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1. |
Mack Forster Award for 1990 |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 339-339
Alan M. McGregor,
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ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01867.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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2. |
1990 MACK FORSTER PRIZE LECTURE REVIEW: The Molecular Genetics of the a globin gene family |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 340-347
D. R. HIGGS,
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ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01868.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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3. |
Postprandial exocrine pancreatic function during long‐term treatment with the somatostatin analogue SMS 201–995 in acromegalic patients |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 348-353
P. A. VAN LIESSUM,
W. P. M. HOPMAN,
G. F. F. M. PIETERS,
A. G. H. SMALS,
A. TANGERMAN,
J. B. M. J. JANSENJ,
G. ROSENBUSCH,
C. B. H. W. LAMERS,
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摘要:
Abstract.Long‐term treatment with the somatostatin analogue SMS 201–995 (SMS) might impair exocrine pancreatic function, secretion of cholecystokinin (CCK) and pancreatic polypeptide (PP), and pancreatic size. In five acromegalics on chronic treatment with SMS, we investigated postprandial 6‐h urinary excretion of p‐aminobenzoic acid (PABA) and p‐aminosali‐cylic acid (PAS) after s.c. injection of 100 μg SMS or placebo and after ingestion of 2 mmol nBT‐PABA and 2 mmol PAS.In the acromegalics, urinary PABA/PAS ratio (reflecting exocrine pancreatic function) after SMS was similar to that after placebo (P>0.10) and higher than in healthy volunteers (n= 8,P=0–05). The initial inhibition of plasma CCK secretion by SMS was cancelled during the 3rd h after the meal, whereas PP release remained completely abolished. Pancreatic size as measured by ultrasonography, was not reduced in seven acromegalics compared with 14 healthy volunteers.It is concluded that despite a blunted release of the trophic hormone CCK, long‐term treatment with SMS 201–995 neither induces an abnormally small pancreas nor deterioration of postprandial exocrine pancreatic function in pati
ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01869.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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4. |
Detection of autoantibodies to Sm antigen in systemic lupus erythematosus by immunodiffusion, ELISA and immunoblotting: variability of incidence related to assays and ethnic origin of patients |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 354-359
N. ABUAF,
C. JOHANET,
P. CHRETIEN,
B. I. ABSALON,
J. C. HOMBERG,
J. F. BURI,
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摘要:
Abstract.Autoantibodies to small nuclear ribonucleo‐proteins (snRNP) were studied using the techniques of immunodiffusion, ELISA, and immunoblotting in the sera of 150 patients with systemic lupus erythematosus (SLE), and of 29 patients with mixed connective tissue disease; 900 control patients and 100 normal blood donors were examined simultaneously. The incidence of anti‐Sm antibodies in French SLE patients was low compared with the occurrence observed in similar studies in USA (even when highly sensitive assays were used) but was of the same magnitude as European results. Frequency of anti‐Sm antibodies in SLE patients varied moderately when detected by immunodiffusion (12%), or by immunoblotting (17%), however, it seems that the ethnic and/or genetic background of patients induces more significant differences. SLE patients from the French West Indies had anti‐Sm antibodies in 39% of cases when detected by immunodiffusion and in 50% when immunoblotting was used. In these patients the incidence of the antibodies was five times more frequent than that of mainland French patients. Immunization against snRNP does not seem to be a common feature of all SLE p
ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01870.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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5. |
Castration inhibits glomerular hypertrophy and proteinuria in uninephrectomized male rats |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 360-365
U. GAFTER,
M. BEN‐BASSAT,
J. LEVI,
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摘要:
Abstract.Renal mass reduction may lead to glomerular hypertrophy, proteinuria and focal glomerulo‐sclerosis (FGS) in humans and rats. In humans and rats, females are less susceptible than males to these phenomena. This study was undertaken to evaluate the effect of male rat castration on the pathogenesis of proteinuria and FGS. Urinary protein was measured in 60‐day‐old male and female rats. Uninephrectomy was performed in all rats, and castration in half of the males. After 180 days, proteinuria, glomerular filtration rate (GFR) and blood biochemistry were determined. Kidneys were resected, weighed and subjected to morphologic studies. Following uninephrectomy, male rats developed severe proteinuria:132.3 pM 40.9 mg 24 h‐1, most of which was accounted for by an albuminuria of 70.9 pM 19.3 mg 24 h‐1. In contrast, protein excretion in female and castrated male rats remained within normal limits: 8.0 pM 1.8 and 4.2 pM 0.5 mg 24 h‐1, respectively. Mean glomerular volume in male rats was 1.18 pM 0.08 times 106μm3; much higher than in female rats, 0.84 pM 0.04 times 106μm3, and castrated male rats, 0.87 pM 0.03 times 106μm3(P<0.005). On light and electron microscopy, glomeruli of female and castrated male rats were completely normal. In contrast, in four of seven male rats, mild glomerular changes were observed. They consisted mainly of mesangial expansion, electron‐dense deposits and collapse of capillary loops. These data suggest that castration confers protection against the development of glomerular hypertrophy and proteinuria in uninephrectomized male rats. Endogenous testosterone may be associated with t
ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01871.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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6. |
Cellular targets and receptors for interleukin‐6 I. In vivo and in vitro uptake of IL‐6 in liver and hepatocytes |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 366-370
O. SONNE,
O. DAVIDSEN,
B. K. MØLLER,
C. MUNCK PETERSEN,
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摘要:
Abstract.Interleukin‐6 (IL‐6) is a potent stimulator of the hepatic synthesis of acute‐phase proteins.125I‐labelled IL‐6 disappeared from the blood of rats with an overall half‐time of about 1.5 min; 41% of the injected tracer dose was recovered in the liver by 15 min. The clearance was biphasic. The simultaneous injection of tracer and an excess of unlabelled IL‐6 eliminated the initial rapid phase, and reduced the hepatic uptake to 14%. Light microscopic autoradio‐graphy showed 5% of the grains over non‐hepatocytes, and 80% over hepatocytes, accumulating in areas around the bile canaliculi. Thereafter, degradation products accumulated in the bile. At 4d̀C, isolated rat hepatocytes bound IL‐6 with an apparentKdof 39 pmol 1‐1to a uniform class of 4500 receptors per cell with an apparent molar mass of 115–120 kg mol‐1. The HepG2 human hepatocellular cell line bound IL‐6 with an apparentKdof 21 pmol 1‐1to a uniform class of 1200 receptors per cell with an apparent molar mass of 155–160 kg mol‐1. At 37d̀C, both cell types endocytosed the bound ligand slowly, and degradation products appeared in the medium after a relatively long lag period (40 min in h
ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01872.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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7. |
Cellular targets and receptors for interleukin‐6 II. Characterization of IL‐6 binding and receptors in peripheral blood cells and macrophages |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 377-384
C. MUNCK PETERSEN,
O. DAVIDSEN,
S. K. MOESTRUP,
O. SONNE,
A. NYKJÆR,
B. K. MØLLER,
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摘要:
Abstract.Within 15 min, approximately 2–5% of125I‐labelled interleukin‐6 (IL‐6) injected intravenously into rats was taken up by the spleen. As determined by light microscopic autoradiography, uptake was mainly (60%) accounted for by macrophages in the red pulp.125I‐IL‐6 binding in rat peritoneal macrophages was quantitatively similar to that in cultured human monocytes and T‐cells. By comparison, IL‐6 binding to polymorphonuclear granulocytes and freshly isolated monocytes was low. Stimulation with antigen, but not with mitogen (PWM), induced receptor presentation in B‐cells, whereas antigen and mitogen downregulated the binding in T‐cells.At 4 C, labelled IL‐6 bound to cells with a half‐time of about 1.5 h. Binding appeared reversible, but dissociation was slow and incomplete. The apparentKdfor IL‐6 binding was about 30 pmol 1‐1in most cell types, however, values of approximately 120 pmol 1‐1were obtained in polymorphonuclear granulocytes. At 37cC,125I‐IL‐6 was rapidly internalized by T‐cells and monocyte‐macrophages, and after a lag time, TCA‐soluble radioactivity was released from the cells following a sigmoidal curve. Polyacrylamide gel electro‐phoresis of radiolabelled IL‐6 cross‐linked to its binding sites in T‐cells, yielded receptor‐ligand complexes with molar masses of 70–80 and 120–140 kg mo‐1. This would
ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01873.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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8. |
Further studies on the mechanism of the natriuretic response to low‐dose dopamine in man: effect on lithium clearance and nephrogenic cAMP formation |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 385-391
D. F. SCHOORS,
A. G. DUPONT,
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摘要:
Abstract.The effect of intravenous infusion of low‐dose dopamine on electrolyte excretion, lithium clearance, nephrogenous cAMP formation and renal hae‐modynamics was investigated in healthy volunteers. Dopamine significantly increased the urine flow rate by 70.6% and urinary sodium excretion by 72%, but did not change creatinine clearance, PRA or plasma levels of AVP, ANP and cAMP. Renal plasma flow significantly increased by 48.6%; the glomerular filtration rate was not changed.Lithiumper seincreased basal PRA, but had no effect on the increments of urine flow rate, sodium excretion and renal blood flow induced by dopamine. Dopamine significantly increased the fractional excretion of lithium (representing fractional excretion of sodium at the proximal level). The increase in urinary sodium excretion during dopamine infusion, significantly correlated with the increase in fractional excretion of lithium (r= 0.94;P0.01). No correlation was found between the increase in urinary sodium excretion and the increase in renal blood flow.In conclusion, this study confirms that low‐dose dopamine increases renal blood flow and urinary sodium excretion in healthy volunteers. This natriuretic response appears to be due to interaction with proximal tubular dopamine receptors, which are positively coupled to adenylate cyc
ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01874.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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9. |
Dexamethasone increases preproparathyroid hormone messenger RNA in human hyperplastic parathyroid cells in vitro |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 392-397
M.‐N. PERALDI,
E. RONDEAU,
V. JOUSSET,
A. EL M'SELMI,
R. LACAVE,
F. DELARUE,
J.‐M. GAREL,
J.‐D. SRAER,
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摘要:
Abstract.To determine if parathyroid hormone release in man is directly stimulated by glucocorticoids, dispersed human parathyroid cells from hyperplastic glands obtained from eight renal transplant recipients were studied in vitro. Dexamethasone (10‐11to 10‐6mol 1‐1) increased PTH release in a time‐ and dose‐dependent manner. A plateau was reached at 10‐8mol 1‐1(1015pM 149 vs. 230pM27 pg 10‐4cells for control value, after 24 h incubation;P<0.0001). An interaction with a glucocorticoid receptor was suggested since 10‐6mol 1‐1RU 486 blunted the dexamethasone‐induced PTH release. By Northern blot analysis, dexamethasone was found to increase the amount of preproPTH mRNA in these cells. The effect of dexamethasone was probably at the gene level since (1) 1,25 dihydroxy vitamin D3inhibited both iPTH and pre‐proPTH mRNA increases induced by dexamethasone and (2) alpha‐amanitin (1,25 μg ml‐1) also completely suppressed the dexamethasone‐induced PTH release. Thus, for the first time, we demonstrate that dexamethasone induces an increase of PTH synthesis, probably by increasing PTH gene transcription. This effect may play an important pathogenic role in persisting hyper‐parathyroidism and steroid‐induced bone complicatio
ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01875.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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10. |
Platelet aggregability in humans: contrastingin vivoandin vitrofindings during sympatho‐adrenal activation and relationship to serum lipids |
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European Journal of Clinical Investigation,
Volume 20,
Issue 4,
1990,
Page 398-405
P. T. LARSSON,
P. HJEMDAHL,
G. OLSSON,
B. ANGELIN,
G. HORNSTRA,
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摘要:
Abstract.Platelet aggregability was studied in 18 healthy volunteers during mental stress (a colour word test; CWT) and low‐ and high‐dose adrenaline infusions using an ex vivo technique (filtragometry) and conventional in vitro aggregometry. CWT and high‐dose adrenaline (3–4 nmol 1‐1in plasma) shortened filtragometry readings, suggesting increased platelet aggregabilityin vivo. Low‐dose adrenaline had no effect despite higher adrenaline levels in plasma (0.9 nmol I‐1) than during CWT (0.4 nmol I‐1). Platelet sensitivity to ADPin vitrowas reduced following CWT and further reduced following adrenaline infusions.In vitro, adrenaline (50 nmol I‐1) had little effect on platelet aggregationper se, but enhanced aggregability evoked by ADP (at ED50). Adrenaline potentiation of ADP‐induced aggregation was enhanced after CWT, but was not related to filtragometry responsiveness to stressin vivo. Serum LDL‐cholesterol levels were inversely correlated to filtragometry readings at rest, suggesting an adverse influence on platelet aggregabilityin vivo.HDL‐cholesterol levels were inversely correlated to platelet sensitivity to ADPin vitro, suggesting a positive influence. Thus, sympathp‐adre‐nal activation enhances platelet aggregabilityin vivo(as assessed by ex vivo filtragometry), but adrenaline alone cannot explain the pro‐aggregatory effect of mental stress. Serum lipoprotein alterations associated with increased risk for atherosclerosis seem to enhance platelet aggregability. The conventionalin vitrotechnique may poorly reflect p
ISSN:0014-2972
DOI:10.1111/j.1365-2362.1990.tb01876.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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