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  • 1
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford : Blackwell Science Ltd
    Anaesthesia 54 (1999), S. 0 
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A postal survey of all 269 acute hospital trusts identified in the United Kingdom was carried out to study the work of Clinical Directors of anaesthesia. Initial responses from 163 Clinical Directors and 129 completed questionnaires were analysed. Four main areas of concern revealed by the survey were contracts and objectives, funding of managerial sessions, access to information and perceived need for support. Most Clinical Directors had no job description and most had no formal written objectives, despite a substantial body of advice that these should be provided. There was generally substantial underfunding of managerial hours compared with those actually worked and approximately 20% of Clinical Directors surveyed had no funding for managerial duties. Clinical Directors' ratings of the information available to assist their decision making were also a cause of concern. Clinical Directors perceived that they need better networking, more training particularly on human resource management and improved management information.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-5233
    Keywords: Diabetes mellitus ; Hypertension ; Urban blacks ; Sub-Saharan Africa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Little is known of the natural history of blood pressure (BP) levels in diabetic patients from sub-Saharan Africa. BP levels were therefore recorded in such patients in Dar es Salaam, Tanzania, over 2, 5, and 7 years. Hypertension was found in 5% of insulin-treated diabetes mellitus (IDDM) and 29.2% of non-insulin-dependent diabetes mellitus (NIDDM) patients at presentation with diabetes. Hypertension developed in a further 2 IDDM (3.7%) and 27 NIDDM (15.6%) patients at 2 years, and in 3 IDDM (13.0%) and 9 NIDDM (9.8%) patients at 5 years. Seven NIDDM (18.4%) patients had developed hypertension by 7 years. In NIDDM patients with normal BP initially, the mean systolic BP rose from 131 to 141 mmHg (P〈0.001) 2 years later (n=146); from 131 to 138 mmHg (P〈0.001) for those followed for 5 years (n=82); and from 131 to 138 mmHg (P〈0.05) for those followed for 7 years (n=31). The mean diastolic BP was 83 mmHg initially and 84 mmHg (NS) for those followed for 2 years (n=146). There was no observed rise in mean diastolic BP at 5 or 7 years of follow-up. In IDDM patients without hypertension, only the systolic BP rose significantly by 5 years, from 124 to 132 mmHg (P〈0.001;n=20). These changes were independent of age, sex, body mass index, and proteinuria. We conclude that: (1) in black Tanzanians, as in other ethnic groups, it is likely that hypertension is significantly associated with diabetes; (2) rates of hypertension and BP levels continue to increase with time, particularly in NIDDM subjects; and (3) BP measurements should be a regular feature of diabetes care in the African diabetic population as in other populations.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-2307
    Keywords: Key words Nitric oxide ; Myocardium ; Hypertension ; Stereology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Structural changes in the myocardium following inhibition of nitric oxide synthesis were studied quantitatively within two different periods. Four groups of 10 rats were studied: control and L-NAME (N G-nitro-methyl-ester-L-arginine) groups for 25 and for 40 days. L-NAME was administered at 50 mg/kg per day in the drinking water. On the 26th and 41st days, the hearts were examined. Volume densities of myocytes (Vv[m]), cardiac interstitium (Vv[int], numerical density of myocytes (Nv[m]) and mean cross-sectional area of the myocytes (A[m]) were determined. Comparing the L-NAME animals with their respective controls showed the arterial pressure (AP) and the heart weight (HW) to be increased in the L-NAME animals. At 25 days, and more obviously at 40 days, the myocytes were hypertrophied with increase of myofibrils (A[m], greater in L-NAME rats). There were some areas with ischaemic lesions, inflammatory infiltrates and perivascular and interstitial fibrosis. The intramyocardial arteries had a thick tunica media and tunica intima. At 25 days the myocardium showed no stereological difference between L-NAME and controls, but by 40 days there was decreased Vv[m] and Nv[m] and increased Vv[int] in the exposed group. Inhibition of NO synthesis provoked a time progressive myocardial change, quantified by stereology.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 38 (1995), S. 35-37 
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Non-esterified fatty acids ; insulin sensitivity ; muscle indirect calorimetry ; non-insulin-dependent diabetes mellitus ; acipimox
