111 results on '"JONES, T. HUGH"'
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102. Andrology: Identifying late-onset hypogonadism in older men
- Author
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Jones, T. Hugh
- Published
- 2010
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103. Response to Comment on: Jones et al. Testosterone Replacement in Hypogonadal Men With Type 2 Diabetes and/or Metabolic Syndrome (the TIMES 2 Study). Diabetes Care 2011;34:828--837.
- Author
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JONES, T. HUGH, HOWELL, JULIAN D., and CHANNER, KEVIN S.
- Subjects
- *
LETTERS to the editor , *TESTOSTERONE , *TYPE 2 diabetes - Abstract
A response by T. Hugh Jones to letter to the editor about his article "Testosterone Replacement in Hypogonadal Men With Type 2 Diabetes and/or Metabolic Syndrome (the TIMES2 Study)," is presented.
- Published
- 2011
- Full Text
- View/download PDF
104. Testosterone therapy improves exercise duration and symptoms in men with chronic congestive heart failure
- Author
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Pugh, Peter J., West, John N., Jones, T. Hugh, and Channer, Kevin S.
- Published
- 2002
- Full Text
- View/download PDF
105. Testosterone is a potent inhibitor of L-type Ca2+ channels
- Author
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Scragg, Jason L., Jones, Richard D., Channer, Kevin S., Jones, T. Hugh, and Peers, Chris
- Subjects
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TESTOSTERONE , *SMOOTH muscle , *ISCHEMIA , *CORONARY disease - Abstract
Testosterone administration is beneficial in alleviating myocardial ischaemia in men with significant coronary artery disease (CAD), a condition which is associated with hypotestosteronaemia. Infusion of physiological concentrations of testosterone into coronary arteries at angiography results in rapid vasodilatation in patients with CAD. Whilst the cardiovascular benefits of testosterone have long been documented, the underlying mechanism(s) have not yet been revealed. Here, we have investigated whether testosterone might act like widely prescribed antihypertensive dihydropyridines, as an endogenous Ca2+ channel antagonist. To do this, we used the whole-cell patch-clamp technique to record Ca2+ currents from the A7r5 smooth muscle cell line and HEK 293 cells stably expressing either L- or T-type Ca2+ channels. We demonstrate that testosterone directly inhibited both native and human recombinant vascular L-type Ca2+ channels in a manner that was voltage-independent and, crucially, displayed an IC50 value of 38 nM, a value within the physiological range. At higher (supraphysiological) concentrations both native and human recombinant T-type channels were also inhibited by testosterone. Our data indicate that testosterone acts like widely prescribed antihypertensive dihydropyridines to reduce Ca2+ influx into vascular smooth muscle and so promote vasodilation. This effect is likely to account for its beneficial cardiovascular actions. [Copyright &y& Elsevier]
- Published
- 2004
- Full Text
- View/download PDF
106. Testosterone and mortality.
- Author
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Muraleedharan V and Jones TH
- Subjects
- Cardiovascular Diseases blood, Cardiovascular Diseases drug therapy, Cardiovascular Diseases mortality, Diabetes Mellitus, Type 2 blood, Diabetes Mellitus, Type 2 drug therapy, Diabetes Mellitus, Type 2 mortality, Humans, Hypogonadism blood, Hypogonadism drug therapy, Hypogonadism mortality, Male, Metabolic Syndrome blood, Metabolic Syndrome drug therapy, Metabolic Syndrome mortality, Testosterone therapeutic use, Testosterone blood
- Abstract
Epidemiological studies have found that men with low or low normal endogenous testosterone are at an increased risk of mortality than those with higher levels. Cardiovascular disease accounts for the greater proportion of deaths in those with low testosterone. Cancer and respiratory deaths in some of the studies are also significantly more prevalent. Disease-specific studies have identified that there are higher mortality rates in men with cardiovascular, respiratory and renal diseases, type 2 diabetes and cancer with low testosterone. Obesity, metabolic syndrome, type 2 diabetes, cardiovascular disease and inflammatory disorders are all associated with an increased prevalence of testosterone deficiency. Two major questions that arise from these findings are (1) is testosterone deficiency directly involved in the pathogenesis of these conditions and/or a contributory factor impairing the body's natural defences or is it merely a biomarker of ill health and the severity of underlying disease process? (2) Does testosterone replacement therapy retard disease progression and ultimately enhance the clinical prognosis and survival? This review will discuss the current state of knowledge and discuss whether or not there are any answers to either of these questions. There is convincing evidence that low testosterone is a biomarker for disease severity and mortality. Testosterone deficiency is associated with adverse effects on certain cardiovascular risk factors that when combined could potentially promote atherosclerosis. The issue of whether or not testosterone replacement therapy improves outcomes is controversial. Two retrospective studies in men with diagnosed hypogonadism with or without type 2 diabetes have reported significantly improved survival., (© 2014 John Wiley & Sons Ltd.)
