bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accelerated cholesteryl ester transfer in patients with insulin‐dependent diabetes mellitus
Authors: BAGDADE J. D. , RITTER M. C. , SUBBAIAH P. V. 
Published: March 2008

Abstract. Abnormalities in cholesteryl ester transfer (CET) may play a role in the development of diabetic arterial vascular complications. To assess this important step systematically in reverse cholesterol transport, we have studied 20 treated, clinically stable, normolipidaemic patients. Contrary to the impairment in CET described previously in NIDDM, the mass of CE transferred from HDL to VLDL+LDL was significantly greater in IDDM patients than in controls at 1,2, and 4 h (P<0.001). When the d<1.063 plasma fractions from IDDM subjects were combined with controls d<1.063 fractions, an accelerated CET response was observed which was identical to that found in intact IDDM plasma. This finding, which indicates that this disturbance in CET was associated with the acceptor lipoproteins, was confirmed when we found that it was reproduced by the addition of IDDM VLDL and not LDL to control d>1.063 fractions.Changes observed in lipoprotein core lipid composition were consistent with accelerated CET occurring in IDDM in vivo: the TG/CE core lipid ratio was decreased in VLDL from six subjects (diabetic 9.5±0.8 vs control 12.9±3.4; P<0.1) and increased in their HDL (diabetic 0.55±0.11 vs control 0.42±0.04; P<0.025). No correlation was demonstrable between estimates of diabetic control (glycoalbumin, fasting glucose) and CET. These data indicate that CET may be abnormally increased in normolipidaemic IDDM patients. A defect of this type may be atherogenic because it increases the number of lipoprotein particles in plasma which resemble cholesteryl ester‐enriched chylomicron and VLDL remnants but whose normal receptor‐mediated catabolism may be altered.
Haemodynamic and renal effects of urodilatin bolus injections in patients with congestive heart failure
Authors: KENTSCH M. , LUDWIG D. , DRUMMER C. , GERZER R. , MÜLLER‐ESCH G. 
Published: March 2008

Abstract. Urodilatin (ANF(95–126)) is an analogue of the atrial natriuretic factor (ANF(99–126)), which has been isolated from human urine. Recently we have shown in healthy volunteers, that intravenous bolus injections of synthetic urodilatin produce more pronounced reductions of pulmonary arterial pressure than ANF(99–126). To compare haemodynamic and renal effects of synthetic urodilatin with those of ANF(99–126) in congestive heart failure (CHF), 12 patients (66.3 ± 1.4 years) received either two high dose intravenous bolus injections of 4 μg kg‐1 bw Urodilatin (URO) at a 30 min interval (n= 6) or the same doses of ANF(99–126)(n = 6).Prior to i.v. URO, no URO immunoreactivity was found in human plasma (specific RIA, no crossreactivity to ANF). Similar to ANF, the increase in diuresis (1.4 ± 0.7 to 3.7+1.6 ml min‐1) and natriuresis (169 ±114 to 430 ± 197 μmol min‐1) was moderate after URO in CHF. During the 90 min study period, mean plasma cyclic GMP levels increased much more after URO (by 53.4 ±15.1 nM) than after ANF (by 13.1 ± 30 nM; P= 0.04). In contrast to ANF, i.v. bolus injections of URO produced sustained haemodynamic effects in CHF lasting up to 90 min: The average (0–90 min) reduction of systemic vascular resistance was more pronounced after URO (‐ 578 ± 148) than after ANF (‐ 204 ± 65 dyn*s*cm‐5, P= 0.04). Average increase of stroke volume index (URO: 9.5 ±1.9; ANF: 2.8 ±1.4 ml min‐1 m‐2; P= 0.02) and reduction of pulmonary capillary wedge pressure (URO: — 10.8 ± 2.1; ANF: ‐ 3.9 ± 1.6 mmHg; P= 0.03)were more prominent after URO.These data indicate that urodilatin bolus injections produce sustained beneficial haemodynamic effects in patients with congestive heart failure, which are prolonged and more pronounced than after ANF. The larger increase in plasma cyclic GMP levels in CHF suggests that in the cardiovascular system of heart failure patients, URO may induce a more potent stimulation of guanylate cyclase coupled ANF receptors than ANF(99–126).
Erythrocyte Li+/Na+ and Na+/H+ exchange, cardiac anatomy and function in insulin‐dependent diabetics
Authors: SEMPLICINI A. , LUSIANI L. , MARZOLA M. , CEOLOTTO G. , MOZZATO M. G. , ZANETTE G. , DONADON V. , STEFANINI M. G. , ZANUTTINI D. , PESSINA A. C. 
Published: March 2008

