bluuebunny/crossref_metadata_2025_split huggingface dataset:
Change in Blood Pressure during Altered Sodium Intake is not Associated with Calciotropic Hormone Level
Authors: Ozono Ryoji , Oshima Tetsuya , Matsuura Hideo , Ishibashi Katsuhiko , Watanabe Mitsuaki , Yoshimura Mitsuisa , Kajiyama Goro , Kambe Masayuki 
Published: August 2015

1. We evaluated the effects of the dietary restriction of sodium chloride on blood pressure and systemic calcium metabolism in 19 in-patients with essential hypertension (11 men and 8 women, mean age 49.9 ± 12.1 years).
2. All patients received a high-sodium diet (250 mmol/day) for 1 week, followed by a low-sodium diet (10 mmol/day) for another week. Intake of potassium (100 mmol/day) and of calcium (15 mmol/day) were kept constant throughout the study.
3. Sodium restriction significantly reduced the mean blood pressure (from 114.0 ± 1.9 to 105.0 ± 13.7 mmHg, P &lt; 0.01). Urinary calcium excretion was significantly reduced (from 5.1 ± 2.4 to 2.2 ± 1.0 mmol/day, P &lt; 0.01).
4. The change in mean blood pressure after sodium restriction was not correlated with a change in any parameter of calcium metabolism [whole blood ionized calcium, plasma intact parathyroid hormone, or 1,25-(OH)2 vitamin D3].
5. Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism.
6. We conclude that sodium restriction reduces blood pressure and decreases urinary calcium excretion. However, we observed no significant role of extracellular calcium concentration or of calciotropic hormone concentration in the mechanism of sodium sensitivity.
Non-invasive Measurement of Cardiac Output and Ventricular Ejection Fractions in Chronic Cardiac Failure: Relationship to Impaired Exercise Tolerance
Authors: Steele Ian C. , Moore ANN , Nugent Anne-Marie , Riley Marshall S. , Campbell Norman P. S. , Nicholls D. Paul 
Published: August 2015

1. The role of cardiac output limitation in the pathophysiology of exercise in patients with chronic failure remains undefined. During steady-state submaximal exercise, oxygen uptake is similar in patients and control subjects, but it is not known if cardiac output is also similar. We wished to determine if the reduced exercise tolerance of patients with chronic cardiac failure during such exercise is related to reduced cardiac output, or to peripheral factors.
2. Ten male patients with stable chronic failure and ten age-matched male normal controls were studied at rest and during exercise. Each subject performed a familiarization exercise test, a symptom-limited maximal exercise test and two submaximal exercise tests. Cardiac output was measured by a carbon dioxide rebreathing method. We also measured oxygen consumption, ventilation, Borg score of perceived exertion and venous lactate concentration, and ejection fractions.
3. As expected, patients had lower peak oxygen consumption [median (range) 1.18 (0.98–1.76) versus 1.935 (1.53–2.31) 1/min; P &lt; 0.001], lower peak venous lactate concentration but a similar overall level of perceived exertion. At the same submaximal workload, patients and control subjects had similar oxygen consumption [0.67 (0.59–0.80) versus 0.62 (0.52–0.82) 1/min] and cardiac output [6.92 (5.79–9.76) versus 7.3 (5.99–10.38) 1/min] but the patients had a greater perceived level of exertion [Borg score: 4 (1–6) versus 3 (1–5); P &lt; 0.005], higher venous lactate concentration [1.6 (1–3.3) versus 1.14 (0.7–1.7) mmol/l; P &lt; 0.05] and higher heart rate [106 (89–135) versus 87 (69–112) beats/min;P &lt; 0.005].
4. During submaximal exercise at a similar absolute workload, patients with cardiac failure have a similar oxygen uptake and cardiac output but greater anaerobiosis and increased fatigue when compared with normal subjects. These findings appear to relate predominantly to changes that occur in the periphery rather than abnormalities of central cardiac function.
Beneficial Effect of the Calcium-Sensitizing Drug EMD 57033 in a Canine Model of Dilated Heart Failure
Authors: Drake-Holland Angela J. , Lee John A. , Hynd John , Clarke Sinéad B. , Noble Mark I. M. 
Published: August 2015