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of the study was to evaluate an acute decrease in NEFA levels during an oral glucose tolerance test and its effects on glucose tolerance, muscle glucose uptake and muscle indirect calorimetry in ten lean non-insulin-dependent diabetic subjects. Two 75-g oral glucose tolerance tests were performed in random order. Placebo or 250 mg acipimox (to inhibit lipolysis) were administered orally 2 h before the start of the oral glucose tolerance test. Two hours after acipimox administration (time 0), non-esterified fatty acid, glycerol and 3-hydroxybutyrate levels decreased by 84, 68 and 77% respectively, compared to basal levels. Concomitantly, muscle lipid oxidation and non-oxidative glycolysis also decreased significantly. After placebo administration, non-esterified fatty acids, glycerol and 3-hydroxybutyrate and lipid oxidation increased by 29, 28, 106 and 33%, respectively (NS vs basal levels; p〈0.001 vs acipimox). There was a negative rate of net glucose storage (interpreted as glycogenolysis) during post-absorptive conditions and at time 0 after administration of both drugs. After oral glucose tolerance test, the incremental areas of blood glucose and insulin were significantly decreased by 18 and 19% after acipimox compared to placebo. In addition, the ratio between the incremental area of forearm muscle glucose uptake and the insulin levels was significantly increased by 45% during acipimox compared to placebo administration. Glucose oxidation and non-oxidative glycolysis were significantly higher while lipid oxidation was significantly lower after acipimox than after placebo. In conclusion, our study found that in lean non-insulin-dependent diabetic subjects, an acute decrease in non-esterified fatty acid levels improves glucose tolerance, muscle glucose uptake, glucose oxidation and non-oxidative glycolysis, but is unable to normalize glucose storage.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0428
    Keywords: Hexokinase II ; candidate gene analysis ; insulin resistance ; familial non-insulin-dependent diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hexokinase II (HKII) plays a central role in the intracellular metabolism of glucose in skeletal muscle, catalysing the phosphorylation of glucose to glucose 6-phosphate. It is therefore considered to be a potentially important candidate gene in the development of insulin resistance and non-insulin-dependent diabetes mellitus (NIDDM). The aim of this study was to screen the HKII gene for mutations in NIDDM subjects from insulin-resistant families. Insulin sensitivity was assessed in unaffected first degree relatives from families with two or more living NIDDM subjects, and 15 families were identified as being insulin resistant. In 15 NIDDM subjects (one from each family) and 4 normoglycaemic control subjects, all 18 exons of the HKII gene were amplified by the polymerase chain reaction, and the products screened for mutations using a combination of single-stranded conformational polymorphism analysis and direct sequencing. Six sequence variations were detected in the NIDDM subjects; four silent polymorphisms [GAT vs GAC at codon 251 in exon 7, AAT vs AAC at codon 692 in exon 15, CCG vs CCC at codon 736 in exon 15, and CTG vs CTA at codon 766 in exon 16]; a single base change [T→C], 22 base pairs distal to the exon-intron junction of exon 17 in the 5′-splice donor; and a single amino acid substitution [Gln142→His] in exon 4, which was identified in 6 of the 15 NIDDM subjects. The frequency of the mutated codon 142 allele however, was comparable between NIDDM subjects with familial NIDDM (n=56) and normoglycaemic control subjects (n=48) (18.8% and 14.6% for NIDDM subjects and control subjects respectively; χ2=0.6, p〉0.25). In addition, measures of insulin sensitivity were comparable in normal glucose tolerant subjects with (n=20) and without (n=40) the codon 142 polymorphism. In conclusion: (1) mutations in the coding regions of the HKII gene are unlikely to be major determinants in the development of insulin resistance and familial NIDDM; although (2) the influence of the codon 142 mutation in combination with other abnormalities of the insulin-signalling pathway on insulin action remain to be addressed.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0428
    Keywords: Key words Impaired glucose tolerance ; insulin sensitivity ; hepatic glucose output ; insulin secretion ; labelled infusion technique.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent evidence suggests that the postprandial hyperglycaemia in impaired glucose tolerance is primarily due to impaired suppression of basal hepatic glucose output. This in turn appears to be secondary to decreased first phase insulin secretion, although decreased hepatic insulin sensitivity, which is a feature of non-insulin-dependent diabetes mellitus, might also play a role. Eight mildly overweight subjects with impaired glucose tolerance and eight closely matched control subjects with normal glucose tolerance underwent an intravenous glucose tolerance test to assess first phase insulin secretion. Insulin sensitivity was examined by a 150-min hyperinsulinaemic-euglycaemic clamp. Somatostatin was infused from 150 min to suppress endogenous insulin secretion, and glucagon and insulin were replaced by constant infusion. Glucose with added dideuterated glucose (labelled infusion technique) was infused to maintain euglycaemia. First phase insulin secretion (Δ 0–10 min insulin area 7 Δ 0–10 min glucose area) was significantly decreased in the subjects with impaired glucose tolerance (median [range]: 1.2 [0.2–19.4] vs 9.1 [2.6–14.5] mU · mmol−1; p 〈 0.01). During the clamp, circulating insulin (93 ± 8 [mean ± SEM] and 81 ± 10 mU · l−1) and glucagon (54 ± 4 and 44 ± 6 ng · l−1) levels were comparable. Total glucose disposal was decreased in subjects with impaired glucose tolerance (2.78 ± 0.27 vs 4.47 ± 0.53 mg · kg−1· min−1; p 〈 0.02), and was primarily due to decreased non-oxidative glucose disposal. However, hepatic glucose output rates were comparable during the clamp (0.38 ± 0.10 and 0.30 ± 0.18 mg · kg−1· min−1). Therefore, the main defects in subjects with impaired glucose tolerance are decreased first phase insulin secretion and peripheral non-oxidative glucose disposal, but hepatic glucose output shows normal responsiveness to insulin. [Diabetologia (1995) 38: 699–704]
    Type of Medium: Electronic Resource
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