bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pretreatment with Methylprednisolone in Coronary Artery Bypass Grafting Influences the Levels of Histamine and Tryptase in Serum but Not in Bronchoalveolar Lavage Fluid
Authors: van Overveld F. J. , De Jongh R. F. , Jorens P. G. , Walter P. , Bossaert L. , De Backer W. A. 
Published: August 2015

1. The presence of histamine and tryptase in serum during and after coronary artery bypass grafting may be an indication of the induction of inflammation.
2. One group of patients received no glucocorticoids and a second group received methylprednisolone before extracorporeal circulation. In the steroid group no effects were seen on the basal levels of histamine (2.84 + 0.12 ng/ml) and tryptase (030 + 0.05 ng/ml) during and after surgery. In the other group two peak levels of histamine were observed: one at 10 min after starting extracorporeal circulation (4.19 +1.79 ng/ml) and another at 4h after surgery (8.26 +4.85 ng/ml). In this group tryptase was only elevated during the period of extracorporeal circulation (1.54+ 0.16 ng/ml).
3. There were no differences between the two groups in complement activation. C3a levels rose to 170 +8% and 180 +10% of the initial value in the steroid and non-steroid group, respectively.
4. It was concluded that during surgery mast cells were activated, but since tryptase levels decreased in the post-operative period, the second increase in the histamine level can be explained by activation of basophils or by an unknown mechanism for the release of histamine but not tryptase by mast cells.
5. In the bronchoalveolar lavage fluid the levels of histamine and tryptase showed no differences between the two groups of patients, but histamine was enhanced compared with normal levels.
Heterogeneity of Human Biliary Mucin: Functional Implications
Authors: Klinkspoor J. Henriëtte , van Wijland Michel J. A. , Koeleman Carolien A. M. , van Dijk Willem , Tytgat Guido N. J. , Groen Albert K. 
Published: August 2015

1. Human gallbladder mucin has been implicated as playing a role in the pathogenesis of gallstones. In previous studies no differences have been found in the content or composition of mucins derived from control bile or cholesterol gallstone bile. Until now, no differences were also found between these two groups of mucins with regard to their ability to cause cholesterol nucleation. In the accompanying paper we have reported that there is a strong heterogeneity of gallbladder mucins derived from individual patients (M. J. A. van Wijland, J. H. Klinkspoor, L. Th. de Wit, R. P. J. Oude Elferink, G. N. J. Tytgat and A. K. Groen, Clin Sci 1994; 86: 67–74). In the present study we further investigated a possible patient to patient heterogeneity of mucin by means of immunological and functional characterization of mucins isolated from hepatic bile of six different patients with gallstones.
2. Considerable heterogeneity was found. Two of the mucins barely reacted with a polyclonal anti-mucin antibody, whereas the other four mucins reacted very strongly. Lectin-binding studies indicated that the glycans of these two mucins expressed less D-N-acetylgalactosamine residues than the other four mucins. This was confirmed by analyses of the glycan compositions. These studies furthermore indicated that the glycans were of the O-linked type, contained α-D-N-acetylglucosamine and were fucosylated, sialy-lated and sulphated to different extents. Except for a strong heterogeneity in the sugar composition of the mucins, heterogeneity was also found in the biological activity of the mucins. The two immunologically diverging mucins nucleated cholesterol from model bile 1–2 days earlier and also caused an almost threefold more rapid rupture of cholesterol/phospholipid vesicles than the other mucins.
3. We conclude that considerable differences exist between mucins derived from individual patients and that the heterogeneity in glycan composition might play a role in the pathogenesis of gallstone disease.
Secretion of Ions and Pharmacological Responsiveness in the Mouse Paw Sweat Gland
Authors: Sato K. , Cavallin S. , Sato K. T. , Sato F. 
Published: August 2015