Abstract. It has been proposed that an increased activity of cell membrane Na+/H+ exchange, mirrored by increased erythrocyte Li +/Na+ exchange, may facilitate cell hypertrophy and hyperplasia.Patients with insulin‐dependent diabetes mellitus may develop a specific cardiomyopathy with systolic and diastolic abnormalities and increased thickness of the left ventricle.Therefore, we have investigated the relationships between erythrocyte Li+/Na+ and Na+/H+ exchange and echocardiographic parameters in 31 male insulin‐dependent diabetics (aged 17–68), in good metabolic control. Three had untreated mild hypertension. In all patients the urinary albumin excretion rate was less than 200 μg min‐1.Ten patients had a Li+/Na+ countertransport higher than 0.37 mmol 1‐1 cell h‐1 the upper normal limit for our laboratory (0.49 ± 0.10, mean ± SD). In comparison with the patients with normal counter‐transport, they had increased interventricular septum thickness and relative wall thickness (h/r). End diastolic volume and cardiac index were reduced while blood pressure and urinary albumin excretion rate were similar.In the whole study group, interventricular septum thickness was significantly correlated to Li+/Na+ exchange (r= 0.61, P< 0.001) and Na +/H+ exchange (r= 0.35, P<0.05), independently of the effect of age and blood pressure.Posterior wall thickness was correlated to Li+/Na+ exchange (r= 0.38, P<0.05) and h/r to Li+/Na + exchange (r= 0.41, P < 0.05) and to Na +/H + exchange (r= 0.44, P<0.05). Li +/Na+ exchange was negatively correlated to cardiac index (r=—0.37, P<0.05). Urinary albumin excretion rate was negatively correlated to posterior wall thickness (r=— 0.40, P < 0.05) and h/ r (r=—0.44,P<0.05), and positively to cardiac index (r= 0.40, P<0.05) and it did not influence the correlations between erythrocyte Na+ transport and echocardiographic parameters.An increased activity of the erythrocyte Li+/Na+ and Na+/H+ exchange may, therefore, indicate high risk of developing cardiac hypertrophy in male insulindependent diabetics. A widespread abnormality of cell Na+/H+ exchange is likely to contribute to the development of cardiac hypertrophy and diabetic cardiomyopathy in these patients.
Central obesity and hyperinsulinaemia in women are associated with polymorphism in the 5‘ flanking region of the human insulin gene
Authors: WEAVER J. U. , KOPELMAN P. G. , HITMAN G. A. 
Published: March 2008

