Publications by authors named "Hough F"

The present experiment used the trapped rat model to explore whether pharmacological manipulation of distress affects the likelihood of helping behavior. 120 Sprague-Dawley rats (30 male pairs and 30 female pairs) completed 12 consecutive, daily trials assessing helping behavior. During an individual trial, a trapped rat was placed in a restrainer in the center of an open field, while its cagemate could move around freely and possibly open the restrainer by lifting a door.

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Subjects with type 1 diabetes mellitus (T1DM) have decreased bone mineral density and an up to sixfold increase in fracture risk. Yet bone fragility is not commonly regarded as another unique complication of diabetes. Both animals with experimentally induced insulin deficiency syndromes and patients with T1DM have impaired osteoblastic bone formation, with or without increased bone resorption.

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Genomic medicine is based on the knowledge that virtually every medical condition, disease susceptibility or response to treatment is caused, regulated or influenced by genes. Genetic testing may therefore add value across the disease spectrum, ranging from single-gene disorders with a Mendelian inheritance pattern to complex multi-factorial diseases. The critical factors for genomic risk prediction are to determine: (1) where the genomic footprint of a particular susceptibility or dysfunction resides within this continuum, and (2) to what extent the genetic determinants are modified by environmental exposures.

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Osteoporosis is a common, costly and serious disease, which is still too often regarded as an inevitable part of the normal ageing process and therefore sub-optimally treated, especially in the elderly--in fact, only two out of every 10 patients who sustain a hip fracture receive any form of assessment or prophylactic therapy for osteoporosis. One out of five patients die within 1 year after a hip fracture, and < 50% are capable of leading an independent life. Yet very effective anti-fracture therapy, capable of reducing fracture risk by 35 - 60%, is available.

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Although the presence of adipocytes in the bone marrow is a normal physiological phenomenon, the role of these cells in bone homeostasis and during pathological states has not yet been fully delineated. As osteoblasts and adipocytes originate from a common progenitor, with an inverse relationship existing between osteoblastogenesis and adipogenesis, bone marrow adiposity often negatively correlates with osteoblast number and bone mineral density. Bone adiposity can be affected by several physiological and pathophysiological factors, with abnormal, elevated marrow fat resulting in a pathological state.

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The number of mature osteoblasts and marrow adipocytes in bone is influenced by the differentiation of the common mesenchymal progenitor cell towards one phenotype and away from the other. Consequently, factors which promote adipogenesis not only lead to fatty marrow but also inhibit osteoblastogenesis, resulting in decreased osteoblast numbers, diminished bone formation and, potentially, inadequate bone mass and osteoporosis. In addition to osteoblast and bone adipocyte numbers being influenced by this skewing of progenitor cell differentiation towards one phenotype, mature osteoblasts and adipocytes secrete factors which may evoke changes in the cell fate and function of each other.

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Background And Objective: Hypothalamic-pituitary-adrenal axis suppression (HPAS) when treating children with corticosteroids is thought to be rare. Our objective was to determine the prevalence of and predictive factors for various degrees of HPAS.

Methods: Clinical features of HPAS, doses, adherence, asthma score, and lung functions were recorded in 143 asthmatic children.

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Adipose-derived stromal cells (ADSCs) can be differentiated in vitro into several mesenchyme-derived cell types. We had previously described depot-specific differences in the adipocyte differentiation of ADSCs, and consequently we hypothesized that there may also be depot-specific differences in osteoblast differentiation of ADSCs. For this study, the osteoblast differentiation potential of rat subcutaneous ADSCs (scADSCs) and perirenal visceral ADSCs (pvADSCs) was compared.

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Visceral adiposity is more strongly linked to insulin resistance than subcutaneous adiposity. High insulin levels can be mitogenic or adipogenic to adipocytes, but little is known regarding these effects of insulin on stromal cells from visceral and subcutaneous fat depots. Consequently, we measured adipogenesis and mitosis in response to elevated insulin levels in rat adipose-derived stromal cells (ADSCs) from visceral (perirenal) and subcutaneous depots.

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Skeletal mass is maintained by a balance between formation and resorption, cell proliferation and apoptosis. In vitro, glucocorticoids (GCs) decrease extracellular signal-regulated kinases (ERK) activation by mitogens, thus inhibiting osteoblast proliferation. Both ERK activity and proliferation are restored by co-treatment with the protein tyrosine phosphatase inhibitor, vanadate.

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Steroid-induced osteoporosis is a common side effect of long-term treatment with glucocorticoid (GC) drugs. GCs have multiple systemic effects that may influence bone metabolism but also directly affect osteoblasts by decreasing proliferation. This may be beneficial at low concentrations, enhancing differentiation.

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A central feature of glucocorticoid (GC)-induced osteoporosis is decreased bone formation, secondary to decreased numbers of functional osteoblasts. We find that ERK activity is essential for serum-induced osteoblast proliferation in vitro because inhibition of MAPK/ERK kinase activity by U0126 completely abolished both serum-induced activation of ERK and proliferation of mouse (MBA-15.4) and human (MG-63) osteoblast cell lines.

