 +/- 5) compared with their controls (147 +/- 3). In senescent RH rats left ventricular (LV) end-diastolic pressure increased fivefold. LV mass increased with age but not with treatment. LV minimal coronary vascular resistance (MCVR, mmHg.ml-1.min-100 g) increased significantly both with age and treatment (8 mo: Con = 0.07 +/- 0.01, RH = 0.14 +/- 0.01; 24 mo: Con = 0.11 +/- 0.01, RH 0.17 +/- 0.02). Treatment affected similar changes in the right ventricular MCVR. LV endocardial-to-epicardial perfusion ratio during rest was lower in the senescent groups but was not altered by hypertension. These data indicate that 1) both aging and this model of hypertension compromise maximal coronary perfusion and reserve in Fischer 344 rats, and 2) aging is associated with an increase in coronary vascular resistance in both ventricles at rest and in a relative reduction in maximal endocardial perfusion in the left ventricle.

Aging↗