Biomass accumulation over the first 150 years in coastal Oregon Picea‐Tsuga forest

Abstract. Production and mortality are the component processes that together determine the biomass dynamics of forests. Due to the significant role of forests in the global carbon cycle, it is important to assess how these two processes affect the maximum biomass attained by forests, as well as the dynamics leading up to and following peak biomass. We address these questions for two sets of plots in Picea sitchensis‐Tsuga heterophylla forest on the northern Oregon coast that originated from a catastrophic wildfire in the 1840s, using new data on dynamics of live trees and stocks of coarse woody debris (CWD). The set of plots closest to the ocean and occupying steeper, more dissected terrain with areas of thin soils has lower biomass, lower net primary production (NPP) of bole wood and higher tree mortality as a fraction of standing biomass. The two sets of plots have similar CWD levels, most of which has accumulated in the last 25 yr. The present disparity in biomass between the two sets of plots appears to be the result of lower NPP on the low‐biomass plots for the entire 140+ yr history of the forest. Over the 58 yr that the high‐biomass plots have been measured (from stand age 85 to 143 yr), NPP of bole wood has declined by 41%. Only ca. 6% of this decline can be accounted for by an increase in maintenance respiration of woody tissues. For both sets of plots relative constancy of biomass in the long term appears likely, due to a short time lag in tree regeneration, asynchronous tree mortality and little overall decline in NPP of bole wood in recent decades. However, since tree mortality as a fraction of standing biomass is higher on the low‐biomass plots, and NPP of bole wood is slightly lower, the difference in biomass between the two sets of plots should increase if current rates of production and mortality persist.     

Developmental interactions of cells mutant for Strong's luxoid gene with normal cells in chimeric mice

Mouse chimeras were made by fusing embryos from the albino BALB/cFo normal skeleton strain producing a slow variant isozyme of glucose phosphate isomerase (GPI) with embryos from the black pigmented SH strain carrying Strong's luxoid gene (symbol: 1st) for skeletal anomalies and producing a fast GPI variant. All chimeras were estimated to bALB/cFo mice to determine the mosaic status of their gonads. In addition, the quantitative proportions of BALB/cFo and SH cells in skin and limb muscles of chimeras were determined by visual estimation of the degree of coat pigmentation and by a serial dilution method applied to electrophoresis and GPI isozyme reaction of limb muscle homogenates. Skeletons of all chimeras and of representative samples of BALB/cFo and SH mice were examined and graded for expression of a number of normal and mutant skeletal characteristics. The most important conclusion of this study is that there was a definite quantitative effect on the development of skeletal characteristics exerted by the relative amount of BALB/ cFo and SH cells present in a chimera such that a structure could vary from normal to entirely mutant, depending on the proportion of each type of cell present.     

Characterization of β-defensin prepropeptide mRNA from chicken and turkey bone marrow

Four avian β-defensin prepropeptide cDNA sequences [gallinacins: Gal 1 (synonym CHP 1, chicken heterophil peptide 1), and Gal 2; turkey heterophil peptides: THP 1 and THP 2] were amplified from chicken or turkey bone marrow mRNA samples, respectively. Partial chicken β-defensin cDNA sequences were obtained using degenerate primers based on chicken peptide sequences (Gal 1/CHP 1 and Gal 2). The complete cDNA sequences of the chicken β-defensins were then determined by designing specific intrapeptidal primers, from the newly acquired sequence, and pairing one primer with a specific poly A primer tail sequence (3' end) and the other primer with an adapter primer in a 5' rapid amplification of cDNA ends (RACE) reaction. The two, turkey β-defensins were amplified from turkey marrow using primers designed from chicken β-defensin preproregions. The complete amino acid sequences for the prepropeptides were deduced for all four avian β-defensins. Previously, only partial mature peptide sequences for the turkey β-defensins and complete mature peptide sequences for the chicken β-defensins were known. All sequences obtained translated accurately to complete and partial amino acid sequences reported for β-defensins purified from chicken and turkey heterophil granules except for one additional amino acid for Gal 1/CHP 1. The four deduced β-defensin proregions lack the long, negatively charged propiece reported in classical defensin proregions. These regions are thought to stabilize and inactivate the positively charged mature peptide and target the propeptide to the storage granule. Instead, these β-defensin proregions are shorter and similar to storage granule-free β-defensins proregions reported for bovine tracheal antimicrobial peptide (TAP) and lingual antimicrobial peptide (LAP). These are the first prepropeptide β-defensins from leukocyte granules to be completely characterized.     

Influence of hydrocortisone acetate on pancreas and mucosal weight, amylase and disaccharidase activities in 14-day-old pigs.

1. One litter of 12 pigs was used to evaluate the effects of hydrocortisone acetate injection on organ weight and carbohydrase activities. 2. Pigs were injected with hydrocortisone acetate or an equal volume of saline at 7 days of age and killed at 14 days, and tissues were collected, weighted, and analyzed for carbohydrase activities. 3. Hydrocortisone had no effect (P greater than 0.40) on daily gain, liver weight, spleen weight, or small intestinal length. 4. Hydrocortisone increased pancreatic weight by 29% and total pancreatic alpha-amylase content by 38%. 5. Hydrocortisone increased duodenal mucosal weight by 23%, duodenal lactase activity by 44%, duodenal maltase activity by 163%, and duodenal sucrase activity by 214%.