Stable isotopes were used to evaluate water sources for co-occurring Jeffrey pine (Pinus jeffreyi Grev & Balf.) and greenleaf manzanita (Arctostaphylos patula Greene) in the southern Sierra Nevada, California, where soils averaged only 75 cm thick but were underlain by up to 5 m of weathered granitic bedrock. Soils and underlying weathered bedrock were sampled three times during both the 1997 and 1998 growing seasons, in 25 cm increments, from 0 to 400 cm or until hard bedrock was reached, and plant stem tissue was sampled simultaneously. Extracted water from the soil/bedrock substrate and plant tissue was analyzed for delta(18)O and/or deltaD, and depth of water source was determined by inference in conjunction with moisture status of the substrate. Water source utilization over the growing seasons for both plants generally followed a pattern similar to that observed for water depletion. Predominant water use was initially from the surface soils. Progressively deeper water sources, including weathered bedrock to a depth of several meters, were exploited as the season progressed and the overlying substrate was depleted of moisture. Early in the growing season, stable isotope values were slightly lower for pine than for manzanita (e.g., average deltaD in June 1997 was -81 per thousand for pine and -77 per thousand for manzanita), and suggest that the functional rooting depth for pine may have been slightly greater than for manzanita. In September 1997, manzanita deltaD values averaged -57 per thousand while pine values averaged -85 per thousand, indicating that manzanita opportunistically utilized summer precipitation while pine used more dependable bedrock water. In 1998, soils remained moist through July due to a late snowfall. Unlike the previous year, pine and manzanita deltaD values were not significantly different in mid- and late-growing season, and both plants exploited bedrock-derived water as soil water was depleted. Water held within bedrock was essential for meeting plant transpirational requirements over the summer drought.

The clinical, genetic, and pathologic findings, and the pertinent case histories in two families with idiopathic hemochromatosis are presented. These studies support the view that idiopathic hemochromatosis is a disease inherited in at least two ways. In one of these families, inheritance appeared to occur in an autosomal recessive manner, whereas in the other, autosomal dominant expression seemed evident. Evidence that an inability of the reticuloendothelial cells to handle iron may play a major role in the pathogenesis of hemochromatosis is presented. The early age of onset and poorer prognosis associated with the recessive inheritance suggest that the defect in reticuloendothelial cell function present in such cases is different from or more severe than those associated with dominant inheritance.

A deterministic aerosol deposition model, previously validated by data from adult inhalation exposure experiments, is used to study particle deposition within the developing human lung. Here, two age-dependent lung morphologies are presented, in which the number of tracheobronchial (TB) generations is complete at birth but airway dimensions vary with age; the number of pulmonary (P) generations, however, changes with age, as do the alveolated airway dimensions. Deposition patterns within the two morphologies are compared. For the light and heavy respiratory-activity levels considered, regional TB and P, and total (TB + P) lung deposition fractions are calculated. For all particle sizes (0.2-9.0 microns diameters) tested, total deposition in both morphologies was minimal for the 30-y-old adult and maximal for either of the youngest subjects (7 and 22 mo old). A breakdown of total deposition into lung compartments was specifically addressed for one morphological model. Age-dependent deposition models are intended to aid in future extrapolation efforts to assess the threat to human health from airborne contaminants.

Experimental inj ections of histamine can produce increased vascular permeability and vasomotor changes resembling those seen very early in certain acute inflammatory reactions,. 1, '' Moreover, there is evidence that histamine release is involved in the pathogenesis of the earliest phase of some types of acute inflammatory reaction. 3-6 In contrast, there is little to support a role for histamine in the pathogenesis of the later stages of inflammation in which leukocytic sticking and emigration are prominent features. The extent to which histamine can induce sticking and emigration of leukocytes under experimental conditions is unclear.Serotonin is known to have permeability-increasing effects in rats and mice, animals in which histamine is relatively ineffective.7 Conversely, serotonin lacks these effects in other, more histamine-sensitive animals (e.g., rabbits).In the present experiments, the effects of histamine and serotonin upon the microcirculation have been observed directly in an improved rabbit ear chamber. This technique affords a dynamic view of the reactions resulting from these substances, revealing especially the temporal relationships between the various components of the reactions. MATERIALS AND METHODSRabbit ear chamber. The rabbit ear chamber used in our laboratory has been described previously.8 A further modification of the Sandison-Clark chamber,°~ 1° it incorporates two features which permit the observation of very early inflammatory changes. One is a valve through which substances can be injected onto the tissue with negligible trauma, an innovation originally proposed by Sanders.ll The other is the greater thickness of the tissue over the chamber table (70-100 0), affording greater stability so that repeated injections and comparisons of the effects of various substances can be made in the same chamber.Each test material was injected through the valve into the chamber with the aid of a syringe microburet by a method previously described.8 Microscopic observations were made at 2, 5, 10, 20, 30, 45, 60, 90, and 120 min. after injection. In some experiments, further observations were made after 120 min. The method of recording the observations has been described.8 The number of leukocytes &dquo;rolling&dquo; and &dquo;sticking&dquo; in each of two preselected venular segments was recorded. A cell moving along the venular endothelium at a rate slower than that of the axial stream of the venule was said to be &dquo;rolling.&dquo; A cell firmly adherent to the endothelium was said to be &dquo;sticking.&dquo; Numbers of roll-