Das Wachstum des Geweihes von Cervus elaphus,Cervus barbarus und Cervus canadensis

Ohne Zusammenfassung     

The hard lives of trees in African savanna—Even without elephants

The ongoing loss of large trees and densification of shrubs are two prevalent processes that take place in African savannas, with profound consequences for their structure and function. We evaluated herbivore impacts on savanna woody communities using a long-term exclosure experiment in the Kruger National Park, South Africa, with three treatments: the exclusion of large mammals only (i.e. elephant and giraffe), exclusion of all herbivores larger than a hare, and areas open to all herbivores. We asked three questions: (1) How did variable exclusion of herbivores affect woody density and structure across the catena (i.e. riparian, sodic and crest vegetation)? (2) Did the exclusion of herbivores result in unique woody species composition? (3) Did herbivore exclusion result in a higher proportion of palatable species? After 17 years, we found that herbivores mainly affected the heights and densities of existing species, rather than leading to turnover of woody species assemblages. Although densities of individuals increased in the full exclosure (350 ha⁻¹), the change was more moderate than expected. By contrast, mixed mega-and meso-herbivores decreased the number of trees and shrubs (decreases of 780 ha⁻¹) via a variety of physical impacts. Meso-herbivores alone, on the other hand, had less impact on individual density (i.e. no change), but limited average height growth and canopy dimensions in certain habitat types. Where elephants are present, they are effective at reducing the density of woody stems to the point of counteracting woody encroachment, but at the same time are actively preventing the persistence of large trees (>5 m) as well as preventing trees from recruiting to larger size classes. However, the lack of massive recruitment and woody cover increases with elephant exclusion, especially for more preferred species, suggests that factors beyond elephants, such as dispersal limitation, seed predation, and drought, are also acting upon species.     

Isolation and partial characterization of the human erythrocyte band 7 integral membrane protein.

Monoclonal antibodies to the Mr 31,000 major integral membrane protein of the human erythrocyte band 7 region were used to identify the corresponding polypeptide chain and epitope-carrying fragments on immunoblots. Analysis of the erythrocyte membrane, membrane fractions, and cytosol revealed that the Mr 31,000 band 7 integral membrane protein is unique and not related to any of the other water-soluble or membrane-bound band 7 components. Cross-reacting proteins were identified in the membranes of other mammalian erythrocytes and in cell lines of epithelial and lymphoid origin. Proteolytic digestion of intact human erythrocytes or erythrocyte membranes demonstrated that the band 7 integral membrane protein has an intracellular domain larger than Mr 12,000; it does not have an extracellular one. One of the monoclonal antibodies was employed for the isolation of band 7 integral membrane protein by immunoaffinity chromatography; subsequent Edman degradation revealed a blocked N-terminus.     

Molecular cloning and expression of human and rat tumor necrosis factor receptor chain (p60) and its soluble derivative, tumor necrosis factor-binding protein.

Tumor necrosis factor-alpha (TNF-alpha), a protein released by activated macrophages, is involved in a wide variety of human diseases including septic shock, cachexia, and chronic inflammation. TNF binding protein (TNF-BP), a glycoprotein with high affinity to TNF-alpha isolated from urine, acts as an inhibitor of TNF-alpha by competing with the cell-surface TNF receptor. We report here the partial amino acid sequencing of human TNF-BP as well as the isolation, sequence, and expression of cDNA clones encoding a human and rat TNF receptor. The calculated Mr of the mature human and rat TNF receptor chains is 47,526 and 48,072, respectively. The extracellular ligand binding domain represents the soluble TNF-BP which is released by proteolytic cleavage. TNF-BP contains 24 cysteine residues and three potential N-glycosylation sites and shows sequence homology to the extracellular portions of TNF-R p80 chain and nerve growth factor receptor. Transfection of the human TNF receptor cDNA into mammalian cells resulted in increased binding capacity for TNF-alpha and increased reactivity with a monoclonal antibody directed against the human TNF receptor chain p60. When a stop codon was introduced into the cDNA at the site corresponding to the carboxyl terminus of TNF-BP, transfected cells secreted a protein that reacted with antibodies raised against natural TNF-BP.     

