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Biomedical subjects

P Manhem

Publications and source records attributed to P Manhem.

At least 19 recordsLinked to original sources

Upgrading and expansion of the Käppala wastewater treatment plant. Operational experiences and results.

Käppala Association has the responsibility to receive and treat wastewater from 11 municipalities situated just north of Stockholm in Sweden. Running a tunnel system, 60 km long, and a treatment plant meets this responsibility. The plant is situated in Lidingö, northeast of Stockholm. The load 2002 corresponds to about 520,000 p.e. During the 1990s the plant was upgraded and expanded to meet an increasing population and more stringent discharge limits. Nitrogen removal was introduced. The expansion was done in two steps; the first step comprised a new plant beside the old one both situated in rock. This part, which included the filtration step, was taken into operation in 1998. Then the old plant was upgraded to the same technical standard as the new part. His Majesty the King of Sweden inaugurated the whole new and upgraded plant in April 2000. A total of 1.3 billion Swedish crowns were invested corresponding to about 140 million euro. The plant's performance is good. There is no trouble keeping the discharge limits, 10 mg/l for BOD7 and total nitrogen and 0.3 mg/l for phosphorus. However the bio-P process has not been altogether successful. We haven't been able to fulfill our goal to reduce the use of iron sulphate. We will during 2003 go on in our investigations concerning running the plant with a combination of bio-P and chemical precipitation.

Bioreactors↗

Metaiodobenzylguanidine (MIBG) scintigraphy and computed tomography (CT) in clinical practice. Primary and secondary evaluation for localization of phaeochromocytomas.

OBJECTIVE: To determine the diagnostic value of metaiodobenzylguanidine (MIBG) scintigraphy compared with computed tomography (CT) for the localization of phaeochromocytomas in clinical practice. DESIGN: Retrospective comparison between MIBG scintigrams and CT for localization of phaeochromocytomas in all patients successively examined with MIBG scintigraphy in Malmö from 1984 until January 1997. SETTING: Malmö University Hospital, Sweden. SUBJECTS: Sixty-four patients with clinically suspected phaeochromocytomas. MAIN OUTCOME MEASURES: MIBG scintigrams and CTs classified as positive or negative based on original interpretations (primary evaluation) and in a secondary evaluation by one blinded examiner are assessed through histological confirmation or clinical rule out of phaeochromocytomas. RESULTS: Twenty-five patients had surgically removed phaeochromocytomas. The remaining 39 patients had no proof of phaeochromocytomas. In the secondary evaluation, sensitivity for MIBG scintigraphy was 88% (22/25) and for CT was 100% (25/25). The specificity for MIBG scintigraphy was 89% (35/39) but only 50% for CT (18/36). Two out of a total of six extra-adrenal tumours were amongst the false-negative MIBG scintigrams. CONCLUSIONS: MIBG scintigraphy for the localization of phaeochromocytomas is superior to CT as far as specificity, whereas CT has a higher sensitivity. After biochemical diagnosis, CT will detect most phaeochromocytomas. MIBG scintigraphy can be of value in patients who show inconclusive results with biochemical testing and CT.

3-Iodobenzylguanidine↗

Inhibition of the rise in FFA by Acipimox partially prevents GH-induced insulin resistance in GH-deficient adults.

To test the hypothesis that GH-induced insulin resistance is mediated by an increase in FFA levels we assessed insulin sensitivity after inhibiting the increase in FFA by a nicotine acid derivative, Acipimox, in nine GH-deficient adults receiving GH replacement therapy. The patients received in a double blind fashion either Acipimox (500 mg) or placebo before a 2-h euglycemic (plasma glucose, 5.5 +/- 0.2 mmol/liter) hyperinsulinemic (serum insulin, 28.7 +/- 6.3 mU/liter) clamp in combination with indirect calorimetry and infusion of [3-(3)H]glucose. Acipimox decreased fasting FFA by 88% (P = 0.012) and basal lipid oxidation by 39% (P = 0.015) compared with placebo. In addition, the insulin-stimulated lipid oxidation was 31% (P = 0.0077) lower during Acipimox than during placebo. Acipimox increased insulin-stimulated total glucose uptake by 36% (P = 0.021) compared with placebo, which mainly was due to a 47% (P = 0.015) increase in glucose oxidation. GH induced insulin resistance is partially prevented by inhibition of lipolysis by Acipimox.

Adult↗

Effect of 6 months of GH treatment on myosin heavy chain composition in GH-deficient patients.