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Glucocorticoid-induced osteoporosis is characterized by decreased osteoblast numbers and a marked impairment of new bone formation. We found that, in vitro, dexamethasone inhibits both preosteoblast proliferation and mitogenic kinase activity in response to mitogens, and that inhibition of protein tyrosine phosphatases (PTPs) using sodium orthovanadate prevents this. Therefore, dexamethasone may act by either upregulating antiproliferative PTPs or downregulating promitogenic tyrosine-phosphorylated substrates.

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Increased dietary protein consumption is thought to cause calciuresis, a negative calcium balance and increased bone loss that may result in skeletal deformities and fracture. To explore this hypothesis, 40 approximately 100-day-old meat-type Merino ram lambs were fed, for 6 months, diets with an increasing crude protein (CP) content (114, 142, 171 and 190 g/kg DM) but approximately on an iso-nutrient basis with regard to metabolisable energy, calcium and phosphorus. Increased protein consumption modestly (NS) enhanced calciuresis and resulted in significant (P < or = 0.

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Chronic glucocorticoid therapy causes rapid bone loss and clinical osteoporosis. We found that although the glucocorticoid, dexamethasone, stimulated osteoblast maturation, it also inhibited proliferation of a preosteoblastic cell line, MBA-15.4.

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Aims: To assess the effect of season and latitude on the in vitro formation of previtamin D3 and vitamin D3 from 7-dehydrocholesterol (7-DHC) by sunlight in two cities in South Africa, Cape Town and Johannesburg.

Methods: An in vitro study utilising vials containing 7-DHC, which were exposed to sunlight for a period of 1 hour between 8:00 and 17:00 on 1 day a month for a year. Previtamin D3 and vitamin D3 were separated from 7-DHC by high-performance liquid chromatography, and the amounts formed were calculated with the use of external standards.

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No single test has a 100% diagnostic accuracy, and combinations of tests are required. We routinely obtain 3 baseline IRMA-ACTH levels, followed by CRF stimulation and overnight high-dose (8 mg) dexamethasone suppression (HDS). If ACTH-independent adrenal disease is suspected, thin-section CT (with or without isotope scanning) of the adrenals is performed.

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Twenty-two patients with chronic renal failure were randomly assigned to a conventional low-protein diet containing 0.6 g protein/kg/day or a very-low-protein diet containing 0.4 g protein/kg/day supplemented with essential amino acids; they were followed up for 9 months.

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Despite the vast number of risk factors that apparently predispose to the development of osteoporosis (OP), they have not been accurately identified and given relative priority. In order to analyse possible risk factors prospectively in a local patient population with overt OP (histomorphometrically confirmed and characterised) and compare it with an appropriately matched non-OP control group (with normal bone mass on dual-energy X-ray absorptiometry), a detailed general history, risk factor analysis, dietary history and anthropometric data were obtained from 56 OP and 125 non-OP subjects. In females a positive family history of OP (P = 0.

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On initial diagnosis or when metabolic control is poor, subjects with type 1 (insulin-dependent) diabetes mellitus often exhibit decreased high density lipoprotein (HDL) cholesterol levels, which have been associated in numerous studies in non-diabetic subjects with atherosclerosis and coronary artery disease. We measured the activities of plasma lecithin:cholesterol acyltransferase (LCAT), post-heparin lipoprotein lipase, and the composition of the HDL subfractions HDL2 and HDL3, in ten poorly controlled type 1 diabetic patients admitted to a metabolic ward (six women and four men, aged 18-37 years). The measurements were repeated after metabolic control had been optimised and again a week after discharge.

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Persistent micro-albuminuria (MA) in patients with diabetes mellitus identifies a high-risk group for the development of vascular complications. Since the methodology involved in measuring MA has not been standardised, MA in 40 diabetic patients was measured in order to compare nephelometry with radio-immunoassay (RIA). The effect of storage (7 days), the influence of freezing and thawing on MA levels, and possible differences between glass and plastic containers were also assessed.

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The role of moderate exercise in the prevention of high-turnover osteoporosis was investigated by the use of an animal model. The effect of chronic training on gravimetric, mineral, physical, and histological parameters of normal bone was also examined. Fifty-six adult female Long-Evans rats were divided into four groups: sedentary (C) and exercising controls (E) and sedentary (O) and exercising osteoporotics (EO).

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Using both a 25 mM Lithium di-iodosalicylic acid (LIS) and a 2M NaCl extraction procedure to extract nuclear matrices from white cells we have identified a 0.9 kb nuclear matrix associated region (MAR) in the human pro alpha 2(I) collagen gene. The MAR is located towards the 3' coding end of the gene, it is completely associated with the matrix in transcriptionally inactive white cells but is incompletely associated with the matrix in transcriptionally active fibroblasts.

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