Search

Your search keyword '"Feher, M.D."' showing total 39 results
Start Over Author "Feher, M.D."
39 results on '"Feher, M.D."'

2. Diabetes: preventing coronary heart disease in a high risk group

Author

Feher, M.D.

Subjects
Diabetics -- Care and treatment, Diabetics -- Diseases, Coronary heart disease -- Risk factors, Coronary heart disease -- Prevention, Coronary heart disease -- Patient outcomes, Comorbidity -- Prevention, Health
Published
2004

11. History of chickenpox and steroid cards: a new warning?

Author

Feher, M.D., Simms, J.P., and Lant, A.F.

Subjects
Identification cards -- Standards -- Health aspects, Chickenpox -- Risk factors, Adrenocortical hormones -- Health aspects, Health, Standards, Risk factors, Health aspects
Abstract

National steroid cards were designed to inform patients treated with corticosteroids of the dose and potential hazards of treatment. Recent reports of severe chickenpox associated with steroid treatment(1)(2) have highlighted [...]

Published
1996

23. Calcium channel blocker induced gum hypertrophy: no class distinction

Author

Samarasinghe, Y.P., Cox, A., and Feher, M.D.

Subjects
Health
Abstract

A 49 year Afro-Caribbean man, with a 10 year history of resistant hypertension, was referred for further management on the following medications: amlodipine 20 mg, atenolol 200 mg, and enalapril [...]

Published
2003

28. Letters.

Author

Al-Mrayat, M., Samarasinghe, Y., Treml, H., Munro, N., Shotliff, K., McIntosh, C., and Feher, M.D.

Subjects
LETTERS to the editor, BRAIN diseases
Abstract

Presents a letter to the editor about a new cause of neuroglycopenia.

Published
2004
Full Text
View/download PDF

29. Refsum's disease: a peroxisomal disorder affecting phytanic acid α-oxidation.

Author

Wierzbicki, A.S., Lloyd, M.D., Schofield, C.J., Feher, M.D., and Gibberd, F.B.

Subjects
REFSUM disease, PEROXISOMAL disorders, METABOLISM, CLONING, ENZYMES, PEROXISOMES
Abstract

Refsum's disease (hereditary motor sensory neuropathy type IV, heredopathia atactica polyneuritiformis) is an autosomal recessive disorder the clinical features of which include retinitis pigmentosa, blindness, anosmia, deafness, sensory neuropathy, ataxia and accumulation of phytanic acid in plasma- and lipid-containing tissues. The transport and biochemical pathways of phytanic acid metabolism have recently been defined with the cloning of two key enzymes, phytanoyl-CoA 2-hydroxylase (PAHX) and 2-hydroxyphytanoyl-CoA lyase, together with the confirmation of their localization in peroxisomes. PAHX, an iron(II) and 2-oxoglutarate-dependent oxygenase is located on chromosome 10p13. Mutant forms of PAHX have been shown to be responsible for some, but not all, cases of Refsum's disease. Certain cases have been shown to be atypical mild variants of rhizomelic chondrodysplasia punctata type 1a. Other atypical cases with low-plasma phytanic acid may be caused by α-methylacyl-CoA racemase deficiency. A sterol-carrier protein-2 (SCP-2) knockout mouse model shares a similar clinical phenotype to Refsum's disease, but no mutations in SCP-2 have been described to-date in man. This review describes the clinical, biochemical and metabolic features of Refsum's disease and shows how the biochemistry of the α-oxidation pathway may be linked to the regulation of metabolic pathways controlled by isoprenoid lipids, involving calcineurin or the peroxisomal proliferator activating α-receptor. [ABSTRACT FROM AUTHOR]

Published
2002
Full Text
View/download PDF

31. Low‐density lipoproteins increase intracellular calcium in aequorin‐loaded platelets

Author

Dunn, R.C., Schachter, M., Miles, C.M.M., Feher, M.D., Tranter, P.R., Bruckdorfer, K.R., and Sever, P.S.

Abstract

Low‐density lipoproteins activate isolated human platelets. The mechanism of this activation is unknown, but may involve increased phosphoinositide turnover. We have examined the effect of low‐density lipoproteins on intracellular calcium concentrations in platelets loaded with the photoprotein aequorin. The lipoproteins induced concentration‐dependent increases in intracellular calcium, associated with shape change and aggregation. These responses could be partially inhibited by the removal of extracellular calcium and by pre‐incubation with acetylsalicylic acid. They were also antagonised by agents which increase cellular concentrations of cyclic adenosine and guanosine monophosphates. It is not clear whether the platelet‐lipoprotein interaction involves a ‘classical’ lipoprotein receptor.

Published
1988
Full Text
View/download PDF

33. Diabetes and Hypertension

Author

Feher, M.D.

Abstract

Hypertension occurs more often in patients with diabetes than in individuals without diabetes. This 1.5-2-fold excess of hypertension can be accounted for by several clinical and pathophysiological factors including diabetic nephropathy, altered neuroendocrine and sodium-volume determinants of blood pressure, disturbed vascular tone and altered blood pressure regulation (Figure 1). Hypertension is also a major cause of diabetic nephropathy. The prevalence of hypertension in type 2 diabetes has been reported to be 30-80%. In type 1 diabetes, the prevalence is up to 25%, and hypertension is usually seen in association with nephropathy.

Published
2002
Full Text
View/download PDF

37. DRUG POINTS.

Author

Rademaker, J., Severs, M., Bewley, A.P., Feher, M.D., Staughton, R.C.D., Woolfrey, S., Gammack, N.S., Dewar, M.S., Brown, P.J.E., Tidswell, P., and d'Assis-Fonseca, A.

Subjects
DRUG side effects, OPIUM, LUNG diseases, WARFARIN
Abstract

Examines the side effects of several drugs in Great Britain. Incidence of opiate toxicity among elderly patients with chronic lung disease; Effects of fluoxetine and warfarin interaction; Contribution of terfenadine in the existence of generalized seizure.

Published
1993

38. Non-steroidal anti-inflammatory drugs and metformin: a cause for concern?

Author

Chan, N.N., Fauvel, N.J., and Feher, M.D.

Subjects
*TREATMENT of diabetes, *ACUTE kidney failure, *BACKACHE, *HYPOGLYCEMIC agents, *INDOMETHACIN, *TYPE 2 diabetes, *NONSTEROIDAL anti-inflammatory agents, *LACTIC acidosis, *METFORMIN, *THERAPEUTICS
Abstract

States that patients with type 2 diabetes who are treated with metformin are at risk of metformin-associated lactic acidosis. Possible consequence of impaired renal function; The case of a 57-year-old Asian woman with type 2 diabetes; What the absence of diabetic retinopathy and proteinuria would suggest; The large number of patients with diabetes who have likely received this drug.

Published
1998
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results