OBJECTIVE: To investigate the effect of GH on myosin heavy chain (MHC) isoform composition, physical fitness and body composition in GH-deficient (GHD) patients. DESIGN: Twenty-two GHD patients were randomized in a double blind manner and half were treated with recombinant human GH (rhGH) and half were treated with placebo for 6 months. Twelve age-matched controls were also included in the study. METHODS: MHC isoform composition in biopsies obtained from the vastus lateralis muscle was determined using SDS-PAGE. Physical fitness was determined on a bicycle ergometer and body composition was determined using bioelectrical impedance analysis. RESULTS: More MHC IIX (28.9 +/- 4.1% and 10.0 +/- 3.1% in GHD and controls respectively (means +/- S.E.M.)) and less MHC I (36.2 +/- 2.4% and 51.7 +/- 3.9% in GHD and controls respectively (means +/- S.E.M.)) were present in the GHD patients compared with the controls. No significant difference in the amount of MHC IIA was detected. Linear regression was used to determine the relationship between variables. There were no significant relationships between the concentration of insulin-like growth factor-I (IGF-I) or the body composition and the MHC composition. Maximal oxygen uptake (VO(2)max) per kg body weight (BW) (litres/min per kg) correlated significantly with the amount of MHC I (r=0.60) and MHC IIX (r=-0.72) but not with the amount of MHC IIA (r=0.35). Treatment of GHD patients with rhGH for 6 months increased the concentration of IGF-I, lean body mass and decreased fat mass but had no effect on MHC composition and physical fitness. CONCLUSIONS: We conclude that a major part of the differences in MHC composition between GHD patients and age-matched controls can be explained by variation in physical fitness. The severity of the GHD and the body composition does not seem to be important for the MHC composition. Furthermore, treatment with GH for 6 months does not affect MHC composition in GHD patients.

Adult↗

The individual responsiveness to growth hormone (GH) treatment in GH-deficient adults is dependent on the level of GH-binding protein, body mass index, age, and gender.

The aim of the present trial was to study the individual responsiveness to GH treatment in terms of body composition and to search for possible predictors of the response in GH-deficient adults. Sixty-eight patients (44 men and 24 women) with a mean age of 44.3 (1.2) yr and verified GH deficiency participated in a 2-phase treatment trial with an initial randomized, double blind, placebo-controlled, 6-month period, followed by an open treatment period, thereby ensuring all patients 12 months of GH treatment. Recombinant human GH was administered sc daily at bedtime, with a target dose of 12 micrograms/kg x day. GHBP was measured by ligand-mediated immunofunctional assay, and serum insulin-like growth factor I (IGF-I) was determined by RIA after acid-ethanol extraction, using a truncated IGF-I analog as the radioligand. Lean body mass (LBM) and body fat (BF) were determined by dual energy x-ray absorptiometry, and total body water (TBW) was determined by bioelectrical impedance. During the placebo control period, serum IGF-I,LBM, and TBW increased (P < 0.001), whereas BF decreased (P < 0.001) and serum GHBP was unchanged in the group treated with GH compared with the patients treated with placebo. After 12 months of GH treatment, the individual changes in BF ranged from -12.5 to 4.3 kg and from -4.5 to 10.1 kg in LBM. Age (P < 0.05) and baseline GHBP level (P < 0.01) were inversely correlated with the increase in LBM. The GH-induced increment in IGF-I and TBW was greater in men than in women (P < 0.01), whereas the decreases in BF were similar in men and women. This trial demonstrates the variability in responsiveness to GH administration in GH-deficient adults. The best response to GH was obtained in younger patients with low GHBP levels. Furthermore, men responded better than women.

Absorptiometry, Photon↗

Reduced bone mineral density in adults with growth hormone (GH) deficiency: increased bone turnover during 12 months of GH substitution therapy.

