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Biomedical subjects

B A Brooks

Publications and source records attributed to B A Brooks.

At least 19 recordsLinked to original sources
PubMed2001

Augmentation of central arterial pressure in Type 2 diabetes.

AIMS: Aortic systolic blood pressure has been shown to be augmented in Type 1 diabetes, indicative of more rapid pulse wave reflection due to increased arterial stiffness. This abnormality is more pronounced in diabetic males. The aim of this study was to examine the effects of diabetes on augmentation of aortic systolic pressure in subjects with Type 2 diabetes. METHODS: Radial artery pressure waveforms were obtained non-invasively by applanation tonometry. A central aortic waveform can be derived using a transfer function obtained from previous studies during cardiac catheterization. A total of 88 subjects with Type 2 diabetes (51 men and 37 women, aged 55.8 years (interquartile range (IR) 49.7-64.1), duration of diabetes 7.5 years (IR 2.4-12.4), HbA1c 7.6% (IR 6.6-8.7)) and 85 controls subjects (40 men and 45 women, aged 55.3 years (IR 44.2-66.4)) were studied. The central aortic waveform allowed determination of the: (i) aortic augmentation index and (ii) subendocardial viability ratio. RESULTS: Similar to Type 1 diabetic subjects, patients with Type 2 diabetes had a significantly higher aortic augmentation index (136.1 +/- 18.0% vs. 128.3 +/- 19.2%, t = 2.8, P = 0.006) and lower subendocardial viability ratio (137.4 +/- 25.0% vs. 155.1 +/- 25.9%; t = 4.6, P = 0.0001) compared with controls. Multivariate analysis identified diabetes as an important determinant of aortic augmentation index (t = 4.0, P = 0.0001). The higher aortic augmentation index was due mainly to the male cohort (t = 2.6; P = 0.01) and was not apparent for females with diabetes (P = 0.2). CONCLUSIONS: Type 2 diabetes is characterized by higher augmentation of aortic systolic pressure and unfavourable ratio of myocardial perfusion to cardiac workload. These results are consistent with increased arterial stiffness. The age-related progression of arterial stiffness is similar in Type 1 and Type 2 diabetes. Anti-hypertensive agents that reduce wave reflection and augmentation may help to prevent systolic hypertension and cardiac hypertrophy in diabetes.

Aorta↗
PubMed1998

Administration of ascorbic acid and an aldose reductase inhibitor (tolrestat) in diabetes: effect on urinary albumin excretion.

The important role of ascorbic acid (AA) as an anti-oxidant is particularly relevant in diabetes mellitus where plasma concentrations of AA are reduced. This study was conducted to evaluate the effects of treatment with AA or an aldose reductase inhibitor, tolrestat, on AA metabolism and urinary albumin excretion in diabetes. Blood and urine samples were collected at 0, 3, 6, 9, and 12 months from 20 diabetic subjects who were randomized into two groups to receive either oral AA 500 mg twice daily or placebo. Systolic and diastolic blood pressures, HbA1c, plasma lipids, urinary albumin, and total glycosaminoglycan excretion were measured at all time points, and heparan sulphate (glycosaminoglycan) was measured at 0 and 12 months. The same parameters, as well as urinary AA excretion, were determined at 0 and 3 months for 16 diabetes subjects receiving 200 mg tolrestat/day. AA treatment increased plasma AA (ANOVA, F ratio = 12.1, p = 0.004) and reduced albumin excretion rate (AER) after 9 months (ANOVA, F ratio = 3.2, p = 0.03), but did not change the other parameters measured. Tolrestat lowered plasma AA (Wilcoxon's signed-rank test, p < 0.05), but did not change AER or the other parameters measured. The ability of AA treatment to decrease AER may be related to changes in extracellular matrix or improvement in oxidative defence mechanism. Unlike the rat model of diabetes, inhibition of aldose reductase did not normalize plasma AA or AER in humans. In fact, tolrestat reduced the plasma AA concentration, a phenomenon which may be due to increased utilization of AA. Dietary supplementation of AA in diabetic subjects may have long-term benefits in attenuating the progression of diabetic complications.

Administration, Oral↗
PubMed1997

Very low calorie diet (VLCD): a useful alternative in the treatment of the obese NIDDM patient.

