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  • 1
    Electronic Resource
    Electronic Resource
    Effects of propranololin vitro andin vivo on platelet function and thromboxane formation in normal volunteers (1983)
    Springer
    Inflammation research 13 (1983), S. 29-34 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In vitro andex vivo effects of propranolol on platelet aggregation, formation of thromboxane B2 (TXB2) and platelet sensitivity to prostacyclin were studied in healthy men. Propranolol, addedin vitro to platelet rich plasma (PRP) inhibited platelet aggregation and TXB2 formation induced by ADP, 1-epinephrine, collagen and arachidonic acid. Concentration of 20–100 μM propranolol were effective when ADP, 1-epinephrine and collagen were used as stimuli. Higher concentrations (250–500 μM) were needed to inhibit aggregation induced by arachidonic acid. Oral administration of propranolol either as a single dose (120 mg) or for one week (3×40 mg/day) did, however, not affect platelet aggregation, thromboxane formation and platelet sensitivity to prostacyclin. In addition, withdrawal of propranolol was without effect on these parameters. Although propranolol has potent effects on platelet functionin vitro, it seems that the blood levels achievable by oral administration of propranolol are too low to affect platelet aggregation and TXB2 formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01994278
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  • 2
    Electronic Resource
    Electronic Resource
    Renal factors in juvenile hypertension (1980)
    Springer
    Journal of molecular medicine 58 (1980), S. 1099-1104 
    Details
    ISSN: 1432-1440
    Keywords: Juvenile Hypertonie ; Niere ; Prostaglandine ; Kallikrein ; Renin ; Juvenile hypertension ; Kidney ; Prostaglandins ; Kallikrein ; Renin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Essential hypertension in infancy, once believed to occur rarely if ever, is now increasingly recognized as a potential precursor of essential hypertension in adulthood. The mechanisms responsible for hypertension in childhood and adolescence are only beginning to be delineated. Renal factors assumed to be operative in juvenile hypertension are involving either volume control (by renal regulation of sodium-chloride and water balance) or vasoactive substances like the kallikrein-kinin, the renin-angiotensin and the prostaglandin system and other less well defined hormones. There is a close interrelationship of all these hormones with each other as well as a close linking of these vasoactive compounds to the renal regulation of sodium-chloride and water balance, thus interfering with a major environmental factor necessary for the development of essential hypertension. At present, data are insufficient to delineate a single hormone or a single hemodynamic abnormality as the only primary factor in juvenile hypertension. Further research into the pathomechanisms responsible for the elevation of blood pressure at its very beginning will improve our understanding of hypertension and possibly benefit its management by early intervention.