Abstract. presented to the European Association for the Study of Diabetes, September 1990 and the 6th International Congress on Obesity, October 1990Abstract. Obesity is a multifactorial disease with a marked genetic component. The situation is further complicated by the heterogeneity of obesity demonstrated by the topographical distribution of body fat, e.g. upper body (central) and lower body (gluteal) obesity. Furthermore, the distribution of fat shows a stronger heritable tendency compared with total body fat. Central obesity is characterized by hyperinsulinaemia and insulin resistance, a feature in common with non‐insulin dependent diabetes mellitus, hypertension and atherosclerosis. In order to study the molecular genetics of central obesity we have examined 56 severely obese (mean body mass index 40), unrelated British Caucasoid young non‐diabetic women for associations of restriction fragment length polymorphism of candidate genes with anthropometric measurements and indices of insulin secretion and resistance. The candidate genes examined were insulin receptor, insulin sensitive glucose transporter and insulin.An association of the class 3 allele of the hypervari‐able region in the 5′ flanking region of the insulin gene was found with upper segment obesity (P=0.005). Furthermore, the class 3 allele was also associated with fasting hyperinsulinaemia (P=0.01), stimulated insulin secretion (P= 0.01) and insulin resistance as calculated from the homeostatic model of assessment (HOMA; P= 0.008). No such associations were found with the other candidate genes studied.This data suggests that polymorphisms in the 5′ flanking region of the insulin gene may affect expression of the gene and thereby modulate insulin production in severely obese female subjects.
Regional effects and clearance of endothelin‐1 across pulmonary and splanchnic circulation
Authors: WAGNER O. F. , VIERHAPPER H. , GASIC S. , NOWOTNY P. , WALDHÄUSL W. 
Published: March 2008

Abstract. To determine the impact of i.v. endothelin‐1 on systemic, pulmonary and splanchnic circulation, as well as the peptide's regional clearance, hepatic venous and right heart catheterization was performed in healthy volunteers. During the peptide's continuous i.v. administration (0.4 pmol x kg‐1 x min‐1, 60 min) its plasma concentration rose from 21±0.5 to 9.5 ± 5.3 pmol/1 (pulmonary artery), from 2.1±0.9 to 5.0±1.6 pmol/1 (femoral artery), and from 1.5 ± 0.6 to 2.9±1.2 pmol/1 (hepatic vein). This was accompanied by an increase in mean systolic arterial pressure from 127±14 to 131 ± 12mmHg(P<0.05). Concomitantly, cardiac output and heart rate decreased from 7.0 ±1.1 to 5.8 ±1.01/min and from 63 ± 6 to 56 ± 5 beats/min, respectively, while total vascular resistance increased from 964 ± 273 to 1204 ±338 dyn x cm x s‐5 (P<0.01). No major changes in pulmonary circulation were observed, while splanchnic vascular resistance increased from 4472±1056 to 5361 ± 1420 dyn x cm x s‐5 (P<0.01) and estimated hepatic blood flow decreased from 1403 ± 218 to 1218 ± 219 ml min‐1 (P<0.01).During endothelin‐1 infusion the pulmonary vascular bed accounted for approximately 53% of the peptide's overall disposal. Since the splanchnic area receives blood previously cleared during passage across the pulmonary vascular bed and the splanchnic plasma flow represented only 25 to 30% of the pulmonary plasma flow, the absolute amount of endothelin‐1 disposed in the splanchnic region represented only about 3%. However, the regional fractional extraction rates were comparable (mean splanchnic fractional extraction: 35.5 ± 2.1 %; mean pulmonary fractional extraction: 49.2 ± 14.9%), and thereby indicate a potentially similar efficacy of the pulmonary and splanchnic vascular bed to extract endothelin‐1.In conclusion we showed pulmonary clearance to be a main cause of the short half‐life of endothelin‐1 in man. Furthermore, the hemodynamic changes induced by the slight increases in regional concentrations of endothelin‐1 provide evidence for a role of endothelin‐1 in the regulation of circulation under (patho‐) physiological conditions.
Haemodynamic and renal effects of urodilatin in healthy volunteers
Authors: KENTSCH M. , LUDWIG D. , DRUMMER C. , GERZER R. , MÜLLER‐ESCH G. 
Published: March 2008