Conventional treatment of obese noninsulin dependent diabetes mellitus (NIDDM) patients is often unsatisfactory. In this study the efficacy of Modifast, a commercial very low calorie diet (VLCD), was evaluated in a population of obese poorly controlled NIDDM patients. The mechanisms of action of VLCD in these patients were also studied by comparing: (i) Plasma insulin and glucose profiles after a VLCD and an isocaloric mixed meal and (ii) plasma amino acid levels, both at baseline and after four weeks of VLCD treatment. A total of 14 obese NIDDM patients (M/F 7/7. median body mass index (BMI) 38.7 kg-2, interquartile range (IQ) 34.7-46.5 kg-2, waist circumference 116 cm, IQ 106-139 cm, insulin treated 7/14) with poor diabetic control (HbA1c 8.6%, IQ 7.8-10%) were studied. Patients were given a VLCD (425 kcal/day) for 12 weeks. At baseline, VLCD and isocaloric meal tests were performed on consecutive mornings. Fasting plasma amino acid levels were also determined at baseline and after 4 weeks of VLCD treatment. Weight, waist circumference, HbA1c, blood pressure, fasting plasma insulin, total cholesterol and triglyceride levels all fell significantly following VLCD treatment. Insulin therapy was able to be ceased in the seven insulin treated patients. Oral hypoglycaemic agent dosage fell from a median of eight (IQ 6-12) to two (IQ 0-8) tablets per day (P = 0.03) in patients initially on this form of therapy. Insulin secretion was higher after VLCD than isocaloric meal (P = 0.04). Fasting plasma alanine level fell from 512.0 (IQ 412.0-563.0) to 374.0 (IQ 342-472.0) mumol/l (P = 0.04) following VLCD treatment. In conclusion, the short term use of a VLCD is very effective in rapidly improving glycaemic control and promoting substantial weight loss in obese NIDDM patients. Moreover, a VLCD diet increases insulin secretion and reduces substrate for gluconeogenesis. Thus, VLCD treatment may improve glycaemic control by factors more than caloric restriction alone.

Adult↗
PubMed1995

Incorporating nursing theory into a nursing department strategic plan.

Corporations, including health care organizations, have used the strategic planning process as a means to plan, coordinate, and direct activities of the organization. Research has shown that nursing departments that conduct strategic planning perform better. But few nursing departments develop strategic plans. Our nursing department recently developed a strategic plan, but the unique aspect of our department's plan is the incorporation of nursing theory. This article will review the strategic planning process, describe the selection of a nursing theory to incorporate into a nursing department strategic plan, and give examples of the integration of strategic planning and nursing theory.

Empathy↗
PubMed1993

The Ah receptor nuclear translocator gene (ARNT) is located on q21 of human chromosome 1 and on mouse chromosome 3 near Cf-3.

We have mapped the Ah receptor nuclear translocator (ARNT) gene to a conserved linkage group located on mouse chromosome 3 and human chromosome 1. EcoRI-digested DNA from a panel of 17 human x mouse somatic cell hybrids was probed with a cDNA fragment of the human ARNT gene. Six of the 17 independent mouse x human hybrids were positive for human bands. Human chromosome 1 showed complete cosegregation with the gene, whereas discordant segregation was observed for all other human chromosomes. The human gene was localized to 1q21 by using DNA from mouse x human hybrid clones that retain translocations involving human chromosome 1, by segregation analysis in nine informative CEPH families, and by in situ hybridization. The mouse homologue was mapped to mouse chromosome 3 using a panel of 16 hamster x mouse somatic cell hybrids. Six of 16 mouse x hamster hybrids were positive for mouse bands, showing complete concordance with mouse chromosome 3. The mouse Arnt gene was regionally mapped on chromosome 3, using linkage analysis in an interspecific backcross. The results indicate that the mouse gene resides about 40 cM from the centromere and about 10 cM proximal to Cf-3, the gene for tissue factor.

Animals↗
PubMed1992

Midbrain dopaminergic cell loss in Parkinson's disease and MPTP-induced parkinsonism: sparing of calbindin-D28k-containing cells.