Organismen als Holismen

Zusammenfassung Ziel der Abhandlung ist die Untersuchung der grundlegenden Prinzipien einer autonombiologischen Kausalität. Wenn die Biologie in autonomer Weise auf ihr gemässe Prinzipien gegründet werden soll —wie das die Physik in ihrer Sphäre auch durchgeführt hat —, dann muss das biologische Denken sich zunächst von einem Idol befreien, das ihr von der klassischen Physik aufgezwungen ist. Das ist der Begriff des Mechanismus, der bei seiner Schaffung gewiss von grossem Werte auch für die Biologie gewesen ist, der aber heute dem biologischen Denken grossen Schaden dadurch zufügt, dass er es in eine ihm völlig fremde Richtung zwängt.Die Organismen und alle ihre Organe von der einfachsten Zellorganelle bis zum komplexesten Organsystem sind aber keine Mechanismen sondern Holismen (Smuts). Es wird versucht, die wesentlichen Kriterien des Holismusprinzips zu bestimmen. Zunächst gilt für sie das Axiom von v.Ehrenfels, demzufolge jeder Holismus mehr ist als die Summe seiner Teile. Das wird im einzelnen genauer analysiert. Weiterhin gilt für Holismen das Kompensationsprinzip vonGoethe. Damit im Zusammenhang stehen die Prinzipien der spezifischen Energie vonJohannes Müller, das Prinzip vonRedi (Omne Vivum ex Vivo), das Prinzip vonVernadsky über die Konstanz der Biosphäre, das Prinzip der phylogenetischen Kompensationen und das Prinzip von der Ektropie der Biosphäre.Alle diese Prinzipien werden im einzelnen diskutiert und analysiert. In engstem Zusammenhang miteinander bilden sie ein autonomes Axiomengefüge für die Biologische Erkenntnis, durch welches wiederum die eigentümlich biologische Kausalität charakterisiert ist. Genau in diesem Sinne sind Holismen verae causae (Smuts).

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Contenido El presente ensayo tiene por fin supremo la investigación de los principios basicos de una autónoma causalidad biologica. Si se quiere fundar la Biologia en sus propios principios autónomos —como se lo ha hecho también con la Fisica misma —, entonces será primeramente necesario que la Biologia se delibera de una ideologia completamente extraña para ella, la cual la Fisica clásica le ha transferido. Esto es el concepto del mecanismo, que en su origin ha sido de gran valor también para la Biologia, pero que hoydia produce enorme daño a la Biologia.Los organismos y todos sus órganos de la mas simple organela celular hasta el mas complicado sistema de órganos sin embargo de ninguna manera no son mecanismos sino al contrario holismos (Smuts). Ahora se ensaya de determinar los criterios esenciales del principio del holismo. Primero es valido para los holismos el axioma de v.Ehrenfels que dice que cada Organismo representa más que la suma de sus partes. Además vale para holismos el principio de la compensación deGoethe. Con esto están relacionados los principios de la energia especifica deJuan Müller, el axioma deRedi (Omne Vivum ex Vivo), el principio deVernadsky acerca de la constancia de la biósfera, el principio de las compensaciones filogenéticas y el principio de la ectropia de la biósfera.Todos los mencionados principios y axiomas serán discutidos y analizados en sus particularidades. En su conjunto representan ellos un sistema de axiomas autónomos para el conocimiento biológico, el cual como tal caracteriza también la asi llamada causalidad biologica. Precisamente en tal sentido son los holismos verae causae (Smuts).

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Diese Abhandlung ist Herrn Prof. Dr. v.Buddenbrock in Verehrung zum 70. Geburtstag dargebracht.     

Regulation of diacylglycerol levels in carbachol-stimulated pancreatic acinar cells: relationship to the breakdown of phosphatidylcholine and metabolism to phosphatidic acid.

Rat pancreatic acinar cells prelabeled with [14C]palmitic acid and then exposed to carbachol (CCh) exhibited a time-dependent increase in 1,2-[14C]diacylglycerol ([14C]DAG) levels, which was first detected at 2 min and then continued to rise in a linear manner. There was a concomitant increase in [14C]phosphatidic acid, which plateaued after 2 min and then remained at steady-state levels. CCh also promoted the release of phosphocholine, but not choline, within 60 s and caused a decrease in [14C]phosphatidylcholine in cells prelabeled with [14C]glycerol after 15 min. The inability to detect a rise in [14C]phosphatidylethanol accumulation and a fall in [14C]phosphatidate levels in [14C]palmitate prelabeled cells after exposure to CCh plus ethanol documented the absence of a phospholipase D-mediated pathway. The rapid phosphorylation of diglyceride in homogenates from unstimulated and carbachol-treated cells increased with increasing concentrations of exogenous substrate, thereby affirming that carbachol stimulates the phosphorylation of DAG by promoting the accumulation of the diglyceride. These collective findings provide evidence for the existence of an integrative control mechanism for regulating endogenous DAG levels during pancreatic acinar cell activation involving phosphatidylcholine-specific phospholipase C and DAG kinase.