- Published
- 2014
- Full Text
- View/download PDF
107. Testosterone and the metabolic syndrome.
- Author
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Muraleedharan V and Jones TH
- Abstract
Metabolic syndrome and testosterone deficiency in men are closely Linked. Epidemiological studies have shown that Low testosterone Levels are associated with obesity, insulin resistance and an adverse Lipid profile in men. Conversely in men with metabolic syndrome and type 2 diabetes have a high prevalence of hypogonadism. Metabolic syndrome and Low testosterone status are both independently associated with increased all-cause and cardiovascular mortality. Observational and experimental data suggest that physiological replacement of testosterone produces improvement in insulin resistance, obesity, dyslipidae-mia and sexual dysfunction along with improved quality of Life. However, there are no Long-term interventional studies to assess the effect of testosterone replacement on mortality in men with Low testosterone Levels. This article reviews the observational and interventional clinical data in relation to testosterone and metabolic syndrome.
- Published
- 2010
- Full Text
- View/download PDF
108. Testosterone for the aging male; current evidence and recommended practice.
- Author
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Stanworth RD and Jones TH
- Subjects
- Age of Onset, Aged, Aging metabolism, Androgens administration & dosage, Blood Glucose metabolism, Body Composition physiology, Bone Density physiology, Clinical Trials as Topic, Diabetes Mellitus, Type 2 metabolism, Erectile Dysfunction physiopathology, Humans, Hypogonadism diagnosis, Hypogonadism epidemiology, Male, Obesity metabolism, Osteoporosis physiopathology, Prostatic Neoplasms blood, Prostatic Neoplasms epidemiology, Prostatic Neoplasms pathology, Testosterone administration & dosage, Androgens therapeutic use, Testosterone therapeutic use
- Abstract
An international consensus document was recently published and provides guidance on the diagnosis, treatment and monitoring of late-onset hypogonadism (LOH) in men. The diagnosis of LOH requires biochemical and clinical components. Controversy in defining the clinical syndrome continues due to the high prevalence of hypogonadal symptoms in the aging male population and the non-specific nature of these symptoms. Further controversy surrounds setting a lower limit of normal testosterone, the limitations of the commonly available total testosterone result in assessing some patients and the unavailability of reliable measures of bioavailable or free testosterone for general clinical use. As with any clinical intervention testosterone treatment should be judged on a balance of risk versus benefit. The traditional benefits of testosterone on sexual function, mood, strength and quality of life remain the primary goals of treatment but possible beneficial effects on other parameters such as bone density, obesity, insulin resistance and angina are emerging and will be reviewed. Potential concerns regarding the effects of testosterone on prostate disease, aggression and polycythaemia will also be addressed. The options available for treatment have increased in recent years with the availability of a number of testosterone preparations which can reliably produce physiological serum concentrations.
- Published
- 2008
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109. Physiologic testosterone therapy has no effect on serum levels of tumour necrosis factor-alpha in men with chronic heart failure.
- Author
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Pugh PJ, Jones RD, Malkin CJ, Hall J, Nettleship JE, Kerry KE, Jones TH, and Channer KS
- Subjects
- Administration, Oral, Cross-Over Studies, Double-Blind Method, Enzyme-Linked Immunosorbent Assay, Humans, Lipopolysaccharides metabolism, Male, Middle Aged, Testosterone blood, Heart Failure blood, Heart Failure therapy, Hormone Replacement Therapy methods, Testosterone administration & dosage, Tumor Necrosis Factor-alpha metabolism
- Abstract
Physiological testosterone therapy increases exercise capacity and reduces symptom scores in men with chronic heart failure (CHF). Tumour necrosis factor-alpha (TNF-alpha) exerts a significant pathologic activity in CHF, and physiologic testosterone replacement therapy is associated with reduced serum levels of TNF-alpha in hypogonadal men with concomitant coronary artery disease. It is unknown whether testosterone exerts a similar immunomodulatory action in men with CHF. Testosterone therapy administered in three placebo-controlled studies, for either 6 hours (two 30-mg buccal tablets, n=12) or 3 months (fortnightly 100 mg intra muscular injection, n=20; or daily 5 mg transdermally, n=62). The effects of testosterone were also assessed on lipopolysaccharide (LPS)-induced TNF- production in whole blood obtained from 27 men with CHF. Incubation with testosterone (10 nM, 1 M, and 100 M) resulted in a reduction in LPS-induced TNF- production from 12.6 +/- 1.3 to 11.2 +/- 1.1 (P = 0.053), 10.3 +/- 1.1 (P = 0.0046), and 9.2 +/- 1.1 (P = 0.000066) ng/ml, respectively. However in men with CHF, serum levels of TNF- were similar before and after treatment with testosterone or placebo, irrespective of the length of study or route of administration. The clinically beneficial actions of testosterone in men with CHF are unlikely to be mediated by reducing TNF-alpha.