    Notes: Zusammenfassung Abweichend von früheren Auffassungen wird heute zunehmend die essentielle Hypertonie als eine Erkrankung auch des Kindes- und Jugendalters angesehen, aus der sich später die essentielle Hypertonie des Erwachsenen entwickelt. Die zur Entstehung der juvenilen Hypertonie führenden Pathomechanismen wurden in klinischen, epidemiologischen und tierexperimentellen Studien untersucht. Zu den renalen Mechanismen, die wahrscheinlich bei der Entstehung der juvenilen Hypertonie eine Rolle spielen, gehören Faktoren, die die renale Kontrolle der Salz-Wasser-Bilanz beeinflussen und vasoaktive Substanzen wie das renale Kallikrein-Kinin-System, das Renin-Angiotensin-System, das Prostaglandin-System und andere bislang weniger gut definierte Hormone. Diese renalen Hormone haben zahlreiche Wechselwirkungen untereinander. Neben ihren direkten Wirkungen auf die Gefäßwand können sie die Salz-Wasser-Bilanz beeinflussen bzw. werden von ihr beeinflußt, wodurch eine enge Verbindung mit Kochsalz, dem wohl entscheidendsten Umweltfaktor für die Entstehung der essentiellen Hypertonie, hergestellt ist. Fortgesetzte Bemühungen um die Aufklärung insbesondere der renalen Pathomechanismen, die am Beginn der Blutdruckerhöhung im Kindes- und Jugendalter wirksam sind, werden das Verständnis der essentiellen Hypertonie verbessern und unter Umständen durch frühzeitige Intervention sogar die Prävention dieser Erkrankung ermöglichen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01476880
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  • 3
    Electronic Resource
    Electronic Resource
    Arachidonic acid metabolites, hypertension and arteriosclerosis (1982)
    Springer
    Journal of molecular medicine 60 (1982), S. 479-488 
    Details
    ISSN: 1432-1440
    Keywords: Prostaglandins ; Hypertension ; Kidney ; Platelets ; Arteriosclerosis ; Prostaglandine ; Hypertonie ; Niere ; Thrombozyten ; Arteriosklerose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Blutdruckhöhe wird durch komplexe Wechselwirkungen verschiedener Mechanismen bestimmt, die sowohl den Blutfluß als auch den Widerstand des Gefäßsystems beeinflussen. Ein Übergewicht der Faktoren, die den Gefäßwiderstand oder das Extrazellulärvolumen vergrößern, führt zu einem Anstieg des Blutdrucks. Solch ein Ungleichgewicht kann z.B. durch eine erhöhte Aktivität des sympathischen Nervensystems und des Renin-Angiotensin-Systems oder durch eine gesteigerte Mineralocorticoid-Sekretion verursacht sein. Ebenso könnte eine verminderte Aktivität blutdrucksenkender Faktoren wie der Prostaglandine oder des Kallikrein-Kinin-Systems zu einem Anstieg des Blutdrucks führen. In dieser Arbeit wird die mögliche Rolle der Prostaglandine für die Pathophysiologie der essentiellen Hypertonie und degenerativer Gefäßerkrankungen dargestellt, basierend auf der Beteiligung von Prostaglandinen an der Kontrolle des Gefäßwiderstandes, der renalen Regulation des Extrazellulärvolumens und der Thrombozyten-Gefäßwand-Wechselwirkung. Ein Ungleichgewicht der Synthese bestimmter Prostaglandin-Endoperoxid-Metabolite könnte zur Hochdruckentstehung beitragen, auch ohne Vorliegen einer erhöhten Aktivität der bekannten blutdrucksteigernden Faktoren. Dabei könnte die Beteiligung der Prostaglandine an der Entstehung von Hochdruck und degenerativer Gefäßerkrankung sowohl auf einer primären Abnormalität beruhen als auch in einer Mittlerrolle für bekannte Risikofaktoren wie hohe Kochsalz-und Fettzufuhr bestehen. Spezifische Blockade oder Stimulation bestimmter Biosynthesewege, die zu gegensätzlich wirksamen Prostaglandinen führen, oder Änderung der nutritiven Zufuhr von Prekursor-Fettsäuren sollte zu einem besseren Verständnis zugrunde liegender Pathomechanismen und zu neuen Ansatzpunkten für Therapie oder Prävention dieser Herz-Kreislauferkrankungen führen.
