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Biomedical subjects

N C Turner

Publications and source records attributed to N C Turner.

At least 19 recordsLinked to original sources

BRCA1 dysfunction in sporadic basal-like breast cancer.

Basal-like breast cancers form a distinct subtype of breast cancer characterized by the expression of markers expressed in normal basal/myoepithelial cells. Breast cancers arising in carriers of germline BRCA1 mutations are predominately of basal-like type, suggesting that BRCA1 dysfunction may play a role in the pathogenesis of sporadic basal-like cancers. We analysed 37 sporadic breast cancers expressing the basal marker cytokeratin 5/6, and age- and grade-matched controls, for downregulation of BRCA1. Although BRCA1 promoter methylation was no more common in basal-like cancers (basal 14% vs controls 11%, P=0.72), BRCA1 messenger RNA expression was twofold lower in basal-like breast cancers compared to matched controls (P=0.008). ID4, a negative regulator of BRCA1, was expressed at 9.1-fold higher levels in basal-like breast cancer (P<0.0001), suggesting a potential mechanism of BRCA1 downregulation. BRCA1 downregulation correlated with the presence of multiple basal markers, revealing heterogeneity in the basal-like phenotype. Finally, we found that 63% of metaplastic breast cancers, a rare type of basal-like cancers, had BRCA1 methylation, in comparison to 12% of controls (P<0.0001). The high prevalence of BRCA1 dysfunction identified in this study could be exploited in the development of novel approaches to targeted treatment of basal-like breast cancer.

BRCA1 Protein↗

Basal-like breast cancer and the BRCA1 phenotype.

Breast cancers arising in germline carriers of BRCA1 mutations have a characteristic phenotype that has been shown in many studies to differentiate BRCA1 tumours from sporadic tumours. Recently, it has become clear that the characteristic phenotype of BRCA1 tumours is due to expression of the basal-like phenotype. We review these phenotypes, the evidence for BRCA1 pathway dysfunction in sporadic basal-like cancers, and discuss the clinical significance of the basal-like phenotype for cancer genetics and treatment.

Breast Neoplasms↗

Paraneoplastic "stiff person syndrome" with metastatic adenocarcinoma and anti-Ri antibodies.

A 43-year-old woman presented with clinical and electrophysiologic features of stiff person syndrome (SPS), without abdominal or lumbar paraspinal muscle involvement. Investigations revealed metastatic adenocarcinoma of the lung with positive anti-Ri antibodies. Her clinical condition improved with diazepam, baclofen, tizanidine, and palliative chemotherapy. Screening for an underlying malignancy and anti-Ri antibodies should be considered in patients with SPS when clinical presentation is atypical.

Adenocarcinoma↗

Hepatitis C and B-cell lymphoma.

The association between the hepatitis C virus and B-cell non-Hodgkin's lymphomas is controversial. We review the epidemiological evidence behind the association, and look at the reasons behind the variation in study findings. There is increasing evidence of the pathogenesis of hepatitis C-associated lymphoma. Treatment of the hepatitis C virus with antiviral therapy may lead to the regression of some low-grade lymphomas. The management of other hepatitis C-associated lymphomas is similar to that of conventional lymphoma, although viral reactivation and subsequent immune reconstitution hepatitis can complicate chemotherapy.

Hepatitis C↗

An improved heat pulse method to measure low and reverse rates of sap flow in woody plants.

The compensation heat pulse method (CHPM) is of limited value for measuring low rates of sap flow in woody plants. Recent application of the CHPM to woody roots has further illustrated some of the constraints of this technique. Here we present an improved heat pulse method, termed the heat ratio method (HRM), to measure low and reverse rates of sap flow in woody plants. The HRM has several important advantages over the CHPM, including improved measurement range and resolution, protocols to correct for physical and thermal errors in sensor deployment, and a simple linear function to describe wound effects. We describe the theory and methodological protocols of the HRM, provide wound correction coefficients, and validate the reliability and accuracy of the technique against gravimetric measurements of transpiration.

Eucalyptus↗

Gas exchange by pods and subtending leaves and internal recycling of CO(2) by pods of chickpea (Cicer arietinum L.) subjected to water deficits.