1. Some of the basic functional features of the mouse paw eccrine sweat gland were delineated to allow comparison with those of transgenic mice in the future.
2. The mouse sweat secretory coil responds to methacholine, elaborating a K+-rich (&gt; 120 mmol/l), Na+-poor (&lt; 70 mmol/l) primary fluid as does the rat paw sweat gland, as previously reported. The methacholine-induced sweat rate increases with age in parallel with the growth of the sweat gland over the first 6 weeks of life.
3. The sweating response to cyclic AMP-elevating agents, such as isoprenaline or forskolin, is as much as 40% of the methacholine-induced sweat rate at 1 week of age, but falls to 10% by 6 weeks of age despite the fact that the agonist-induced tissue accumulation of cyclic AMP expressed on a per μg of protein basis triples with age over the same period.
4. A marked K+ outflux was also noted in response to methacholine and a small K+ outflux was seen in response to cyclic AMP-elevating agonists in super-fused adult mouse secretory coils in vitro.
5. Since sweat secretion is usually associated with activation of either K+ channels or Cl− channels or both, and since the sweating occurred in response to cyclic AMP-elevating agonists, we speculate that the cyclic AMP-activated Cl− channels (the mouse version of the cystic fibrosis transmembrane conductance regulator) may also occur in the mouse sweat gland, but that the degree of their expression may be influenced by the age of the mice.
Insulin—like Growth Factor-1 is Partially Responsible for Fibroblast Proliferation Induced by Bronchoalveolar Lavage Fluid from Patients with Systemic Sclerosis
Authors: Harrison Nicholas K. , Cambrey Alison D. , Myers Allen R. , Southcott Anne M. , Black Carol M. , du Bois Roland M. , Laurent Geoffrey J. , McAnulty Robin J. 
Published: August 2015

1. Interstitial lung disease is a common complication of systemic sclerosis. The mechanism by which excess collagen is deposited in the lung is poorly understood, but is thought to involve release of mediators which activate lung fibroblasts. In this study we investigated and partially characterized the fibroblast proliferative activity of bronchoalveolar lavage fluid from 29 patients with systemic sclerosis, 19 with and 10 without evidence of lung disease assessed by thin-section computed tomography.
2. Bronchoalveolar lavage fluid from both groups of patients stimulated fibroblast proliferation compared with control subjects: systemic sclerosis with normal computed tomography, 27.7 (range 10.5–57.9)% above control; systemic sclerosis with abnormal computed tomography, 26.7 (range 5.0–47.8)% above control, P &lt; 0.02 in both cases.
3. The activity was reduced by about one-third by neutralizing antibodies to insulin-like growth factor-1 but not platelet-derived growth factor. Levels of insulin-like growth factor-1 of bronchoalveolar fluid were increased in patients with systemic sclerosis [2.10 (range 1.10–3.48) ng/ml of bronchoalveolar lavage fluid] compared with controls [1.45 (range 1.10–2.05) ng/ml; P &lt; 0.01]. When patients were subdivided into those with abnormal computed tomography [2.10 (range 1.20–3.48) ng/ml] and those with normal computed tomography [1.85 (range 1.10–2.90) ng/ml] only the values for the group with evidence of lung disease were increased compared with control subjects (P &lt; 0.02). Platelet-derived growth factor could not be detected in bronchoalveolar lavage fluid from any group. Fractionation of bronchoalveolar lavage fluid demonstrated activity in several fractions consistent with the molecular masses of insulin-like growth factor-1 associated with binding proteins.
4. We conclude that bronchoalveolar lavage fluid from patients with systemic sclerosis contains increased levels of insulin-like growth factor-1 and this contributes to the increased fibroblast-growth-promoting activity of this fluid. The data also suggest that other mitogens are involved, but we were unable to demonstrate a role for platelet-derived growth factor.
Tumour Necrosis Factor Receptor Levels Are Linked to the Acute-Phase Response and Malnutrition in Human-Immunodeficiency-Virus-Infected Patients
Authors: Süttmann U. , Selberg O. , Gallati H. , Ockenga J. , Deicher H. , Müller M. J. 
Published: August 2015

1. Increased release of tumour necrosis factor is thought to contribute to human-immunodeficiency-virus-associated wasting syndrome. Elevated serum concentrations of tumour necrosis factor have, however, mainly been found during acute opportunistic infections and were not correlated with the degree of wasting. This finding may be explained by the paracrine release and the rapid inactivation of tumour necrosis factor. Serum levels of the two recently detected soluble tumour necrosis factor receptor proteins (p55 and p75) are assumed to reflect tumour necrosis factor release.
2. Serum levels of soluble tumour necrosis factor receptors 55 and 75 were measured by an enzyme-linked immunological and biological binding assay in 45 human-immunodeficiency-virus-infected patients and seven healthy control subjects. Patients were followed up for survival. Serum albumin, prealbumin, total iron-binding capacity (transferrin) and C-reactive protein concentrations were measured using standard laboratory methods. Body composition was determined by bioelectrical impedance analysis.
3. Serum concentrations of soluble tumour necrosis factor receptor 55 and 75 were both significantly increased in human-immunodeficiency-virus-infected patients as compared with the healthy control subjects (P &lt; 0.05); soluble tumour necrosis factor receptor concentrations were even more increased in patients with elevated C-reactive protein levels (≥ 5 mg/l) as compared with those with normal C-reactive protein levels (&lt; 5 mg/l; P &lt; 0.0001 and P &lt; 0.01, respectively). An association was observed between serum soluble tumour necrosis factor receptor 55 and 75 concentration and (i) serum albumin concentration (r = −0.46, P &lt; 0.005 and r = −0.63, P &lt; 0.001, respectively), (ii) serum prealbumin concentration (r = −0.42, P &lt; 0.005 and r = −0.57, P &lt; 0.001, respectively), and (iii) serum total iron-binding capacity (transferrin; r = −0.31, P &lt; 0.05 and r = −0.44, P &lt; 0.005, respectively). A correlation was also found between serum soluble tumour necrosis factor receptor 55 level and the extracellular mass-body cell mass quotient (r = 0.63, P &lt; 0.001).
4. The present data provide evidence that the tumour necrosis factor system is involved in the genesis of human-immunodeficiency-virus-associated malnutrition. Serum levels of soluble tumour necrosis factor receptors may be useful for diagnosis and management of the wasting syndrome.
Glucose Polymer in the Fluid Therapy of Acute Diarrhoea: Studies in a Model of Rotavirus Infection in Neonatal Rats
Authors: Thillainayagam A. V. , Dias J. A. , Salim A. F. M. , Mourad F. H. , Clark M. L. , Farthing M. J. G. 
Published: August 2015

