CABI:20153174020Understanding how plants are constructed - i.e., how key size dimensions and the amount of mass invested in different tissues varies among individuals - is essential for modeling plant growth, carbon stocks, and energy fluxes in the terrestrial biosphere. Allocation patterns can differ through ontogeny, but also among coexisting species and among species adapted to different environments. While a variety of models dealing with biomass allocation exist, we lack a synthetic understanding of the underlying processes. This is partly due to the lack of suitable data sets for validating and parameterizing models. To that end, we present the Biomass And Allometry Database (BAAD) for woody plants. The BAAD contains 259634 measurements collected in 176 different studies, from 21084 individuals across 678 species. Most of these data come from existing publications. However, raw data were rarely made public at the time of publication. Thus, the BAAD contains data from different studies, transformed into standard units and variable names. The transformations were achieved using a common workflow for all raw data files. Other features that distinguish the BAAD are: (i) measurements were for individual plants rather than stand averages; (ii) individuals spanning a range of sizes were measured; (iii) plants from 0.01-100 m in height were included; and (iv) biomass was estimated directly, i.e., not indirectly via allometric equations (except in very large trees where biomass was estimated from detailed sub-sampling). We included both wild and artificially grown plants. The data set contains the following size metrics: total leaf area; area of stem cross-section including sapwood, heartwood, and bark; height of plant and crown base, crown area, and surface area; and the dry mass of leaf, stem, branches, sapwood, heartwood, bark, coarse roots, and fine root tissues. We also report other properties of individuals (age, leaf size, leaf mass per area, wood density, nitrogen content of leaves and wood), as well as information about the growing environment (location, light, experimental treatment, vegetation type) where available. It is our hope that making these data available will improve our ability to understand plant growth, ecosystem dynamics, and carbon cycling in the world's vegetation

The pharmacological properties of magnolol and hOnokiol, neolignane derivatives, extracted from Magnolia officinalis, used in Chinese and Japanese traditional medicine, for neurosis and gastrointestinal complaints, were investigated. Magnolol and hOnokiol produced sedation, ataxia, muscle relaxation and a loss of the righting reflex with an increase in dose of 50 to 500 mg/kg i.p. Magnolol and hOnokiol at a dose of 50 mg/kg suppressed spinal reflexes in young chicks in a similar manner, but with a much longer duration of action than mephenesin. Pretreatment of mice with magnolol 100 mg/kg inhibited tonic extensor convulsions and death produced by an intracerebroventricular injection of penicillin 0 potassium 50 tg. In rats, after an intraventricular injection of penicillin G 400 .tg. magnolol suppressed the incidence of spike discharge, but not seizure discharge. Magnolol produced spindle discharges in sensory and motor cortex electroencephalograms and inhibited mid brain reticular formation-and hypothalamus-stimulated responses in the neo-and palaeo-cortex electroencephalograms, respectively. These results suggest that magnolol causes a depression of the ascending activating systems as well as of the spinal cord.

Intracisternal injection of ovine corticotropin-releasing factor (CRF) into the pylorus-ligated rat or the rat with gastric fistula resulted in a dose-dependent inhibition of gastric secretion stimulated with pentagastrin or thyrotropin-releasing hormone. When injected into the lateral hypothalamus--but not when injected into the cerebral cortex--CRF suppressed pentagastrin-stimulated acid secretion. The inhibitory effect of CRF was blocked by vagotomy and adrenalectomy but not by hypophysectomy or naloxone treatment. These results indicate that CRF acts within the brain to inhibit gastric acid secretion through vagal and adrenal mechanisms and not through hypophysiotropic effects.