Terminal drought markedly reduces leaf photosynthesis of chickpea (Cicer arietinum L.) during seed filling. A study was initiated to determine whether photosynthesis and internal recycling of CO(2) by the pods can compensate for the low rate of photosynthesis in leaves under water deficits. The influence of water deficits on the rates of photosynthesis and transpiration of pods and subtending leaves in chickpea (cv. Sona) was investigated in two naturally-lit, temperature-controlled glasshouses. At values of photosynthetically active radiation (PAR) of 900 micromol m(-2) s(-1) and higher, the rate of net photosynthesis of subtending leaves of 10-d-old pods was 24 and 6 micromol m(-2) s(-1) in the well-watered (WW) and water-stressed (WS) plants when the covered-leaf water potential (Psi) was -0.6 and -1.4 MPa, respectively. Leaf photosynthesis further decreased to 4.5 and 0.5 micromol m(-2) s(-1) as Psi decreased to -2.3 and -3.3 MPa, respectively. At 900--1500 micromol m(-2) s(-1) PAR, the net photosynthetic rate of 10-d-old pods was 0.9-1.0 micromol m(-2) s(-1) in the WW plants and was -0.1 to -0.8 micromol m(-2) s(-1) in the WS plants. The photosynthetic rates of both pods and subtending leaves decreased with age, but the rate of transpiration of the pods increased with age. The rates of respiration and net photosynthesis inside the pods were estimated by measuring the changes in the internal concentration of CO(2) of covered and uncovered pods during the day. Both the WW and WS pods had similar values of internal net photosynthesis, but the WS pods showed significantly higher rates of respiration suggesting that the WS pods had higher gross photosynthetic rates than the WW pods, particularly in the late afternoon. When (13)CO(2) was injected into the gas space inside the pod, nearly 80% of the labelled carbon 24 h after injection was observed in the pod wall in both the WW and WS plants. After 144 h the proportion of (13)C in the seed had increased from 19% to 32% in both treatments. The results suggest that internal recycling of CO(2) inside the pod may assist in maintaining seed filling in water-stressed chickpea.

Carbon Dioxide↗

Seed coat cell turgor in chickpea is independent of changes in plant and pod water potential.

Turgor pressure in cells of the pod wall and the seed coat of chickpea (Cicer arietinum L.) were measured directly with a pressure probe on intact plants under initially dry soil conditions, and after the plants were irrigated. The turgor pressure in cells of the pod wall was initially 0.25 MPa, and began to increase within a few minutes of irrigation. By 2-4 h after irrigation, pod wall cell turgor had increased to 0.97 MPa. This increase in turgor was matched closely by increases in the total water potential of both the pod and the stem, as measured by a pressure chamber. However, turgor pressure in cells of the seed coat was relatively low (0.10 MPa) and was essentially unchanged up to 24 h after irrigation (0.13 MPa). These data demonstrate that water exchange is relatively efficient throughout most of the plant body, but not between the pod and the seed. Since both the pod and the seed coat are vascularized tissues of maternal origin, this indicates that at least for chickpea, isolation of the water relations of the embryo from the maternal plant does not depend on the absence of vascular or symplastic connections between the embryo and the maternal plant.

Cicer↗

Acceleration of the development of diabetes in obese diabetic (db/db) mice by nicotinamide: a comparison with its antidiabetic effects in non-obese diabetic mice.