1. Pacing-induced heart failure was studied in eight dogs. Heart failure was induced by right ventricular pacing at 250–260 beats/min for 6 weeks. Evidence of heart failure was determined clinically and by measurement of left ventricular (LV) dimensions by transoesophageal echocardiography.
2. Haemodynamic measurements of LV pressure, maximum rate of rise of LV pressure (LVdP/dtmax), cardiac output, mean arterial pressure, heart rate, pulmonary artery and pulmonary wedge pressures were made during infusion of solvent (control) and the calcium sensitizer EMD 57033 (0.6 mg min−1 kg−1).
3. The degree of heart failure varied from mild to severe in different individuals, but in each case EMD 57033 exerted a positive inotropic effect on LV haemodynamics and dimension.
4. The positive inotropic effect of the calcium sensitizer was manifest by increased peak LVdP/dt with a subsequent increase in cardiac output at the same mean arterial pressure.
5. This study clearly demonstrates that there is the potential for improvement of contractility of the failing myocardium of the intact mammal by an agent with a mechanism of action which does not involve an increase in intracellular calcium.
Plasma Concentration of Total Leptin and Human Lung-Cancer-Associated Cachexia
Authors: Simons Jean Paul F.H.A. , Schols Annemie M.W.J. , Campfield L. Arthur , Wouters Emiel F.M. , Saris Wim H. 
Published: August 2015

1. Adipocyte-derived leptin is postulated to represent the afferent hormonal signal to the hypothalamus in a feedback mechanism that regulates fat mass. In this proposed feedback mechanism, increased fat mass leads to an elevated plasma leptin level that eventually induces a decrease in appetite and an increase in energy expenditure, and vice versa.
2. As anorexia and hypermetabolism play a role in the development of cancer cachexia, we investigated the hypothesis that underlying abnormalities in the leptin feedback mechanism (in particular relatively high plasma leptin levels or, on the other hand, a hypothalamic insensitivity to a fall in leptin levels) might be involved. For this purpose, total plasma leptin, body composition (fat mass and fat-free mass), appetite and resting energy expenditure were assessed in 21 male lung-cancer patients.
3. Total leptin was detectable in six patients and non-detectable in 15. In comparison with the latter, the patients with detectable leptin were characterized by a trend towards less weight loss (3.4% compared with 11.0%, P = 0.07), as being less underweight (body mass index 23.8 kg/m2 compared with 19.4 kg/m2, P = 0.004) and by a higher fat mass (21.4 kg compared with 9.7 kg, P = 0.001). Significant between-group differences in appetite and resting energy expenditure were lacking.
4. Based on these findings, we conclude that in cancer the afferent part of the leptin feedback mechanism functions normally and that, in particular, elevated leptin levels are not involved in the development of cachexia. Since the absence of plasma leptin was not associated with an increased appetite and decreased energy expenditure, disturbances in the hypothalamic part of the feedback mechanism are hypothesized.
Mutations at the Lipoprotein Lipase Gene Locus in Subjects with Diabetes Mellitus, Obesity and Lipaemia
Authors: Zhang Qiuping , Cavallero Elisabeth , Hoffmann Michael M. , Cavanna Julian , Kay Andrea , Charles Aline , Braschi Sylvie , Marz Winfried , Perlemuter Leon , Jacotot Bernard , Galton David J. 
Published: August 2015