Abstract. Urodilatin (ANF(95–126)), an analogue of the atrial natriuretic factor (ANF(99–126)), has recently been isolated from human urine. To study haemodynamic and renal effects of synthetic urodilatin, 18 healthy male volunteers (age 26.1±0.8 years; X ± SEM) received i.v. bolus injections of urodilatin at doses of 1, 2 or 4 μg kg‐1 body weight (bw) (n= 6 per dosage group). Urodilatin dose‐dependently increased heart rate and cardiac index. A dose‐dependent increase in plasma cyclic GMP levels was also observed. Urinary cyclic GMP excretion, urine flow and natriur‐esis increased 7‐fold, 5‐fold and 4‐fold, respectively. Renal effects were not different between dosage groups.Compared with ANF(99–126), after urodilatin the reduction in mean pulmonary arterial pressure (PAP) was more pronounced (2 μg kg‐1, n= 6; ANF ‐1.8 ± 0.5, URO: ‐5.5±1.1 mmHg, P<0.05). Furthermore, after urodilatin the reduction of PAP lasted continuously from 2 up to 90 min after injection, while ANF(99–126) produced only a transient decrease of PAP. Similarily the reduction of pulmonary capillary wedge pressure (PCWP) by urodilatin from 9.3±1.2 to 3.8±0.9 mmHg (P<0.05) was also sustained up to 90 min post administration. These data in healthy volunteers suggest that, due to prolonged reduction of PAP and PCWP with increases of cardiac index and reduction of systemic vascular resistance, urodilatin might exhibit beneficial effects in cardiovascular disease.
Verapamil increases serum ionized calcium and serum phosphate in patients with post‐surgical hypoparathyroidism
Authors: SJÖDÉN G. , ROSENQVIST M. , NORDENSTRÖM J. , BJÖRKHEM I. , ERIKSSON S. A. V. , KRIEGHOLM E. 
Published: March 2008

Abstract. The calcium homeostasis in eight patients with postoperative hypoparathyroidism was examined before and after 2 weeks of administration of verapamil in an oral dose of 80 mg three times daily. Serum ionized calcium increased during verapamil treatment (from mean ± SD of 110 ± 006 to 1.24 ± 0.38 mmol 1‐1; P <0.05), as well as total serum calcium corrected for protein (from 2.11±0.13 to 2.18 ± 0.13 mmol l‐1; P < 0.05). During treatment with verapamil there was an increase in serum phosphate (from 1.08 ±0.15 to 1.19±0.20 mmol l‐1P≤ 0.05) and in the urinary excretion of phosphate (P/creatinine ratio from 1.22±0.69 to 1.83 ± 0.97; P≤0.05). The serum 1,25‐dihydroxyvitamin‐Dj and serum parathyroid hormone were below the detection limits both before and after verapamil treatment. There were no significant changes either of the intestinal absorption of calcium or of the urinary calcium excretion. Serum osteocalcin was insignificantly reduced after treatment (1.60 ± 0.70 before treatment and 1.25 ± 0.71 μg l‐1 after treatment).Thus in patients with post‐surgical hypoparathyroidism verapamil has effects on calcium and phosphorous homeostasis. Since calcium absorption was not influenced by verapamil, it is suggested that verapamil affects bone mineral metabolism.
Functional and structural determinants of glomerulosclerosis in the fawn‐hooded rat
Authors: WESTENEND P. J. , NOOYEN Y. A. , KROGT J. A. VAN DER , BRUMMELEN P. VAN , WEENING J. J. 
Published: March 2008

Abstract. The effect of uninephrectomy (UN) at 4 months of age was studied on several parameters involved in the development of glomerulosclerosis (GS) in male spontaneously hypertensive Fawn‐Hooded rats. Protein excretion per animal was significantly more increased in UN rats at 2 months after operation compared to sham operated controls (202±104 vs. 88±37 mg 24 h‐1, P=0.005) and remained significantly higher throughout the rest of the observation period. At 11 months of age UN rats had a marked increase in the incidence of GS, 37± 16% compared to 5 ± 3% (P < 0.001) in controls. No differences were observed in mean arterial blood pressure.Functional studies in separate groups of rats at 5 months of age showed an increase in single kidney glomerular filtration rate in UN rats (0.40±0.07 vs. 0.28±0.09 ml min‐1 100 g, P= 0.006). Single kidney renal plasma flow and filtration fraction were not altered. Mean glomerular volume was increased 1 month after UN (1.86 ± 0.25 vs. 1.39 ± 0.25 times 106μm3, P=0.003). Urinary noradrenaline excretion per animal (24‐h) showed a high sympathic nervous tone in both sham and UN rats. Total urinary dopamine and kallikrein excretion per animal were not influenced by UN.These data indicate that after UN the development of GS in this rat strain is accelerated in association with compensatory hyperfiltration and glomerular volume expansion, which may play a role in the pathogenesis of GS.
Effect of a somatostatin analogue, octreotide, on renal haemodynamics and albuminuria in acromegalic patients
Authors: DULLAART R. P. F. , MEIJER S. , MARBACH P. , SLUITER W. J. 
Published: March 2008