Computer imaging and immunohistochemical staining techniques were used to determine which midbrain dopaminergic (DA) cells are spared in Parkinson's disease (PD), and in animals treated with the DA neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and whether the spared cells contain the calcium-binding protein, calbindin-D28k (CaBP). The PD patients had more than 55% fewer midbrain DA neurons than age-matched normal subjects. The cell loss occurred within the combined substantia nigra and retrorubral area (greater than 61%; DA nuclei A9 and A8, respectively), and the ventral tegmental area (greater than 42%; DA nucleus A10). The cell loss was greatest within the ventral portion of the nucleus A9. A similar pattern of DA cell loss was observed in MPTP-treated Macaca fascicularis monkeys. The CaBP-containing cells were located specifically in the cell regions spared by PD and by MPTP-treatment in both monkeys and C57BL/6 mice. These data suggest that PD and MPTP both destroy the same population of midbrain DA neurons within nuclei A8, A9, and A10, and that perhaps CaBP protects the DA neurons from cell death caused by both PD and MPTP.

Aged↗
PubMed1992

The effects of chromium supplementation on serum glucose and lipids in patients with and without non-insulin-dependent diabetes.

Seventy-six patients with established atherosclerotic disease were treated daily with either 250 micrograms of chromium orally as chromium chloride or a placebo for a period of 7 to 16 months (mean, 11.1 months). Serum chromium increased from 2.69 +/- 0.09 to 12.12 +/- 0.77 nmol/L (mean +/- SE, P less than .005). Serum triglycerides were lower (1.68 +/- 0.11 and 2.10 +/- 0.14 nmol/L, respectively; P less than .02) in the chromium-treated patients than in the patients who received placebo, and serum high-density lipoprotein (HDL) increased (from 0.94 +/- 0.05 to 1.14 +/- 0.07 mmol/L, P less than .005) in the patients who received chromium. There was no change in serum cholesterol or blood glucose during the study.

Adult↗
PubMed1992

Serum and mononuclear cell potassium, magnesium, sodium and calcium in pregnancy and labour and their relation to uterine muscle contraction.

Thirty women in their third trimester of pregnancy (37-42 weeks), 40 women during and 72 h after labour and 18 non-pregnant controls were studied for changes in serum and mononuclear cell cation content, and their relationship to cervical effacement and intensity of pain as measured by plasma beta endorphin concentrations during labour. Serum magnesium fell from 0.95 +/- 0.01 (mean +/- SEM) to 0.84 +/- 0.02 mmol/litre at late pregnancy and further to 0.76 +/- 0.01 during labour (P < 0.001); serum potassium fell from 4.25 +/- 0.05 to 3.79 +/- 0.06 mmol/litre (P < 0.0001) during labour; and serum calcium fell from 2.40 +/- 0.02 to 2.28 +/- 0.01 mmol/litre at late pregnancy (P < 0.001) and further to 2.25 +/- 0.02 mmol/litre during labour (P < 0.001). Mononuclear cell magnesium content rose from 4.5 +/- 0.3 to 5.6 +/- 0.04 fmol/cell (P < 0.02); potassium content rose from 37.7 +/- 2.0 to 50.9 +/- 3.0 fmol/cell (P < 0.001); and calcium content rose from 4.4 +/- 0.4 to 7.6 +/- 1.1 fmol/cell (P < 0.105). On the other hand, mononuclear cell sodium content fell from 7.2 +/- 0.5 to 3.8 +/- 0.3 fmol/cell (P < 0.001). Plasma beta endorphin concentrations increased with increasing degrees of effacement, as did intracellular Na, whereas intracellular Mg and K showed an inverse trend. A significant correlation was found between intracellular cation and beta endorphin levels (r = -0.98, Mg; -0.99, K; 0.83, Na). These changes are probably due either to intercompartmental cation shifts or possibly to endometrial ischaemia and damage during labour.

Adolescent↗
PubMed1991

Effects of hydrochlorothiazide, diltiazem and enalapril on mononuclear cell sodium and magnesium levels in systemic hypertension.