    Notes: Summary The level of arterial blood pressure is set by complex interactions of several mechanisms which influence both blood flow in and resistance of the vascular system. An imbalance favouring elevation of vascular resistance or extracellular volume will result in hypertension. Such alterations may include increased activity of the sympathetic nervous system, of the renin-angiotensin system, or excessive secretion of mineralocorticoids. Of equal importance may be a reduced activity of blood pressure-lowering factors such as prostaglandins and the kallikrein-kinin system. This paper describes the possible significance of prostaglandins in the pathophysiology of hypertension and in degenerative vascular disease, based on their involvement in the control of vascular resistance, renal regulation of extracellular volume and plateletvessel wall interactions. An abnormality in the biosynthesis of certain prostaglandin endoperoxide metabolites may lead to hypertension even without an increase in the activity of the classic blood-pressure-elevating systems. The contribution of prostaglandins for the development of hypertension and degenerative vascular disease may be based on an inherent abnormality of the prostaglandin system, as well as on the effects of major risk factors such as dietary intake of sodium and fat on prostaglandin synthesis. Specific blockade or stimulation of distinct biosynthetic pathways leading to antagonistically acting prostaglandins and nutritional manipulation of precursor fatty acids should lead to a better understanding of the pathomechanisms involved and may offer new strategies for therapy or prevention of these cardiovascular disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01756093
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  • 4
    Electronic Resource
    Electronic Resource
    Rapid increase of mineralocorticoids after furosemide in low-renin essential hypertension: Evidence for 18-hydroxycorticosterone to be a better marker than aldosterone (1982)
    Springer
    Journal of molecular medicine 60 (1982), S. 847-852 
    Details
    ISSN: 1432-1440
    Keywords: Low-renin essential hypertension ; Furosemide ; Plasma renin activity ; Aldosterone ; 18-Hydroxycorticosterone ; Low-renin Hypertonie ; Furosemid ; Plasmareninaktivität ; Aldosteron ; 18-Hydroxycorticosteron
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das Verhalten der Plasmareninaktivität (PRA), des Plasmaaldosterons, des 18-Hydroxycorticosterons (18-OH-B), des 18-Hydroxydeoxycorticosterons (18-OH-DOC) und des Corticosterons wurde nach Furosemid an 20 Normalpersonen, 16 Patienten mit normal-renin Hypertonie (NREH) und 12 Patienten mit low-renin Hypertonie (LREH) untersucht. Die Blutentnahmen erfolgten unmittelbar vor der Gabe von 40 mg Furosemid i.v. sowie 15 min (im Liegen) und 120 min (aktive Orthostase) danach. Die Normalpersonen zeigten 15 min nach Furosemid einen Anstieg der PRA von 0,8±0,4 ng AI/ml·min (SD) auf 3,4±1,4 (P〈0,01), des Plasmaaldosterons von 109±28 pg/ml auf 139±40 (P〈0,01) und des 18-OH-B von 199±90 pg/ml auf 279±85 (P〈0,01). Bei Patienten mit NREH stieg die PRA signifikant geringer an (P〈0,01). Dementsprechend wurde kein signifikanter Anstieg des Plasmaaldosterons und des 18-OH-B gefunden. Bei Patienten mit LREH blieb die PRA (basal 0,2±0,1) 15 min nach Furosemid praktisch unverändert. Das Plasmaaldosteron jedoch stieg von 111±37 auf 160±66 (P〈0,05) und das 18-OH-B von 162±101 auf 261±71 an (P〈0,01). Der relative Anstieg des 18-OH-B bei Patienten mit LREH war im Vergleich zu Patienten mit NREH signifikant höher. 120 min nach Furosemid lagen die Plasmaspiegel des Aldosterons und des 18-OH-B bei Normalpersonen signifikant höher als in den beiden Patientengruppen (P〈0,01). Die Corticosteron und 18-OH-DOC Plasmaspiegel zeigten zwischen den untersuchten Gruppen kein differentes Verhalten, und es fand sich nur 120 min nach Furosemid in Kombination mit aktiver Orthostase ein signifikanter Anstieg. Die Ergebnisse zeigen, daß die Sekretion der Mineralcorticoide bei Patienten mit LREH unmittelbar nach Furosemid gesteigert ist, obwohl die PRA unverändert bleibt. 18-OH-B ist anscheinend für dieses Phänomen ein empfindlicherer Index als Aldosteron.