1. Unlike standard glucose-electrolyte oral rehydration solutions, solutions containing polymeric glucose as substrate can significantly reduce stool output, duration of diarrhoea and total oral rehydration solution requirements. However, neither the underlying mechanisms nor the optimal size and concentration of glucose polymer has been defined.
2. We have used a model of rotavirus diarrhoea in neonatal rats to compare the effects on water and solute absorption of varying the concentration of a glucose polymer (mean chain length five glucose residues) in experimental oral rehydration solutions. Three polymer (P) solutions were compared with solutions of identical electrolyte content (mmol/l: sodium, 60; potassium, 20; chloride, 60; citrate, 10) containing equivalent amounts of free glucose (G) as substrate by perfusion of the entire small intestine in situ. The polymer (9, 18, 36 mmol/l; 159, 168, 186 mosmol/kg, respectively) and the monomer (45, 90, 180 mmol/l; 195, 240 320 mosmol/kg) solutions were perfused in normal and rotavirus-infected neonatal rats.
3. In normal intestine polymer solutions promoted greater water absorption [P9, mean 291.4 (SEM 16.4); P18, 331.9(13.1); P36, 284.3 (11.8) μl mi−1 g−1] than their equivalent monomer solutions [G45, 220.8 (8.4); G90, 240 (21); G180,79.4 (145) μl min− g−1; P &lt; 0.02]. In rotavirus-infected intestine, water absorption from all solutions declined, but the fall was much less pronounced from the polymer solutions [P9, 232.8 (6); P18, 277.2 (20.5); P36, 166 (18.2) μl min−1 g−1] than from their monomeric counterparts [G45, 116.7 (25.5); G90, 68.7 (12.4); G180, 21 (11.6) μl min−1 g−1; P &lt; 0.005].
4. In both the normal net absorptive state and the net secretory state induced by rotavirus infection, there was a striking inverse correlation between net water absorption and perfusate osmolality (r = −0.94 and r = −0.88, respectively; P &lt; 0.05). In rotavirus-infected intestine, increasing the polymer concentration from 18 to 36 mmol/l resulted in a relative fall in water absorption (P &lt; 0.01). The hypertonic solution G180 was associated with the lowest water absorption (P &lt; 0.01). None of the solutions was able to reverse rotavirus-induced net secretion of sodium, which was similar from all solutions, whether polymer- or monomer-based.
5. These results (i) emphasize the pre-eminence of hypotonicity among the factors promoting water absorption from polymer-based oral rehydration solutions in acute diarrhoea, (ii) confirm the adverse consequence of raising substrate concentration (whether polymer or monomer) beyond certain limits and (iii) indicate that the concentration of this glucose polymer yielding the optimum compromise between substrate availability and low osmolality may be approximately 9–18 mmol/l.
No Mandatory Role for the Spleen in the Exercise-Induced Leucocytosis in Man
Authors: Iversen P. O. , Arvesen B. L. , Benestad H. B. 
Published: August 2015