Abstract. Although insulin‐like growth factor I increases renal function, the renal haemodynamic abnormality underlying the glomerular hyperfiltration in acromegaly is unknown. In normal subjects, amino acids and low doses of dopamine increase the glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), presumably by a predominant vasodila‐tion of the afferent and efferent glomerular arterioles, respectively.We studied baseline GFR and ERPF (determined with 125I‐iothalamate and131I‐hippuran, respectively), the renal stimulatory effects of amino acid and dopamine infusion, and albuminuria before and after 3 months octreotide treatment in seven acromegalic patients with metabolically active disease. Octreotide reduced growth hormone concentrations from 14.7 ± 3.0 to 5.5 ±1.0 μg I‐1 (mean±SEM,n= 7; P< 0.001) and insulin‐like growth factor I levels from 412± 1.31 to 2.44±0.68 kU I‐1 (J><0.02). Glucagon concentrations did not change. Baseline GFR and ERPF declined from 132 ± 5 to 117 ±6 and from 547±32 to 478 ± 31 ml min‐1 1.73 m‐2, respectively (P<0.05 for both). Initially the response to amino acids was impaired (increment in GFR: 4.8±6.0%, NS; ERPF: ‐1.5 ±6.8%, NS), whereas the response to dopamine was normal (GFR: 10.6± 1.1%, P < 005: ERPF: 33.2 ± 3.1%, P<0.01). After octreotide, amino acid infusion increased GFR by 15.0 ± 6.8% (P < 0.02) and ERPF by 11.3 ± 5.6% (P < 0.02), while the dopamine response was unchanged. Initially, six patients were normo‐albuminuric and one had intermittent micro‐albuminuria. Octreotide reduced albuminuria by 22% overnight (median; P<005), and by 65% during the clearance studies (P<0.05).In conclusion, afferent glomerular vasodilation appears to be an important characteristic of the glomerular hyperfiltration in acromegaly. Octreotide reverses this abnormality and reduces albuminuria.
Sodium‐lithium countertransport kinetics in normal and hypertensive human pregnancy
Authors: RUTHERFORD P. A. , THOMAS T. H. , MACPHAIL S. , WILKINSONg R. 
Published: March 2008

Abstract. Erythrocyte sodium‐lithium countertransport activity is increased in a subgroup of patients with essential hypertension but activity also rises temporarily during normal pregnancy. It is not known if the mechanism of raised activity is the same in both of these situations. Standard sodium‐lithium counter‐transport activity and its kinetic characteristics (sodium affinity and maximum velocity) were measured in 15 women with a normal pregnancy. The mechanism of raised sodium‐lithium countertransport activity was an increase in maximum velocity. There was no change in sodium affinity. This contrasts with essential hypertension where the mechanism is increased sodium affinity.Sodium‐lithium countertransport activity was also measured in 14 primigravidae whose pregnancies were complicated by hypertension, and mean activity was not significantly higher than in normal pregnancy. However, six women had increased sodium affinity suggestive of essential hypertension and a different underlying mechanism of hypertension to those with normal sodium affinity. Prospective measurement of sodium‐lithium countertransport kinetics may lead to a better understanding of the pathophysiology of hypertension in pregnancy.
Vasoactive peptides in Bartter's syndrome
Authors: STAHL M. M. S. , VAARA I. , HEDNER P. , EKMAN R. 
Published: March 2008