Destruction of pancreatic beta cells has been implicted in the progression to hyperglycemia in type 1 diabetes. While there is evidence of beta-cell loss in type 2 diabetes, its contribution to the development of the diabetic state is undecided. Nicotinamide has defensive effects against toxic insults to the pancreatic islets and confers protection in both human and animal models of type 1 diabetes, but its effects on type 2 diabetes are less well documented. This report describes a comparison of the outcome of chronic oral administration of nicotinamide on the development of diabetes in obese diabetic (db/db) and non-obese diabetic (NOD) mice models of type 2 and type 1 diabetes, respectively. Nicotinamide was administered in the diet (5 g/kg diet) for 12 (db/db) or 24 (NOD) weeks. Over the 12 weeks of the study, control diabetic (db/db) mice became progressively more hyperglycemic and glycosuric, while serum and pancreatic insulin levels decreased compared with those on day 0. In mice treated with nicotinamide, there was a pronounced acceleration in the development of hyperglycemia and glycosuria, as well as a decrease in pancreatic insulin levels, compared with time-matched controls. In addition, the morphology of the pancreatic islets of nicotinamide-treated diabetic (db/db) mice showed an enhanced islet disorganization. By comparison, in NOD mice, nicotinamide prevented the decline in serum and pancreatic insulin levels and maintained normal islet architecture and insulin content. Our data shows that in contrast to its preventative effects on the development of autoimmune diabetes in NOD mice, chronic nicotinamide administration to obese diabetic (db/db) mice markedly accelerated the progression of diabetes. The results of our study caution against the use of nicotinamide in insulin-resistant states, such as type 2 diabetes.

Animals↗

Insulin resistance, impaired glucose tolerance and non-insulin-dependent diabetes, pathologic mechanisms and treatment: current status and therapeutic possibilities.

Impaired glucose tolerance and non-insulin-dependent diabetes (NIDDM) are the pathologic consequence of two co-incident and interacting conditions, namely insulin resistance and relative insulin deficiency. Recognised by the World Health Authority as a global health problem there are at 1995 estimates at least 110 million diagnosed diabetics world wide with at least the same number undiagnosed. Diabetes is the 4th leading cause of death in developed countries and its management exerts a vast economic and social burden. Insulin resistance is established as the characteristic pathologic feature of patients with glucose intolerance and NIDDM describing a state in which insulin stimulated glucose uptake and utilisation in liver, skeletal muscle and adipose tissue is impaired and coupled to impaired suppression of hepatic glucose output. Although the biochemical mechanisms underpinning both defects are becoming better understood, the genetic and molecular causes remain elusive; and whether insulin resistance or relative insulin deficiency represents the primary defect in patients with NIDDM is the matter of some debate. In this article we review the biochemical and molecular nature of the defects in insulin sensitivity and glucose uptake, and discuss some of the potential causative mechanisms. The genetic and environmental basis of insulin resistance is reviewed and presented, and potential therapeutic targets including thiazolidinediones are discussed.

Diabetes Mellitus, Type 2↗

Potential benefit of inhibitors of advanced glycation end products in the progression of type II diabetes: a study with aminoguanidine in C57/BLKsJ diabetic mice.

Prolonged hyperglycemia in type II diabetic patients is linked both with diabetic complications and with further impairment of glucose homeostasis, possibly due to glucose toxicity of the beta cell. While the connection between the accumulation of extracellular advanced glycation end products (AGEs) and the development of complications is well established, it has only recently been suggested that intracellular glycation may be equally adverse and could be involved in the pathogenesis of glucose toxicity in vitro. Aminoguanidine is a recognized inhibitor of the formation of both extracellular and intracellular AGEs. In this study, we show that the development of diabetes, measured by increased water intake and concomitant midday blood glucose levels in type II genetically diabetic mice, is reduced by treatment with aminoguanidine at a dosage of 500 mg/kg/d for 12 weeks in the diet. In addition, at the end of the study, aminoguanidine reduced the decline in serum and pancreatic insulin levels and the degree of pancreatic islet morphological degeneration, all of which are associated with pancreatic insufficiency following prolonged hyperglycemia in this animal model. These results suggest that AGEs may be involved in the aggravation of type II diabetes in vivo and aminoguanidine may be beneficial in its treatment.

Animals↗

Peroxisome proliferator-activated receptor-gamma agonist, rosiglitazone, protects against nephropathy and pancreatic islet abnormalities in Zucker fatty rats.