- Published
- 2005
- Full Text
- View/download PDF
110. A mathematical comparison of techniques to predict biologically available testosterone in a cohort of 1072 men.
- Author
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Morris PD, Malkin CJ, Channer KS, and Jones TH
- Subjects
- Biomarkers blood, Cohort Studies, Humans, Male, Predictive Value of Tests, Regression Analysis, Sensitivity and Specificity, Sex Hormone-Binding Globulin metabolism, Hypogonadism blood, Hypogonadism diagnosis, Models, Biological, Testosterone blood
- Abstract
Objective: In the absence of widely available measures of determining free and/or bioavailable testosterone (BioT) physicians may use formulae such as the free androgen index (FAI) to estimate free testosterone. We compared the efficacy of calculated markers of androgen status in predicting serum BioT and hypogonadism., Design: Total testosterone (TT), sex hormone binding globulin (SHBG) and BioT were determined in a large cohort of men. Comparison of calculated androgen levels was performed following endocrine assessment., Methods: TT and SHBG were determined by ELISA, and BioT was determined by ammonium sulphate precipitation. From these data we calculated FAI and free testosterone using two other published formulae - FTnw (free testosterone as calculated by the method of Nanjeee and Wheeler) and FTv (free testosterone as calculated by the method of Vermeulen). A novel formula was derived to calculate BioT from given levels of TT and SHBG (BTcalculated). The ability of the methods (FAI, FTnw, FTv, BTcalc) to predict BioT were compared using regression analysis. The ability of these markers of androgen status to predict biochemical hypogonadism was compared using area under receiver operator curve (auROC)., Results: The equation derived from our data was the best predictor of BioT (R(2)=0.73, P<0.0001) although TT was also a good marker (R(2)=0.68, P=0.0001). In the determination of hypogonadism, of all currently available formulae none were better that the TT (auROC: TT=0.93, FAI=0.72, FTnw=0.91, FTv=0.88) although when TT is borderline (7.5
- Published
- 2004
- Full Text
- View/download PDF
111. Testosterone is a potent inhibitor of L-type Ca(2+) channels.
- Author
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Scragg JL, Jones RD, Channer KS, Jones TH, and Peers C
- Subjects
- Calcium Channels, L-Type genetics, Cell Line, Dose-Response Relationship, Drug, Electrophysiology, Humans, Nifedipine pharmacology, Recombinant Proteins drug effects, Recombinant Proteins genetics, Recombinant Proteins metabolism, Transfection, Calcium Channel Blockers pharmacology, Calcium Channels, L-Type drug effects, Calcium Channels, L-Type metabolism, Testosterone pharmacology
- Abstract
Testosterone administration is beneficial in alleviating myocardial ischaemia in men with significant coronary artery disease (CAD), a condition which is associated with hypotestosteronaemia. Infusion of physiological concentrations of testosterone into coronary arteries at angiography results in rapid vasodilatation in patients with CAD. Whilst the cardiovascular benefits of testosterone have long been documented, the underlying mechanism(s) have not yet been revealed. Here, we have investigated whether testosterone might act like widely prescribed antihypertensive dihydropyridines, as an endogenous Ca(2+) channel antagonist. To do this, we used the whole-cell patch-clamp technique to record Ca(2+) currents from the A7r5 smooth muscle cell line and HEK 293 cells stably expressing either L- or T-type Ca(2+) channels. We demonstrate that testosterone directly inhibited both native and human recombinant vascular L-type Ca(2+) channels in a manner that was voltage-independent and, crucially, displayed an IC(50) value of 38 nM, a value within the physiological range. At higher (supraphysiological) concentrations both native and human recombinant T-type channels were also inhibited by testosterone. Our data indicate that testosterone acts like widely prescribed antihypertensive dihydropyridines to reduce Ca(2+) influx into vascular smooth muscle and so promote vasodilation. This effect is likely to account for its beneficial cardiovascular actions.
- Published
- 2004
- Full Text
- View/download PDF
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