1. Short-lasting strenuous physical exercise leads to a marked increase in the blood concentration of leucocytes in healthy humans. The cell sources of this leucocytosis have not been definitely identified, neither has the contribution made by the various subtypes of leucocytes.
2. We have compared the exercise-induced leucocytosis in six splenectomized and six intact subjects. The blood concentrations of leucocytes as well as of most subtypes, except monocytes and eosinophilic granulocytes, increased substantially at the end of a 5 min exercise (200 W) bout.
3. The increases were similar in the splenectomized subjects and in the control subjects. Thirty minutes after completion of the exercise the various leucocyte blood concentrations had returned to pre-exercise levels.
4. The plasma concentrations of several cytokines (interleukins-1α and −6; tumour necrosis factor-α and granulocyte colony-stimulating factor) known to affect leucocyte kinetics did not change appreciably with exercise in either group.
5. We conclude that exercise-induced leucocytosis can take place in the absence of the spleen. There was no evidence that cytokines known to affect leucocyte formation, mobilization and activity are involved in this leucocytosis.
Recovery from Acute Ischaemic Renal Failure is Accelerated by Des-(1–3)-Insulin-Like Growth Factor-1
Authors: Clark Ross , Mortensen Deborah , Rabkin Ralph 
Published: August 2015

1. Acute renal failure carries a high risk of morbidity and mortality, so there is a need for agents that minimize renal injury after an insult and that hasten repair. Insulin-like growth factor-1 is mitogenic for renal tubular cells; in normal kidneys it has haemodynamic effects and it is potently anabolic. We tested the theory that insulin-like growth factor-1 may be of use in the treatment of acute renal failure by administering recombinant des-(1–3)-insulin-like growth factor-1, a truncated form of insulin-like growth factor-1, which occurs naturally. Ischaemic renal failure was induced in normal rats by occluding both renal pedicles for 60 min. Then des-(1–3)-insulin-like growth factor-1 (0.8 mg day−1 kg−1) or vehicle was given by subcutaneous minipump for 7 days. The rats were weighed and bled daily and in one experiment were housed in metabolic cages and urine was collected.
2. Des-(1–3)-insulin-like growth factor-1 caused a lower and earlier peak in both serum creatinine and blood urea-nitrogen levels, and a more rapid and complete return toward basal values than in untreated animals. Also des-(1–3)-insulin-like growth factor-1 significantly increased creatinine clearance and reduced fractional excretion of filtered sodium. Besides these beneficial effects on kidney function, des-(1–3)-insulin-like growth factor-1 was anabolic as treated rats gained weight while control rats lost weight. The mortality in control rats was 28% compared with 6% in treated rats.
3. Thus des-(1–3)-insulin-like growth factor-1 accelerated recovery from acute ischaemic injury and may be useful for the treatment of acute renal failure.
Plasma Endothelin Levels and Vascular Effects of Intravenous l-Arginine Infusion in Subjects with Uncomplicated Insulin-Dependent Diabetes Mellitus
Authors: Smulders Ronald A. , Stehouwer Coen D. A. , Olthof Cornelis G. , Van Kamp Gerard J. , Teerlink Tom , De Vries Peter M. J. M. , Donker Ab J. M. 
Published: August 2015

1. Uncomplicated insulin-dependent diabetes mellitus is associated with generalized vasodilatation. This vasodilatation is believed to contribute to the development of microvascular complications. The endothelium plays an important role in the regulation of vascular tone.
2. To investigate the role of endothelial mediators, we measured plasma endothelin levels and studied the vascular effects of intravenous l-arginine (the precursor of NO) in 10 male type 1 diabetic patients and 10 non-diabetic subjects.
3. The baseline plasma endothelin level was significantly lower in the diabetic patients [mean 1.7 (SD 0.5) versus 2.1 (0.4) pmol/l; P &lt; 0.05] than in the control subjects.
4. During l-arginine infusion, plasma cyclic GMP (the second messenger for NO) increased in the control subjects [from 5.1 (2.9) to 6.9 (2.9) nmol/l; P &lt; 0.05 versus saline] and in the diabetic patients [from 4.6 (1.8) to 5.7 (2.2) nmol/l; P = 0.09]. l-Citrulline (a by-product of NO synthesis from l-arginine) increased in both groups. The responses to l-arginine were not significantly different between the control subjects and the diabetic patients. The plasma atrial natriuretic peptide level did not change in either group during infusion of l-arginine or of an equal volume of isotonic saline.
5. Blood pressure decreased slightly during l-arginine administration in both groups. In control subjects, the extracellular fluid volume in the lower leg increased during l-arginine infusion as compared with saline; in the diabetic patients both l-arginine and saline increased the extracellular fluid volume.
6. In conclusion, the vascular effects of l-arginine are similar in men with uncomplicated insulin-dependent diabetes mellitus and in control subjects. Whether these effects are due to an increase in NO synthesis remains unclear. The increase in extracellular fluid volume during saline infusion in diabetic patients suggests an increase in microvascular permeability in
Blood Flow Responses to Intra-Arterial Acetylcholine in Man: Effects of Basal Flow and Conduit Vessel Length
Authors: Chowienczyk P. J. , Cockcroft J. R. , Ritter J. M. 
Published: August 2015