Rosiglitazone (BRL 49653), a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist and potent insulin action-enhancing agent, was given in the diet (50 micromol/kg of diet) to male Zucker rats ages 6-7 weeks for 9 months (prevention group). In this treatment mode, rosiglitazone prolonged the time to onset of proteinuria from 3 to 6 months and markedly reduced the rate of its subsequent progression. Progression was also retarded when treatment was commenced (intervention group) after proteinuria had become established (4 months; ages 24-25 weeks). In either treatment mode, rosiglitazone normalized urinary N-acetyl-beta-D-glucosaminidase activity, a marker for renal proximal tubular damage, and ameliorated the rise in systolic blood pressure that occurred coincidentally with the development of proteinuria in Zucker fatty control rats. The renal protective action of rosiglitazone was verified morphologically. Thus in the prevention group there was an absence of the various indexes of chronic nephropathy that were prominent in the Zucker fatty control group, namely, glomerulosclerosis, dilated tubules containing proteinaceous casts, a loss of functional microvilli on the tubular epithelium, and varying degrees of chronic interstitial nephritis. An intermediate pathology was observed in the intervention group. Also, pancreatic islet hyperplasia, ultrastructural evidence of beta-cell work hypertrophy, and derangement of alpha-cell distribution within the islet were prominent features of Zucker fatty control rats, but these adaptive changes were ameliorated (intervention group) or prevented (prevention group) by rosiglitazone treatment. These data demonstrate that treatment of Zucker fatty rats with rosiglitazone produced substantial protection over a prolonged period against the development and progression of renal injury and the adaptive changes to pancreatic islet morphology caused by sustained hyperinsulinemia.

Acetylglucosaminidase↗

Elevated renal endothelin-I clearance and mRNA levels associated with albuminuria and nephropathy in non-insulin-dependent diabetes mellitus: studies in obese fa/fa Zucker rats.

1. The obese fa/fa Zucker rat is a genetic model of obesity and insulin resistance which develops a number of metabolic and endocrine features of non-insulin-dependent diabetes, including hypertension, proteinuria and glomerular sclerosis. 2. We have investigated the urinary excretion of the metabolites of thromboxane (thromboxane B2) and prostacyclin (6-keto prostaglandin F1 alpha), and of endothelin and cyclic GMP as markers for changes in the balance of renal haemodynamic factors in the obese Zucker rat. 3. Obese fa/fa Zucker rats were hypertensive compared with their lean counterparts (161 +/- 3 and 138 +/- 3 mmHg respectively, P < 0.01); obese animals were also markedly proteinuric (16.7 +/- 6.7 versus 1.1 +/- 0.1 mg/ml) and albuminuric (8.3 +/- 2.9 versus 0.4 +/- 0.25 mg/ml) and excreted less creatinine than lean animals (all P < 0.01). Urinary excretion of endothelin was greater in obese rats (123 +/- 24 versus 62 +/- 10 pg/15 h, P < 0.05) as was the level of pre-proendothelin mRNA, but excretion of cyclic GMP was depressed (12.5 +/- 1.6 versus 27.2 +/- 3.1 nmol/ 15 h, P < 0.01). Histological examination of kidneys from obese animals showed evidence of focal glomerulosclerosis and cortical tubular damage. 4. These results show that increased urinary endothelin is associated with proteinuria and early stage nephropathy in this animal model of non-insulin-dependent diabetes mellitus. This finding, coupled with a decreased excretion of cyclic GMP, suggests that these increased renal vasoconstrictor/vasodilator forces might contribute to the renal functional changes in non-insulin-dependent diabetes mellitus.

6-Ketoprostaglandin F1 alpha↗

Effects of the glucocorticoid II receptor antagonist mifepristone on hypertension in the obese Zucker rat.