1. The common association of obesity, diabetes mellitus and hyperlipidaemia may have a primary aetiological basis. Insulin resistance has been postulated as a possible cause, but defects in the plasma transport of triacylglycerol or fatty acids could also be primary determinants.
2. We have therefore, studied 18 patients with diabetes mellitus, obesity and severe hypertriglyceridaemia for defects of a key protein involved in the clearance of plasma triacylglycerols, lipoprotein lipase.
3. DNA was prepared from leucocytes of 18 patients with the above syndrome, and exons encoding lipoprotein lipase were amplified by PCR. The products were sequenced using the dideoxy chain-termination method.
4. Eight of the subjects were found to possess genetic variants at the lipoprotein lipase gene locus. These were: (a) G579→A, V108V; (b) G818→A, G188E; (c) C829→T, R192; (d) A1127→G, N291S; (e) C1308→G, F351L;(f) C1338→A, T361T; and (g) C1595→G, S447. Three of these, (c), (e) and (f), have not hitherto been described. Variant (f), appears to be a population polymorphism whose allele frequency in normolipidaemic diabetics was found to be 0.12 (162 chromosomes studied). The others are all rare at frequencies of &lt;0.01 and may contribute to the phenotype by impairing clearance of plasma triacylglycerols.
5. We conclude that genetic variants at the lipoprotein lipase locus occur commonly in subjects with this syndrome (four out of 18 subjects with probably functional mutants) and may affect the individual's response to obesity and diabetes mellitus for the development of lipaemia.
Elevated Post-Prandial Gastric Inhibitory Polypeptide Concentrations in Hypertriglyceridaemic Subjects
Authors: Gama Rousseau , Norris Fiona , Morgan Linda , Hampton Shelagh , Wright John , Marks Vincent 
Published: August 2015

1. We investigated whether abnormalities of gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (7–36 amide) (GLP-1) contribute to the hypertriglyceridaemia and hyperinsulinaemia in hypertriglyceridaemic subjects. Serum triglycerides and plasma glucose GIP, GLP-1 and immunoreactive insulin (IRI) concentrations were measured before and after a mixed meal in 15 hypertriglyceridaemic patients and in eight healthy normotriglyceridaemic control subjects.
2. Integrated post-prandial GIP concentrations were greater than in controls (P &lt; 0.05) and correlated positively with both fasting and integrated post-prandial triglyceride concentrations (P &lt; 0.05 for both). Fasting and integrated post-prandial IRI levels were higher in hypertriglyceridaemic subjects than in controls (P &lt; 0.02 and P &lt; 0.05 respectively) and correlated positively with fasting triglycerides (P &lt; 0.02 and P &lt; 0.001 respectively) and integrated post-prandial triglycerides (P &lt; 0.005 and P &lt; 0.05 respectively). There was no correlation between GIP concentrations and either fasting or post-prandial IRI levels. Fasting and post-prandial concentrations of GLP-1 were similar in patients and controls.
3. Hypertriglyceridaemic subjects have post-prandial hyperGIPaemia in addition to the well-documented hyperinsulinaemia. We found no association between GIP and insulin. There is, however, clear evidence for an association between post-prandial GIP concentrations and triglyceride levels. We suggest that this association may depend on changes in lipoprotein lipase activity and that there may be a feedback loop between GIP and triglyceride lipolysis.
Selective Migration of α-Smooth Muscle Actin-Positive Myofibroblasts toward Fibronectin in the Boyden's Blindwell Chamber
Authors: Kawamoto Masashi , Matsunami Takakuni , Ertl Ronald F. , Fukuda YUH , Ogawa Maki , Spurzem John R. , Yamanaka Nobuaki , Rennard Stephen I. 
Published: August 2015

1. In order to address the hypothesis that migrating fibroblasts have a different phenotype, human fetal lung fibroblasts (HFL-1) cells were evaluated in the Boyden blindwell chamber migration assay followed by immunoelectron microscopy.
2. HFL-1 cells were placed on nucleopore filters and incubated for 2 h using purified human plasma fibronectin (pFn) as a chemoattractant. Filters were then processed for immunoelectron microscopy using antibodies for α-smooth muscle (α-SM) actin as a marker for myofibroblasts, cellular fibronectin (cFn) and VLA-5.
3. Cells which had migrated to the bottom side of the filter were more likely to express α-SM actin, 29.1 ± 3.4% of cells, compared with cells which did not migrate through the filter, 12.4 ± 1.3% (P &lt; 0.05). The total proportion of α-SM-actin-positive cells located on both sides of the filter showed no difference between those which had migrated toward pFn and controls (17.7 ± 1.0% compared with 20.2 ± 2.5%).
4. cFn-positive cells showed minimal differences compared with control cells, while perinuclear and endoplasmic reticulum staining of VLA-5 was observed only in the cells treated with pFn.
5. The results show that HFL-1 cells are heterogenous for α-SM actin expression. Short-term incubation with pFn did not change the proportion of α-SM-actin-positive HFL-1 cells. Cells which migrate, however, are enriched for α-SM actin expression. pFn-induced fibroblast chemotaxis can selectively recruit myofibroblasts with increased α-SM actin expression, a feature which may contribute to the altered population of cells at sites of fibrosis.
Mast Cell Activation in Arthritis: Detection of α- and β-tryptase, Histamine and Eosinophil Cationic Protein in Synovial Fluid
Authors: Buckley M. G. , Walters C. , Wong W. M. , Cawley M. I. D. , Ren S. , Schwartz L. B. , Walls A. F. 
Published: August 2015