1. Acetylcholine relaxes human resistance vessels and releases nitric oxide and other factors from the endothelium. Comparison of responses to acetylcholine with those to an endothelium-independent vasodilator (such as nitroprusside) forms the basis of the so-called acetylcholine test of endothelial function. However, when this test is applied in vivo by intraarterial infusion, the metabolic instability of acetylcholine may result in differential responses to these drugs arising from anatomical rather than functional differences.
2. Vasodilator responses to brachial Artery infusions of acetylcholine (41 and 83 nmol/min) and sodium nitroprusside (11 and 38 nmol/min) were measured in 30 healthy human subjects using venous occlusion plethysmography.
3. Responses to acetylcholine showed a greater dependence on resting blood flow (P &lt; 0.05) and on forearm length (P &lt; 0.05) than those to sodium nitroprusside (results predicted by a simple blood flow model).
4. Correction for forearm length abolished an apparent difference of 59% between responses to acetylcholine in men and women. Conduit vessel geometry and resting blood flow influence the acetylcholine test of endothelial function.
Increased Platelet Volume and Platelet Mass in Patients with Atherosclerotic Renal Artery Stenosis
Authors: Bath Philip M. W. , Missouris Constantinos G. , Buckenham Timothy , MacGregor Graham A. 
Published: August 2015

1. Platelet volume was measured in citrated blood in two groups of patients at risk of having atherosclerotic renal artery stenosis, namely (i) 30 patients with severe hypertension, and (ii) 44 patients with peripheral vascular disease.
2. Platelet volume was increased in patients with hypertension who had atherosclerotic renal artery stenosis diagnosed by angiography: no renal artery stenosis, median 7.2 (interquartile range 0.5) × 10−15/l; renal artery stenosis 7.8 (0.8) × 10−15/l; platelet mass also increased with increasing severity of renal artery stenosis. Platelet volume correlated with severity of renal artery stenosis (rs = 0.391, 2p = 0.033, n = 30). Similarly, platelet volume correlated with severity of renal artery stenosis in patients with peripheral vascular disease (rs = 0.319, 2p = 0.035, n = 44). Serum immunoreactive platelet-derived growth factor (predominantly released from platelets) and plasma immunoreactive interleukin-6 (a cytokine which has been postulated to regulate platelet volume) concentrations were not different between hypertensive patients with and without renal artery stenosis.
3. Since large platelets are hyperactive, increased platelet volume may contribute to the development of atherosclerotic renal artery stenosis. However, the present data do not lend support to the hypothesis that platelet-derived growth factor is central to renal artery atherogenesis. Interleukin-6 does not appear to regulate platelet volume.
Changes in Pulse Transit Time and Pulse Rate as Markers of Arousal from Sleep in Normal Subjects
Authors: Pitson D. , Chhina N. , Knijn S. , van Herwaaden M. , Stradling J. 
Published: August 2015

1. Obstructive sleep apnoea and its variants often provoke hundreds of short arousals that lead to the most important symptom, disabling hypersomnolence. The measurement of sleep in these conditions requires the documentation of these short arousals and this is conventionally done by manual inspection of the sleeping EEG, a laborious procedure.
2. Other markers of ‘arousal’, that are easier to measure and document, include several cardiovascular signals that change as part of the orienting reflex: pulse rate rise, blood pressure rise, skin vasoconstriction, for example.
3. Pulse transit time (measured as the interval from the ECG R-wave until the arrival of the pulse pressure wave at the periphery, about 250 ms) varies inversely with blood pressure and provides a beat-to-beat estimation of blood pressure changes.
4. In eight normal subjects we have assessed the relationship between transient EEG arousals of different length (provoked by external stimuli) and changes in both pulse transit time and heart rate.
5. Significant falls in pulse transit time occurred in response to external stimuli [15.1 (SEM 1.4) ms], indicating a rise in blood pressure, and were significant even when there was no discernible change in the EEG [9.9 (SEM 2.6) ms]. Significant changes in heart rate also occurred [10.3 (SEM 1.2) beats/min], but were slightly less sensitive than changes in pulse transit time.
6. Changes in pulse transit time (and to a lesser extent pulse rate) are sensitive markers of EEG arousal. As such they should be useful to include when monitoring sleep and its disorders, particularly since pulse transit time recorders can easily be made portable for home use.