We have investigated the possible involvement of endogenous corticosteroids in the maintenance of hypertension in aged lean and obese Zucker rats using the type II corticosteroid antagonist mifepristone. At 8 mo of age, the start of the study, obese Zuckers had been hypertensive for at least 2 mo (systolic blood pressure; 153 +/- 4 vs. 136 +/- 5 mmHg; n = 8-9; P < .05) and were hyperinsulinemic (756 +/- 98 vs. 193 +/- 61 microU x ml(-1)) and hypercorticosteronemic (524 +/- 83 vs. 260 +/- 97 ng x ml(-1)) compared to their lean littermates. There were no differences in plasma renin activity between lean and obese animals and plasma renin activity was unaffected by any treatment. Oral treatment of obese rats with mifepristone (40.0 mg x kg(-1) day(-1) for 9 days) resulted in a gradual reduction in SBP to lean levels by day 9. Mifepristone treatment did not affect plasma insulin or corticosterone levels but resulted in a significant reduction in plasma aldosterone concentration. Mifepristone was without significant effect on systolic blood pressure in lean rats. Oral treatment of lean rats with corticosterone-21-acetate (3.0 mg x kg(-1) day(-1) for 9 days) resulted in a rise in systolic blood pressure to levels similar to obese Zuckers after 9 days. Plasma insulin levels were unchanged but corticosterone immunoreactivity was significantly reduced. Plasma aldosterone levels were increased from 564 +/- 3 to 802 +/- 68 pg x ml(-1). Our data suggest that raised glucocorticoids and aldosterone may be factors contributing to hypertension in obesity.

Aldosterone↗

Effects of streptozotocin-induced diabetes on vascular reactivity in genetically hyperinsulinaemic obese Zucker rats.

Although the fa/fa Zucker rat shows many of the features of type II diabetes, the absence of consistent cardiovascular complications in this model may be due to the absence of significant hyperglycaemia. We studied the consequences of streptozotocin (STZ)-induced insulin deficiency and hyperglycaemia on vascular reactivity in the fa/fa Zucker rat. Hyperinsulinaemic obese Zucker rats were rendered diabetic by injection of STZ (50-60 mg/kg intraperitoneally, i.p.), and vascular tissue was removed for study 10-12 weeks later. In isolated aorta, there was no difference in the phenylephrine (PE) concentration-response relation between lean and obese control animals, but the concentration-response curve was shifted to the left in diabetic animals, (pD2 7.56 +/- 0.04 in STZ diabetic animals, n = 8; 7.4 +/- 0.04 in obese control, n = 9, p < 0.05). The maximum response was also enhanced in both aorta and perfused mesentery of STZ-treated animals. In contrast, the potency of serotonin (5-HT) in inducing contractions of isolated aorta were enhanced in tissues from obese as compared with lean animals (pD2 6.63 +/- 0.06, n = 9; 6.17 +/- 0.07, n = 7 respectively; p < 0.01) and was attenuated in animals with STZ-induced diabetes (pD2 6.31 +/- 0.09, n = 8, p = 0.05). The differential effects of hyperglycaemia on PE-and 5-HT-induced vasoconstriction suggest that the long-lasting modulation of vasoconstrictor responses induced by increases in blood glucose level may be specific for some agonists.

Acetylcholine↗

Eicosanoid release in allergen-induced bronchoconstriction in dogs. Its relationship to airways hyperreactivity and pulmonary inflammation.

In vitro studies have demonstrated the release of histamine, PGD2, TXB2, PGE2, PGF2 alpha, 6-keto-PGF1 alpha and the peptidoleukotrienes from sensitized lung. We have assessed the release of these mediators following antigen challenge in vivo. Antigen challenge of allergic dogs resulted in an acute bronchoconstriction and an increase in bronchial reactivity to histamine and an increase in neutrophil and eosinophil numbers recovered by bronchoalveolar lavage (BAL), 2 and 24 h later. The acute response was associated with histamine and PGD2 release but there was no increase in the levels of other eicosanoids in recovered BAL. Bronchial hyperreactivity and pulmonary inflammation, 2 and 24 h post-challenge was not associated with a concommitant (antigen specific) increase in BAL fluid eicosanoid levels. We conclude that although PGD2 is released during the acute response to antigen the subsequent changes (hyperreactivity and inflammation) are not characterised by a maintained elevation in eicosanoid levels detectable by BAL.

Airway Resistance↗

Effects of genetic hyperinsulinaemia on vascular reactivity, blood pressure, and renal structure in the Zucker rat.