1. Although mast cell hyperplasia is a feature of rheumatoid arthritis and osteoarthritis, the extent and nature of mast cell activation in joint disease have not been clearly established.
2. We have investigated the levels of mast cell tryptase and histamine and also of eosinophil cationic protein in synovial fluid collected from 31 patients with rheumatoid arthritis, 14 with seronegative spondyloarthritis and nine with osteoarthritis. Two RIAs for tryptase were employed: one with monoclonal antibody AA5, which was found to bind equally well to both α and β isoforms on Western blots of the recombinant enzyme, and the other with antibody G5, which recognizes predominantly β-tryptase.
3. α-Tryptase, which is likely to be released constitutively from mast cells, appeared to be the major form in synovial fluid, as the assay with antibody AA5 detected appreciably more tryptase than that with antibody G5. β-Tryptase, which is released on anaphylactic activation of mast cells, was detected in 14 out of 45 synovial fluid samples studied, with concentrations of up to 12 μg/l measured by the G5 assay. The apparent levels of β-tryptase, but not of α-tryptase, were closely correlated with those of histamine in the synovial fluid. Patients with osteoarthritis appeared to have a greater proportion of β-tryptase in the synovial fluid than those with rheumatoid arthritis, as well as higher concentrations of histamine. Eosinophil cationic protein was present at high levels in the synovial fluid, although eosinophil numbers were low, and its concentrations were not correlated with the concentrations of the mast cell products.
4. These data suggest that anaphylactic degranulation of mast cells may have occurred to a greater extent in osteoarthritis than in rheumatoid arthritis, despite the relative lack of synovial inflammation in osteoarthritis. Although the eosinophil cationic protein detected may not reflect eosinophilic inflammation in the joint, the presence in synovial fluid of tryptase of both major forms, and of histamine, appears to indicate that mast cell products are secreted constitutively, as well as by processes of anaphylactic degranulation in rheumatoid arthritis, seronegative spondyloarthritis and osteoarthritis.
A Single Dose of Intravenously Injected Poloxamine-Coated Long-Circulating Particles Triggers Macrophage Clearance of Subsequent Doses in Rats
Authors: Moghimi S. M. , Gray T. 
Published: August 2015

1. Adsorption of the block copolymer non-ionic surfactant poloxamine-908 on to the surface of polystyrene nanospheres (60 nm in diameter) produced ‘phagocyte-resistant’ particles (otherwise known as long-circulating particles). This was reflected by a profound reduction in uptake of such engineered nanospheres by macrophages of the reticuloendothelial system and extended blood circulation time, after intravenous administration to rats.
2. A single intravenous administration of poloxamine-908-coated particles dramatically affected the circulation half-life and body distribution of a second subsequent dose. The degree of alteration depended on the interval between the two doses. At 3 days after a single intravenous injection of poloxamine-coated particles, Kupffer cells and spleen macrophages could clear a second dose of long-circulating beads from the blood. When tested at day 14, the second dose of intravenously injected poloxamine-coated particles avoided rapid uptake by liver and spleen macrophages and remained in the blood.
3. The coating polymer (poloxamine-908) apparently triggered bead clearance by resident Kupffer cells and certain sub-populations of spleen macrophages, since a single intravenous dose of an endotoxin-free solution of poloxamine 3 days before the administration of long-circulating particles induced similar effects. When the interval between the two injections was 2 weeks, poloxamine-coated particles again exhibited long circulation half-life. This cycle could be repeated after intravenous administration of a second poloxamine dose 2 weeks after the first poloxamine injection.
4. The mechanism of particle recognition by resident tissue macrophages was found to be independent of opsonization processes.
5. These studies could have important implications in biomedical application, design and engineering of poloxamine-based long-circulating drug carriers for repeated intravenous administration.
Nitric Oxide in Different Types of Hypertension during Pregnancy
Authors: Garmendia Jenny V. , Gutiérrez Ylse , Blanca Isaac , Bianco N. E. , De Sanctis J. B. 
Published: August 2015