Abstract. Patients with Bartter's syndrome exhibit an increased vascular resistance to the pressor effects of angiotensin II and noradrenaline. Further, an increased production of vasodilating renal prosta‐glandins, perhaps mediating the vascular unresponsi‐veness, has been hypothesized in this syndrome based on high urinary prostaglandins. To determine whether different peptides might contribute to blood pressure control in this syndrome, the basal immunoreactive plasma levels of an array of vasoactive peptides and catecholamines were analysed in six patients with Bartter's syndrome. Among the vasoconstrictors analyzed, the mean plasma levels of noradrenaline (NA), adrenaline (A) and neuropeptide Y‐like immunoreac‐tivity (NPY‐LI) were significantly increased as compared to healthy subjects (P= 0.030, 0.046 and 0.001, respectively). The plasma level of the vasodilator substance P (SP‐LI) was also higher in these patients (P = 0.057).These results indicate that in Bartter's syndrome the vasoconstrictive effect of catecholamines and angiotensin II may be enhanced by concomitant NPY release. Whether a release of the vasodilator substance P is an independent mechanism or represents a reflex response to the increased secretion of angiotensin II, catecholamines and/or NPY remains to be established. However, the significance of these biochemical findings for blood pressure maintenance in Bartter's syndrome remains to be settled.
Increased human erythrocyte sodium‐Iithium countertransport in hyperlipidaemic patients may indicate increased membrane lipid fluidity
Authors: DOWD A. , THOMAS T.H. , WILKINSON R. 
Published: March 2008

Abstract. Erythrocyte sodium‐lithium countertransport (SLC) activity, membrane fluidity, plasma trigly‐ceride and cholesterol were measured in hyperlipidaemic patients and normal subjects. Fluidity was assessed by the fluorescence anisotropy (inversely related to fluidity) of the probes 1,6‐diphenyl‐1,3,5‐hexatriene (DPH) and 1,4‐trimethylammonium‐3,5‐hexatriene (TMA‐DPH). In a second group of patients the maximum velocity (Vmax) and external sodium affinity constant (km) of SLC was also measured.In the first group of patients, SLC activity was increased compared with the controls (0.279 ± 0.019 vs. 0.213 ± 0.013, P= 0.006) as was membrane fluidity in the deep hydrophobic regions (DPH anisotropy 0.211 ± 0.0007 vs. 0.215 ± 0.0011, P= 0.007). There was a strong correlation between SLC and DPH anisotropy (Rs= ‐0.72, P= < 0.001) which was due to the correlation between Vmax and DPH anisotropy (Rs=‐0.90, P= < 0.001).Increases in Vmax of SLC in hyperlipidaemic patients may be due to differences in lipid organisation in the deep hydrophobic regions of the membrane which may affect the turnover rate of the transporter.
Cerebral trauma and alcohol abuse
Authors: RÖNTY H. , AHONEN A. , TOLONEN U. , HEIKKILÄ J. , NIEMELÄ O. 
Published: March 2008

Abstract. We report results of clinical examinations, computed tomography, quantitative electroencepha‐lography (QEEG), and cerebral blood flow measurements performed on a series of 56 consecutive brain injury patients including 15 alcohol abusers and 41 non‐alcoholic subjects. Greater volumes of intra‐cranial haemorrhage were noted in the alcoholics for a similar severity of injury and local brain atrophy became more pronounced in them during a follow‐up of 1 year. After this time, the third ventricle width, distance between frontal horns, the sum of lateral ventricle dimensions and cortical sulci were all markedly larger in the alcoholics. The QEEG results also indicated a weaker improvement in the alcoholics. The cerebral blood flow at the site of the injury was initially slow in the alcoholics when compared to the contrala‐teral region of the other hemisphere, although these differences disappeared during the follow‐up. Permanent occupational disability was also found to be associated with pretraumatic alcohol abuse.The findings indicate that ethanol abuse is not only commonly associated with cerebral trauma but is also a risk factor for a more severe brain damage following the injury.