The association between insulin resistance, obesity, and hypertension is well recognised. We examined the hypothesis that hypertension in the obese Zucker rat is related to changes in vascular reactivity. Systolic blood pressure (SBP) in conscious Zucker rats was significantly greater in obese as compared with lean animals (157 +/- 9 and 117 +/- 8 mm Hg). Obese animals also had marked proteinuria and reduced urinary creatinine excretion in 24 h as compared with their lean counterparts. The reactivity of isolated aorta to phenylephrine (PE) and 5-hydroxy-tryptamine (5-HT) was modestly (twofold) increased in obese animals (EC50 13.8 nM as compared with 29.4 nM in lean animals and 0.19 nM as compared with 0.46 nM in lean animals, respectively). In the perfused mesenteric vascular bed, basal perfusion pressure was the same in both phenotypes, as was the pressor response to PE and depressor response to acetylcholine (ACh) and sodium nitroprusside (SNP). In the isolated aorta, from obese animals, insulin attenuated the contractile response to PE but markedly enhanced the vasoconstrictor potency of 5-HT. It had no significant effect on pressor or depressor responses in the perfused mesenteric bed. The data suggest that increased reactivity of central arteries to spasmogenic agents may be involved in the development of systolic hypertension in the hyperinsulinaemic Zucker rat.

Acetylcholine↗

Superoxide generation by guinea-pig peritoneal macrophages is inhibited by rolipram, staurosporine and mepacrine in an agonist-dependent manner.

Platelet-activated factor (PAF) (EC50 -7.9 +/- 0.6 M), formyl-methionyl-leucyl-phenylalanine (fMPL) (EC50 -7.7 +/- 0.1M), phorbol 12-myristate 13 acetate (PMA) (EC50 -8.4 +/- 0.3 M), opsonized zymosan (OPZ) (0.01-1 mg/ml) were potent stimuli to superoxide generated by guinea-pig peritoneal macrophages. Superoxide generation by low (< or = -8M) concentrations but not high (> or = -7M) concentrations of PAF or fMLP were attenuated by rolipram (100 microM) in the presence of 1 microM prostaglandin E2 (PGE2). That stimulated by PMA or OPZ, however, was unaffected. At 1 microM, staurosporine was a potent inhibitor of superoxide generation stimulated by both fMLP and PAF but was without effect on that stimulated by OPZ. Superoxide generation stimulated by fMLP, PAF and OPZ was inhibited by 100 microM mepacrine. We conclude that superoxide generation stimulated by the chemoattractants fMLP and PAF involves a cyclic AMP regulated and cyclic AMP independent process. The cyclic AMP independent process is mediated by protein kinase C. Although protein kinase C seems a central element in the respiratory burst stimulated by fMLP, PAF and PMA that stimulated by OPZ bypasses this mechanism. Phospholipase A2 however, represents a common stage in the signal transduction pathway.

3',5'-Cyclic-AMP Phosphodiesterases↗

Leaf growth, photosynthesis and tissue water relations of greenhouse-grown Eucalyptus marginata seedlings in response to water deficits.

Leaf growth, rate of leaf photosynthesis and tissue water relations of shoots of Eucalyptus marginata Donn ex Sm. (jarrah) seedlings were studied during a soil drying and rewatering cycle in a greenhouse experiment. Rates of leaf growth and photosynthesis were sensitive to water deficits. The rate of leaf growth decreased linearly with predawn leaf water potential to reach zero at -1.5 MPa. Rate of leaf growth did not recover completely within the first three days after rewatering. Midday photosynthetic rates declined to 40% of those of well-watered seedlings at a predawn leaf water potential of -1.0 MPa and reached zero at -2.2 MPa. Photosynthetic rate recovered rapidly following rewatering and almost fully recovered by the second day after rewatering. All tissue water relations parameters, except the bulk modulus of elasticity, changed significantly as the soil dried and recovered completely by the third day after rewatering. Changes in osmotic pressure at full turgor of 0.4 MPa indicated considerable capacity for osmotic adjustment. However, because there was little osmotic adjustment until predawn leaf water potential fell below -1.5 MPa, this capacity would not have enhanced seedling growth, although it may have increased seedling survival. The sensitivity of photosynthesis and relative water content to water deficits suggests that greenhouse-grown E. marginata seedlings behave like mesophytic plants, even though E. marginata seedlings naturally grow in a drought-prone environment.

Journal Article↗