1. Serum nitric oxide (NO) levels (determined by its products of oxidation) were assessed in nonpregnant women, normal pregnant women and patients suffering from mild pre-eclampsia (MPE), severe pre-eclampsia (SPE), chronic hypertension (CHT) and CHT with pre-eclampsia (CHT+PE). The levels of NO products were significantly reduced during pregnancy in MPE (P &lt; 0.001), CHT+PE (P &lt; 0.01) and SPE (P &lt; 0.05). Significant reductions of NO products were also observed in puerperium (P &lt; 0.001) in all groups except CHT+PE (P &lt; 0.05).
2. In normal pregnancy, three events were related to NO levels: (1) negative correlations were found between the levels of nitrite (r = −0.73, P = 0.0003), nitrate (r = −0.53, P = 0.017) and the number of weeks of gestation; (2) in the caesarean section group, the levels of NO at puerperium were significantly lower (P &lt; 0.05) than those during pregnancy; and (3) there was a significant reduction in NO levels in the pregnant women carrying male fetuses as compared with female fetuses (P &lt; 0.05).
3. In SPE, the patients with a family history of hypertension had lower levels of NO compared with the patients without such a history (P &lt; 0.05).
4. A negative correlation was observed between systolic blood pressure, diastolic blood pressure and NO levels in MPE (r = −0.62, P = 0.013 and r = −0.68, P = 0.0049 respectively) and SPE (r = −0.72, P = 0.004 and r = −0.53, P = 0.037 respectively).
5. In SPE, positive correlations were observed between platelet count and nitrite (r = 0.67, P = 0.006) and nitrate levels (r = 0.56, P = 0.028).
6. In MPE, patients with anti-hypertensive treatment showed significantly (P &lt; 0.05) higher levels of NO compared with the non-treated patients.
7. NO may be important in the physiopathology of hypertension during pregnancy, although several factors may affect its levels.
Renovascular Hypertension with Low-to-Normal Plasma Renin: Clinical and Angiographic Features
Authors: Rossi Gian Paolo , Pavan Edoardo , Chiesura-Corona Matteo , Bader Michael , Paganini Giovanni , Cesari Maurizio , De Toni Renzo , Feltrin Gian Pietro , Ganten Detlev , Pessina Achille C. 
Published: August 2015

1. Low-to-normal renin renovascular hypertension (RVH) and the accuracy of renal vein renin ratios were investigated in 129 consecutive patients referred for suspected RVH. Forty-nine had essential hypertension, 24 unilateral renoparenchymal hypertension and 56 renal artery obstruction. Of the latter, 86% were diagnosed retrospectively as RVH, based on fall in blood pressure with correction of renal ischaemia. We measured baseline, captopril-stimulated and renal vein plasma renin activity (PRA) levels, as well as several other parameters.
2. PRA was low-to-normal in 37% of the RVH patients [low-to-normal renin (LNR-) RVH group] and elevated in the remaining 63% [high-renin (HR-) RVH group]. In the LNR-RVH group, low-to-normal renin levels, by immunoreactive active renin and plasma renin concentration measurements, and a blunted response of PRA to captopril, were seen. As compared with HR-RVH, LNR-RVH patients had a longer duration of hypertension (P &lt; 0.05), higher serum K+ (P = 0.04) and lower diastolic blood pressure (P = 0.02). However, they did not differ for the other variables, including the fall in blood pressure after correction of renal ischaemia. Although the number of bilateral stenoses was similar in the two groups, no patient in the LNR-RVH group had total renal artery occlusion compared with 53% in the HR-RVH group (P = 0.00015). The accuracy of renal vein renin indices were high enough to justify their use only in the patients with total occlusion of a renal artery.
3. Thus LNR-RVH is common in patients with longstanding hypertension without a totally occluded renal artery. Since the sensitivity of renin measurements is low, cure of hypertension would be precluded for more than one third of RVH patients, if these tests were a prerequisite for identifying RVH.