To evaluate the consequences of growth hormone (GH) deficiency on bone mineral density and to evaluate the effects of GH substitution therapy, 68 adults (25 females and 43 males) aged 22-61 (mean 44.2 +/- 1.2) years with GH deficiency (GHD) were studied. Fifty-eight patients had panhypopituitarism, three had isolated GHD and in seven patients at least one additional pituitary function was affected. Twenty-one patients had childhood onset GHD. The patients were randomized to receive either GH in daily injections (0.125 IU.kg-1. week-1 for the first 4 weeks and subsequently 0.25 IU.kg-1. week-1) or placebo for 6 months. The trial continued as an open study with GH treatment for 6 to 12 months, with data presented as compiled data of 12 months of GH treatment in 64 patients. Bone mineral density (BMD) was measured by dual energy x-ray absorptiometry and bone turnover was assessed by serum markers of bone metabolism (osteocalcin, procollagen I peptide, cross-linked telopeptide of type I collagen and alkaline phosphatase activity), In women with adult onset GHD (N = 19) and in men with childhood onset GHD (N = 15), total body, spine and hip BMD was significantly reduced at baseline compared to Swedish age- and sex-matched control material. In men with adult onset of GHD (N = 28), BMD did not differ from male controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Decreased blood pressure response to infused noradrenaline in normotensive as compared to hypertensive patients with primary hypothyroidism.

OBJECTIVE AND PATIENTS: To further explore the difference in plasma noradrenaline in normotensive and hypertensive hypothyroid patients we have investigated the pressor response to exogenous noradrenaline in 11 normotensive and five hypertensive patients with primary hypothyroidism before and after thyroxine replacement. Seven healthy subjects served as controls. DESIGN: The patients were studied under metabolic ward conditions and received a Na+ and K+ defined diet for 4 days. The controls received the same diet on an ambulatory basis for 3 days and were admitted to the ward in the evening on the third day. In the morning of day 4 a graded noradrenaline infusion was given. When the increase in systolic blood pressure in two consecutive registrations was at least 20 mmHg as compared to basal values the noradrenaline infusion was stopped. The dose required to increase systolic blood pressure by 20 mmHg (I20) was determined. RESULTS: During hypothyroidism the I20 was 120 ng/kg BW/min in normotensive patients and 39 in hypertensive patients as compared to 62 in controls. The I20 was higher in normotensives as compared to hypertensives (P = 0.041). The I20 was not different in hypertensives as compared to controls. When the patients had become euthyroid I20 decreased to 51 ng/kg BW/min (P = 0.04) in the normotensives, but remained unchanged in the hypertensives. There was no difference in I20 between normotensive and hypertensive patients in the euthyroid state, or when compared to controls. CONCLUSION: The pressor response to noradrenaline was decreased in normotensive hypothyroid as compared to hypertensive hypothyroid patients, indicating a decreased peripheral sensitivity to noradrenaline in normotensive hypothyroid patients. Following thyroxine replacement the decreased response became normal.

Adult↗

Cardiac pheochromocytoma.

Cardiac pheochromocytoma is a rare tumour and may be difficult to localize. We present a 32-year-old male with a cardiac pheochromocytoma that was successfully resected. An initial unenhanced CT did not reveal the tumour. MIBG-scintigraphy indicated the location, but to get full information, a dynamic contrast-enhanced CT of the chest during adequate alpha and beta blockade was essential. ECG-gated MRI gave further information about the anatomical details.

Adult↗

Percutaneous transluminal renal angioplasty versus surgical reconstruction of atherosclerotic renal artery stenosis: a prospective randomized study.

PURPOSE: The purpose of this prospective randomized study was to compare percutaneous transluminal renal angioplasty (PTRA) and operation as initial therapy with regard to technical results, primary and secondary patency, and effects on blood pressure and renal function in patients with atherosclerotic unilateral renal artery stenosis. METHODS: Fifty-eight patients who did not have diabetes, who were less than 70 years of age, and who had severe hypertension and significant stenosis were randomized to receive PTRA or operation. Angiography was performed 10 days, 1 year, and 2 years after treatment to verify patency, and blood pressure and renal function were simultaneously evaluated. RESULTS: Technically, PTRA was successful in 83% and operation in 97% of patients. The primary patency rate after 24 months was 75% in the PTRA group and 96% in the operative group in technically successful cases. The secondary patency rate in the PTRA group was 90% and in the surgical group 97%. To achieve these results four patients in the PTRA group required operation, and one patient in the surgical group required PTRA. Hypertension was cured or improved after additional treatment in 90% of the patients after PTRA and 86% after operation. The corresponding figures for improved or unchanged renal function were 83% and 72%, respectively. After additional treatment, effects on blood pressure and renal function did not differ. Seventeen percent of the patients treated with PTRA required surgical intervention. CONCLUSIONS: PTRA is recommended as first choice of therapy for atherosclerotic renal artery stenosis causing renovascular hypertension if combined with intensive follow-up and aggressive reintervention.

Adult↗

Determination of urinary N-acetyl-beta-glucosaminidase in patients with hypertension and renal artery stenosis.