    Notes: Summary The response of plasma renin activity (PRA), plasma aldosterone, 18-hydroxycorticoster-one (18-OH-B), 18-hydroxydeoxycorticosterone (18-OH-DOC) and corticosterone to furosemide were compared in 20 normal control subjects, 16 patients with normal-renin essential hypertension (NREH) and 12 patients with low-renin essential hypertension (LREH). Analyses were performed before medication, and 15 min (supine) and 120 min (active orthostasis) after IV administration of 40 mg furosemide. In normotensive subjects PRA increased 15 min after administration of furosemide from 0.8±0.4 ng AI/ml·h (SD) to 3.4±1.4 (P〈0.01), plasma aldosterone from 109±28 pg/ml to 139±40 (P〈0.01) and 18-OH-B from 199±90 to 279±85 (P〈0.01). In patients with NREH, PRA increased significantly less (P〈0.01) and no significant increase of plasma aldosterone or 18-OH-B was found. PRA of patients with LREH (0.2±0.1 ng AI/ml·h) remained practically unchanged 15 min after furosemide administration, but in contrast to NREH aldosterone increased from 111±37 to 160±66 (P〈0.05) and 18-OH-B from 162±101 to 261±71 pg/ml (P〈0.01). The relative increase of plasma 18-OH-B was significantly greater in patients with LREH than in patients with NREH. The plasma levels of aldosterone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P〈0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P〈0.01) only at 120 min after furosemide administration combined with active orthostasis. In summary, our results support the concept that sensitivity of the mineralocorticoid-producing cells is enhanced in patients with LREH. Postfurosemide 18-OH-B seems to be a better marker of this phenomenon than aldosterone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01728351
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  • 5
    Electronic Resource
    Electronic Resource
    Clinical and biochemical features of patients with aldosterone-producing adenoma and idiopathic hyperaldosteronism (1983)
    Springer
    Journal of molecular medicine 61 (1983), S. 35-42 
    Details
    ISSN: 1432-1440
    Keywords: Primary aldosteronism ; 18-Hydroxycorticosterone ; 18-Hydroxydeoxycorticosterone ; Saline infusion ; Angiotensin II ; Metoclopramide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Eight patients with aldosterone-producing adenoma (APA) (7 histologically proved) and 6 patients with idiopathic hyperaldosteronism (IHA) (2 histologically proved) were evaluated for differential diagnosis using clinical, radiographic, and biochemical parameters. Mean basal plasma aldosterone (445±146 (SD) pg/ml), 18-hydroxycorticosterone (975±394 pg/ml), and 18-hydroxydeoxycorticosterone levels (374±266 pg/ml) and mean diastolic blood pressure were significantly higher in patients with APA (p〈0.05 andp〈0.01), whereas mean plasma potassium levels and stimulated plasma renin activity were lower in subjects with APA as compared to patients with IHA (p〈0.01 andp〈0.01). Radiographic procedures predicted the correct diagnosis in 3 of 8 operated cases (37%) and selective adrenal vein sampling in 5 of 6 cases (83%). Urinary aldosterone excretion (30±10 µg/24 h) was suppressed inall patients with IHA after a 21 isotonic saline infusion in 2 h (13±6,p〈0.01). Inall patients with APA, however, aldosterone excretion wasnot suppressible (basal: 36±12). Plasma aldosterone levels of some patients with APA could be reduced by saline infusion and the response was not characteristically different between both groups. After 10 mg metoclopramide iv. the slopes of plasma aldosterone levels were similar for patients with APA and normal subjects. Patients with IHA showed a different secretion pattern with a delay of both the increase and the decline of aldosterone levels. Graded angiotensin II infusions (subpressor doses for normotensive individuals) did not increase plasma aldosterone levels in patients with APA. However, in patients with IHA, excessive increases of aldosterone levels were seen (basal: 268±54 pg/ml, after 4 ng A II/kg−1·min−1: 806±262). From these data, we conclude that patients with APA could be reliably identified before operation by determination of urinary aldosterone before and after a simple saline infusion test. Additionally, plasma aldosterone levels after metoclopramide iv. or angiotensin II infusions may be helpful diagnostic tools.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01484437
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  • 6
    Electronic Resource
    Electronic Resource
    Urinary prostaglandins in human neonates: Relationship to kidney function and blood pressure (1980)
    Springer
    Journal of molecular medicine 58 (1980), S. 449-455 
    Details
    ISSN: 1432-1440
    Keywords: Blutdruck ; Neugeborene ; Prostaglandine ; Niere ; Osmolalität ; Blood pressure ; Neonates ; Prostaglandins ; Kidney ; Osmolality
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary We studied the excretion of prostaglandin (PG) E2 and of PGF2α in 172 healthy newborns during the first week of life to detect possible biochemical markers for the individual susceptibility to hypertension. PG excretion was compared to urinary electrolytes, urinary osmolality, and blood pressure. In addition, blood pressure of the newborns was related to the blood pressure of the mothers and to the history of hypertension in parents and/or grandparents. PGE2-excretion increased from 0.7 ng/mg creatinine on the third day to 1.5 ng on the fifth day of life (p〈0.001) while PGF2α excretion remained unchanged at 2 ng/mg creatinine. PGE2 (but not PGF2α) was inversely correlated to urinary osmolality (p〈0.001) while urinary potassium was positively correlated to PGF2α (p〈0.001). On the fifth day of life systolic blood pressure of the newborns was correlated to PGF2α-excretion and to systolic blood pressure of the mother (p〈0.05). Blood pressure was significantly higher in newborns with a history of hypertension in parents or grandparents than in those without hypertension in relatives (p〈0.02). The data suggest that renal PG:s are involved in the regulation of urinary osmolality and potassium excretion in the neonate. The positive correlation between PGF2α excretion and blood pressure may indicate a genetically determined PG-related renal influence on the level of systemic blood pressure.