Sixteen patients (mean age 68 years) with mild to moderate hypertension were treated with either diltiazem or hydrochlorothiazide for 6 weeks, followed by enalapril for a further 6 weeks. A second group of 40 patients (mean age 71 years) was treated with either hydrochlorothiazide or enalapril for 12 weeks; nonresponders received both drugs for 8 weeks. Treatment with hydrochlorothiazide or enalapril resulted in a lowering of systolic and diastolic blood pressures, but diastolic pressure was lower in patients treated with enalapril (89 +/- 2 and 82 +/- 2 mm Hg, respectively; p less than 0.05). Treatment with diltiazem resulted in a decrease in diastolic pressure only. Treatment with hydrochlorothiazide resulted in a 17% decrease in serum potassium (p less than 0.05), which returned to normal when enalapril was substituted. Hydrochlorothiazide also produced a 23% decrease in mononuclear cell sodium content at 4 weeks (p less than 0.01), with a further 15% decrease at 12 weeks (p less than 0.05). Mononuclear cell potassium and magnesium also decreased at 12 weeks by 18 and 16%, respectively (p less than 0.05). All these effects were reversed when enalapril was substituted. A similar pattern of events was seen with diltiazem, which was again reversed with enalapril. Finally, there was no relation between changes in mononuclear cell sodium or other cation content and changes in blood pressure.

Aged↗
PubMed1991

Cloning of a factor required for activity of the Ah (dioxin) receptor.

The aryl hydrocarbon (Ah) receptor binds various environmental pollutants, such as polycyclic aromatic hydrocarbons, heterocyclic amines, and polychlorinated aromatic compounds (dioxins, dibenzofurans, and biphenyls), and mediates the carcinogenic effects of these agents. The complementary DNA and part of the gene for an 87-kilodalton human protein that is necessary for Ah receptor function have been cloned. The protein is not the ligand-binding subunit of the receptor but is a factor that is required for the ligand-binding subunit to translocate from the cytosol to the nucleus after binding ligand. The requirement for this factor distinguishes the Ah receptor from the glucocorticoid receptor, to which the Ah receptor has been presumed to be similar. Two portions of the 87-kilodalton protein share sequence similarities with two Drosophila proteins, Per and Sim. Another segment of the protein shows conformity to the consensus sequence for the basic helix-loop-helix motif found in proteins that bind DNA as homodimers or heterodimers.

Amino Acid Sequence↗
PubMed1991

Genetic and molecular analysis of the Ah receptor and of Cyp1a1 gene expression.

The Ah receptor is a soluble protein complex that mediates carcinogenesis by a wide range of environmental pollutants, including polycyclic aromatic hydrocarbons, heterocyclic amines, and polychlorinated aromatic compounds. The best understood activity of the receptor concerns its role in the induction of cytochrome P450IA1. We undertook a somatic cell genetic analysis of P450IA1 induction using the mouse hepatoma cell line, Hepa-1. Clones of Hepa-1 were isolated that are defective in induction of P450IA1. Evidence was obtained that the clones are mutational in origin. Cell fusion experiments demonstrated that a few of the mutants are dominant, while the majority are recessive. The dominant mutants were shown to synthesize a repressor of P450IA1 transcription. The recessive mutants were assigned to 4 complementation groups (probably corresponding to 4 different genes). Complementation group A corresponds to the P450IA1 structural gene. Mutations in the B, C and D genes all affect functioning of the Ah receptor. A 'reverse selection procedure', whereby cells that express P450IA1 inducibility can be selected from a majority population of cells lacking inducibility, was developed. The reverse selection procedure was used to isolate transfectants of representative recessive mutants in which the mutational defects are complemented by exogenously applied genomic DNA. A human DNA-derived transfectant of a C- mutant was used to clone the human C gene. The C gene is not the ligand-binding subunit of the Ah receptor but is a protein that is required for translocation of Ah receptor-ligand complexes from cytoplasm to nucleus. In analogous experiments the dominant gene from one of the dominant mutants was transfected into wild-type Hepa-1 cells. Success in transfecting the dominant gene should provide the means for cloning it.

Animals↗
PubMed1991

Chromium and cholesterol-induced atherosclerosis in rabbits.

Thirty-three rabbits on a cholesterol-enriched diet were randomized into 6 groups and treated with daily injections of either water, 20 micrograms of potassium chromate or 1, 5, 10 or 20 micrograms of chromium chloride, respectively, for 135 days with a 2- to 10-fold increase in serum chromium. There was a marked reduction in the percentage of aortic intimal surface covered by plaque, in aortic weight and cholesterol content in the treated animals. Rabbits treated with 20 micrograms of chromium chloride showed a better response than those treated with either 10 or 20 micrograms of potassium chromate.

Animals↗
PubMed1991

Serum and intracellular electrolytes in patients with and without pain.