The purpose of the study was to measure the urinary excretion of N-acetyl-beta-glucosaminidase (U-NAG) in patients suspected of having renovascular hypertension and to compare the enzyme excretion before and after active intervention with operation or percutaneous transluminal renal angioplasty (PTRA). Eighty-one patients with severe, therapy-resistant hypertension were examined with regard to renal artery stenosis (RAS). At least one significant renal artery stenosis was found in 61 patients, whilst the remaining 20 patients were classified as having essential hypertension. Enzyme levels were found to be significantly higher in RAS patients as compared with patients with severe hypertension lacking significant renal artery stenosis, 0.66 (0.41-0.91, median value, 1st and 3rd quartiles) versus 0.35 (0.27-0.54); P < 0.01. Both groups of patients had significantly higher U-NAG values than a healthy reference population (0.2, 0.13-0.27; P < 0.01). Forty of the RAS patients were randomized to surgery or PTRA and followed prospectively for 2 years. After either renal vascular surgery or PTRA a significant rise in U-NAG excretion was observed 7-10 days after treatment. Urinary NAG excretion remained elevated during long-term follow-up. It is suggested that U-NAG should be determined in patients with therapy-resistant hypertension with suspicion of renal artery stenosis.

Acetylglucosaminidase↗

80-year-old men have elevated plasma concentrations of catecholamines but decreased plasma renin activity and aldosterone as compared to young men.

Plasma concentrations of adrenaline, noradrenaline, aldosterone and plasma renin activity were determined in a selected group of 80-year-old men (N = 41) in good health without clinical signs of cardiovascular disease, and were compared to levels in young healthy males (N = 20, 24-28 years). Plasma adrenaline and noradrenaline concentrations were higher (0.24 median; 25th-75th percentiles 0.16-0.34 nmol/L vs 0.15; 0.11-0.18 nmol/L, p < 0.01 and 2.22; 1.58-3.27 nmol/L vs 1.15; 1.00-1.74 nmol/L, p < 0.001), and plasma renin activity and plasma aldosterone concentration were lower in the old than in the young men (0.65; 0.35-1.04 micrograms/L/1h vs 2.09; 1.23-2.41 micrograms/L/1h, p < 0.001 and 0.12; 0.09-0.19 nmol/L vs 0.38; 0.28-0.54 nmol/L, p < 0.001). In conclusion, increased plasma concentrations of catecholamines and decreased plasma concentration of aldosterone and plasma renin activity in old men, as compared to young men, must be considered when interpreting data of these hormones in elderly men.

Adult↗

Increased arterial and venous plasma noradrenaline levels in patients with primary hypothyroidism during hypothyroid as compared to euthyroid state.

The use of venous plasma noradrenaline levels as a marker of general sympathetic tone has been questioned as changes in local sympathetic activity may influence the venous levels. To compare arterial and venous plasma noradrenaline levels in patients with primary hypothyroidism, arterial and venous blood were sampled during strictly standardized conditions during hypothyroid and euthyroid states. The patients were hospitalized for 5 days at a metabolic ward on a standardized sodium and potassium intake. On the fourth day catheters were positioned in the axillary artery and vein. Blood samples were drawn simultaneously for noradrenaline and adrenaline determinations during resting conditions. The arterial and venous plasma noradrenaline levels did not differ significantly, neither during hypothyroidism nor during euthyroidism. The arteriovenous difference in plasma adrenaline was similar during hypothyroidism compared to euthyroidism, indicating similar peripheral extraction rate of catecholamines during hypothyroidism as compared to euthyroidism. During hypothyroidism venous and arterial noradrenaline were significantly higher as compared to euthyroidism. In conclusion, there is no difference between arterial and venous noradrenaline levels either in the hypothyroid or the euthyroid state, and the peripheral extraction rate of plasma noradrenaline seems to be similar in hypothyroidism and euthyroidism. The local contribution of noradrenaline from the arm, reflecting local sympathetic nervous activity, is limited during resting conditions. In hypothyroid patients plasma noradrenaline levels are increased as compared to the euthyroid state, indicating increased general sympathetic activity in hypothyroidism.

Adult↗

Plasma neuropeptide Y (NPY) and galanin before and during exercise in type 1 diabetic patients with autonomic dysfunction.