    Notes: Zusammenfassung Auf der Suche nach einem biochemischen Parameter als Marker für die Hypertonie-Gefährdung wurde bei 172 gesunden Neugeborenen am 3. und 5. Lebenstag die Ausscheidung von PGE2 und von PGF2α gemessen und mit dem Blutdruck, der Elektrolytausscheidung sowie der Urinosmolalität verglichen. Daneben wurde der Blutdruck der Neugeborenen in Beziehung gesetzt zum Blutdruck der Mutter und zur Hypertonie-Anamnese in den Familien der Eltern. Die PGE2-Ausscheidung stieg von 0,7 ng/mg Kreatinin am 3. Tag auf 1,5 am 5. Tag (p〈0,001), während die PGF2α-Exkretion bei 2 ng/mg Kreatinin konstant blieb. Es bestand eine inverse Korrelation zwischen PGE2 und der Urinosmolalität (p〈0,001), während die Kalium-Ausscheidung positiv zur PGF2α-Exkretion korreliert war (p〈0,001). Am 5. Lebenstag war der systolische Blutdruck der Neugeborenen signifikant korreliert zu der PGF2α-Ausscheidung (p〈0,05). Es bestand weiterhin eine positive Korrelation des systolischen Blutdrucks der Neugeborenen zum systolischen Blutdruck der Mütter (p〈0,05). Der Blutdruck bei Neugeborenen mit Hypertonie in der Familienanamnese war bereits in der ersten Lebenswoche signifikant höher als der Blutdruck bei Kindern ohne Hypertonie bei Eltern und/oder Großeltern. Die Untersuchungen deuten darauf hin, daß beim Neugeborenen renale Prostaglandine bei der Regulation der Urinosmolalität und der Kalium-Ausscheidung beteiligt sind. Die positive Korrelation zwischen PGF2α-Ausscheidung und Blutdruck wird als möglicher Marker eines genetisch determinierten Einflusses des renalen PG-Systems auf die Blutdruckregulation gedeutet.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01476799
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  • 7
    Electronic Resource
    Electronic Resource
    Niedrig dosierte Acetylsalicylsäure (100 mg/Tag) nach aortokoronarer Bypassoperation (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 458-464 
    Details
    ISSN: 1432-1440
    Keywords: Aspirin® ; Coronary Bypass ; Coronary Heart Disease ; Platlets ; Platlet Inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A prospective, randomized, doubleblind, placebo-controlled trial was conducted to evaluate the efficacy of Acetylsalicylic Acid (ASS) (100 mg/d, starting 24 h after operation) on vein graft patency. Sixty of 88 patients having undergone surgery entered the study; in 24 of 31 patients in the placebo group and 22 of 29 patients in the ASS-group angiography was performed 4 months postoperatively. There were no significant differences between the groups with respect to age, number of diseased vessels or previous myocardial infarctions. Mean number of grafts per patient was 2,2 (placebo) and 1,8 (ASS) for proximal anastomoses (p〈0.10) and 3.4 (placebo) and 2.6 (ASS) for distal anastomoses (p〈0.05). Graft occlusion rate for proximal anastomoses was less in the ASS-group, 10% (4/40), as compared with placebo 32% (17/53) (p〈0.05). Graft occlusion rate for distal anastomoses was also less in the ASS group, 19% (11/57) as compared to 35% (28/81) in the placebo group (p〈0.10). All grafts were patent in 16/22 patients in the ASS group but only in 9/24 in the placebo group (p〈0.05). On designation of patients without postoperative angiograms but cardiovascular events as well as those with at least one graft occluded as “failures”, the incidence of the latter was 9/29 in the ASS group and 20/31 in the placebo group (p〈0.05). Early postoperative bleeding was similar in both groups, no side effects of ASS were observed. In this trial with initiation of low — dose ASS therapy 24 h after operation, antiplatlet therapy reduced the graft occlusion rate significantly.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01726907
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  • 8
    Electronic Resource
    Electronic Resource