The effect of acute stress, with and without pain, on serum and mononuclear cell cation content was studied in 205 healthy women in their last trimester of pregnancy or during normal labour, in patients with acute medical conditions in which pain was or was not present, in acute surgical conditions, and immediately prior to elective surgery. In all subjects there was a fall in serum sodium, potassium, magnesium and calcium concentrations during stress, with an apparent shift into the intracellular space. An inverse correlation was present between the severity of pain and the fall in serum cations.

Adolescent↗
PubMed1990

A routine method for the measurement of the sodium, potassium, magnesium and calcium content of human lymphocytes.

We describe a rapid, single-step procedure for the isolation of human lymphocytes from whole blood, suitable for a routine clinical laboratory. Lymphocyte content of sodium, potassium, magnesium and calcium were measured simultaneously in a group of controls and found to fall within expected ranges. Expression of results per mg protein produced less inter-individual variation than per unit cell. In order to examine another, physiologically different but normal population, women during pregnancy were also studied. The cation content of lymphocytes expressed per mg protein was significantly lower than for controls due to a 44% increase in protein content per cell.

Adult↗
PubMed1988

Glutathione transferase activities of cultured human lymphocytes.

We have detected glutathione transferase (GST) activity towards 1-chloro-2,4-dinitrobenzene (CDNB) and benzo[a]-pyrene 4,5-oxide (BPO) in freshly isolated peripheral lymphocytes, phytohaemagglutinin (PHA)-stimulated lymphocytes, interleukin-2 (IL-2)-dependent T-cells and lymphoblastoid B-cell lines. The detection of conjugating activity with BPO implies the expression of a neutral, 'mu-like' GST form by both resting and cultured lymphocytes. In a sample of 12 unrelated individuals, BPO conjugating activity of freshly isolated lymphocytes showed a polymorphic distribution. In comparison with freshly isolated cells, BPO activity was increased 2- to 5-fold in IL-2-dependent T-cells and 4- to 10-fold in B-cell lines. The CDNB activity of T-cells was not significantly different to that of freshly isolated cells (P greater than 0.05) but activity in B-cell lines showed a significant increase (P less than 0.01). These data indicate that measurement of BPO activity in freshly isolated lymphocytes may allow the study of the human GST-mu polymorphism. However, IL-2-dependent culture of T-cells or viral immortalization of resting lymphocytes appears to cause the activation or induction of a GST form or forms which conjugate BPO efficiently. In the T-cells this effect may be mediated through addition of IL-2 to the culture since PHA treatment alone did not elevate activity.

Benzopyrenes↗
PubMed1988

Effects of enalapril on lymphocyte sodium, potassium, magnesium and calcium levels in patients with severe congestive heart failure.

Fifteen patients (median age 73 years) with severe congestive heart failure were treated with Enalapril for a total of 12 weeks with a significant improvement in their right atrial pressures and in their functional state. Renal function, serum potassium, magnesium and calcium levels were unchanged. Lymphocyte sodium, potassium and calcium levels were generally lower than control values throughout the study but these differences were only statistically significant early in the study. Lymphocyte magnesium levels were unchanged. These findings are in contrast to those previously reported in the literature for such patients treated with conventional diuretics.

Aged↗
PubMed1988

The gene CYP3 encoding P450pcn1 (nifedipine oxidase) is tightly linked to the gene COL1A2 encoding collagen type 1 alpha on 7q21-q22.1.

CYP3, the gene which encodes the hepatic cytochrome P450pcn1, the isozyme responsible for the metabolic oxidation of the calcium channel-blocking drug nifedipine, has recently been mapped to human chromosome 7 using somatic cell hybrids. Using multilocus linkage analysis in CEPH families, we examined the linkage of a cDNA probe (hPCN1) for CYP3 to the oncogene MET, the pro-alpha 2(1) collagen gene COL1A2, and the T-cell receptor beta-chain gene TCRB, together with three arbitrary loci D7S8, D7S13, and D7S16, defined by the anonymous DNA probes pJ3.11, pB79a, and p7C22, respectively. From 70 CEPH parents screened with a StyI RFLP for hPCN1, four informative families were found each with both parental and maternal grandparents and 6-11 children per family. Tight linkage emerged between CYP3 and COL1A2, with a maximum combined lod score of 5.72 at theta = 0, suggesting the most likely subchromosomal localization of CYP3 is 7q21.3-q22.1.

Chromosomes, Human, Pair 7↗