Plasma neuropeptide Y (NPY), plasma galanin and plasma catecholamines were determined before and during an ergometer exercise test in 11 type 1 diabetic patients (age 19-36 years, mean 30; duration of diabetes 2-18 years, mean 9) with autonomic dysfunction and in 13 age-matched healthy controls (age 24-36 years, mean 29). Before exercise, plasma NPY (100 +/- 6 pmol/l vs 144 +/- 7 pmol/l; P less than 0.001) and plasma galanin (54 +/- 3 pmol/l vs 77 +/- 5 pmol/l; P less than 0.005) were significantly lower in patients than in controls. During exercise, plasma NPY, plasma adrenaline, and plasma noradrenaline increased in patients and controls while galanin only increased in patients. Since there was a direct correlation between plasma NPY before exercise and the increment (delta 80%) in noradrenaline during exercise (r = 0.54; P less than 0.01), it is suggested that plasma NPY determined in the basal situation may be a useful marker of sympathetic nerve failure in diabetic patients.

Adult↗

The activity of the renin-angiotensin-aldosterone system before and during submaximal bicycle exercise in relation to circulatory catecholamines in patients with type 1 (insulin-dependent) diabetes mellitus.

To evaluate the renin-angiotensin-aldosterone system in relation to circulatory catecholamines, we determined renin activity, angiotensin II, aldosterone, adrenaline, and noradrenaline in plasma before and during a submaximal bicycle exercise test in 23 Type 1 (insulin-dependent) diabetic patients (aged 19-57 years, mean 37; duration of diabetes 2-32 years, mean 16), 17 with signs of cardiac autonomic neuropathy, and in 18 healthy non-diabetic subjects (aged 24-41 years, mean 29). At rest, Type 1 diabetic patients showed significantly lower aldosterone values than control subjects (0.14 +/- 0.02 nmol/l and 0.22 +/- 0.02 nmol/l; p less than 0.01) while renin activity (1.0 +/- 0.1 nmol.l-1.h-1 and 0.9 +/- 0.1 nmol.l-1.h-1) and angiotensin II (14 +/- 1 nmol/l and 18 +/- 2 nmol/l) did not differ significantly between patients and control subjects. During exercise, increments (increase from the resting value to the value at 80% of maximal working capacity) in renin (1.5 +/- 0.4 nmol.l-1.h-1 and 3.7 +/- 0.5 nmol.l-1.h-1; p less than 0.001), angiotensin II (28 +/- 8 nmol/l and 60 +/- 8 nmol/l; p less than 0.001), aldosterone (0.16 +/- 0.04 nmol/l and 0.25 +/- 0.05 nmol/l; p less than 0.05), adrenaline (1.96 +/- 0.49 nmol/l and 2.92 +/- 0.51 nmol/l; p less than 0.05), and noradrenaline (12.01 +/- 1.25 nmol/l and 18.74 +/- 1.45 nmol/l; p less than 0.01) were significantly lower in the patients than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Impaired responses of plasma catecholamines to exercise in diabetic patients with abnormal heart rate reactions to tilt.

The plasma catecholamine response to a standardized bicycle exercise test was evaluated in 24 insulin-dependent diabetic (IDDM) patients in whom the heart rate reactions to deep breathing (E/I ratio) and to tilt, the immediate acceleration and the transient deceleration (acceleration and brake indices), had been assessed as tests of autonomic neuropathy. Patients with an abnormal acceleration index (n = 8) showed, compared with non-diabetic (n = 18) controls who had participated in previous studies, an impaired increment in noradrenaline during exercise (80% of maximal working capacity) (MWC) (12.38 +/- 1.46 nmol l-1 vs. 18.74 +/- 1.45 nmol l-1; P less than 0.01) and adrenaline (50% of MWC: 0.25 +/- 0.04 nmol l-1 vs. 0.54 +/- 0.08 nmol l-1; P less than 0.05). Similarly, patients with an isolated abnormal brake index (n = 6), i.e. with a normal acceleration index and a normal E/I ratio, showed compared with controls an impaired increment in noradrenaline (9.53 +/- 1.66 nmol l-1 vs. 18.74 +/- 1.45 nmol l-1; P less than 0.01) and adrenaline (1.41 +/- 0.22 nmol l-1 vs. 2.92 +/- 0.51 nmol l-1; P less than 0.05) during 80% of MWC. IDDM patients with abnormal heart rate reactions to tilt, an abnormal acceleration index or an abnormal brake index show impaired catecholamine responses to exercise, which can be demonstrated also in patients without signs of parasympathetic neuropathy.

Acceleration↗