    Prostaglandin excretion after furosemide in normal and low-renin essential hypertension (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 777-782 
    Details
    ISSN: 1432-1440
    Keywords: Prostaglandins ; Furosemide ; Renin ; Potassium ; Kidney function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined the urinary excretion of prostaglandin (PG)E2 and PGF2α before and 15 min after stimulation with the acutely vasodilating agent furosemide in 25 normotensive controls and 81 patients with essential hypertension (EH). After furosemide administration, PGE2 excretion was lower in patients with EH (P〈0.02). Excretion rates of PGF2α and of sodium, and urinary volume in hypertensive patients were not significantly different from the values found in normotensive controls. Patients with low-renin essential hypertension (LREH) had a significantly reduced excretion of both PGE2 and PGF2α before and after administration of furosemide as compared to controls. The difference in PGF2α excretion was also significant when LREH patients were compared to those with normal-renin essential hypertension (NREH). Patients with LREH were older and excreted less potassium than patients with NREH or normotensive controls. We conclude that the reduced PG excretion immediately after furosemide administration in patients with EH reflects a diminished capacity of the hypertensive kidney to generate prostaglandins which exert an overall vasodilating effect. Since renin secretion is under the control of renal PG formation, the decreased responsiveness of plasma renin activity (PRA) observed in patients with EH and predominantly in those with LREH may be the consequence of a decreased renal cortical PG generation. Alternatively, mechanisms that reduce both PRA and PG generation have to be considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01721777
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  • 9
    Electronic Resource
    Electronic Resource
    Electrostatic orientation during electron transfer between flavodoxin and cytochrome c (1983)
    [s.l.] : Nature Publishing Group
    Nature 301 (1983), S. 169-171 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Figure la, b shows the 2kT electrostatic potential fields around tuna ferricytochrome c10 at two ionic strengths. The fields were computed from the crystallographic coordinates11 using a modified Tanford-Kirkwood theory which scales the local dielectric constant of the charged groups according to ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/301169a0
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  • 10
    Electronic Resource
    Electronic Resource
    Photobiology in space: An experiment on Spacelab I (1984)
    Springer
    Origins of life and evolution of the biospheres 14 (1984), S. 825-832 
    Details
    ISSN: 1573-0875
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Geosciences
    Notes: Abstract The joint European/US Spacelab Mission I, scheduled for October 1983 for a 9 day lasting Earth-orbiting flight, provides a laboratory system for various disciplines of science, including exobiology. On the pallet, in the experiment ES 029 “Microorganisms and Biomolecules in Space Hard Environment” 316 dry samples ofBacillus subtilis spores will be exposed to space vacuum and/or selected wavelengths of solar UV radiation. After recovery action spectra of inactivation, mutation induction, reparability and photochemical damage in DNA and protein will be determined. The results will contribute to the understanding of the mechanism of the increased UV sensitivity of bacterial spores in vacuo and to a better assessment of the chance of survival of resistant life forms in space and of interplanetary transfer of life.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00933739
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