Dendrochemical analysis of lead and calcium in southern Appalachian American beech.

The health of the northern hardwood forest in the southern Appalachian Mountains of Tennessee, North Carolina, and Virginia has gained attention from the media and environmental stakeholders due to a purported decline in forest health at higher elevations. This project examined lead (Pb) and calcium (Ca) concentrations in growth rings of an important northern hardwood species, American beech (Fagus grandifolia Ehrh.) at Mount Rogers and Whitetop Mountain, Virginia and attempted to examine concentration relationships with stem growth patterns. Dominant and codominant trees were sampled from 16 research plots at two elevations. Tree cores were crossdated, divided into sections of 10-yr periods, and analyzed using atomic absorption spectroscopy. Lead concentrations correlated negatively with ring width. Elevation and aspect were significantly associated with the Pb concentration, while Ca concentrations were only associated with aspect. Tree core samples taken from higher elevation plots contained higher Pb concentrations than samples collected from lower elevation plots, while the northwest and southwest aspects contained significantly higher amounts of Pb and Ca. Both Pb and Ca concentrations increased during the 1860s and again during the mid-1900s.

Is there synchronicity in nitrogen input and output fluxes at the Noland Divide Watershed, a small N-saturated forested catchment in the Great Smoky Mountains National Park?

High-elevation red spruce [Picea rubens Sarg.]-Fraser fir [Abies fraseri (Pursh.) Poir] forests in the Southern Appalachians currently receive large nitrogen (N) inputs via atmospheric deposition (30 kg N ha(-1) year(-1)) but have limited N retention capacity due to a combination of stand age, heavy fir mortality caused by exotic insect infestations, and numerous gaps caused by windfalls and ice storms. This study examined the magnitude and timing of the N fluxes into, through, and out of a small, first-order catchment in the Great Smoky Mountains National Park. It also examined the role of climatic conditions in causing interannual variations in the N output signal. About half of the atmospheric N input was exported annually in the streamwater, primarily as nitrate (NO3-N). While most incoming ammonium (NH4-N) was retained in the canopy and the forest floor, the NO3-N fluxes were very dynamic in space as well as in time. There was a clear decoupling between NO3-N input and output fluxes. Atmospheric N input was greatest in the growing season while largest NO3-N losses typically occurred in the dormant season. Also, as water passed through the various catchment compartments, the NO3-N flux declined below the canopy, increased in the upper soil due to internal N mineralization and nitrification, and declined again deeper in the mineral soil due to plant uptake and microbial processing. Temperature control on N production and hydrologic control on NO3-N leaching during the growing season likely caused the observed inter-annual variation in fall peak NO3-N concentrations and N discharge rates in the stream.

Rheumatoid arthritis and pregnancy.

Although some 70% of patients with rheumatoid arthritis remit during pregnancy, the mechanism for this is not known. A variety of mechanisms have been invoked but none appear to be sufficiently established as an explanation. The most likely explanation is that a factor, or factors, cause the inhibition of release of lymphokines which thereby have a suppressive effect on rheumatoid inflammation.

Rheumatic diseases in pregnancy.

The effects of pregnancy on the clinical course of the rheumatic diseases is not only variable but often unpredictable. Disease activity at the onset of pregnancy will have great bearing on fetal outcome. Thus the use of potentially harmful drug combinations in pregnancy has to be weighed against theoretical teratogenic effects. This review outlines some of these dilemmas.

Immunosuppressive properties of pregnancy serum on the mixed lymphocyte reaction.

The human fetus may escape immunological attack because of serum factors which have immunomodulatory influence on maternal cellular effector responses. Paired peripheral and retroplacental sera were shown to inhibit the allogenic mixed lymphocyte reaction (MLR) used as an in-vitro model of cell-mediated immunity. There was no correlation between the suppressive effect of the peripheral and retroplacental sera and the serum concentrations of four pregnancy-related proteins (alpha-fetoprotein, pregnancy-associated alpha 2 glycoprotein, pregnancy-associated plasma protein A and Schwangerschaftsprotein 1) to which immunosuppressive properties have been ascribed, but there was a negative correlation between peripheral AFP and MLR inhibition (r = -0.62, P less than 0.001). Hence, the factor or factors responsible for suppressing the MLR are not those investigated in the present study.

Human retroplacental sera inhibit the expression of class II major histocompatibility antigens.

Since factor(s) present in human pregnancy sera may interfere with HLA-DR expression on antigen-presenting cells which could account for fetal immune tolerance, we decided to investigate HLA-DR expression on the human myeloid macrophage cell line U937 using the monoclonal antibody RF DR2 and flow cytometry. Following incubation of U937 cells with recombinant interferon gamma (rIFN gamma) and fetal calf serum, 76% of the cells were HLA-DR positive. In contrast, when U937 cells were incubated with retroplacental serum (RP) only 40% of them were positive for HLA-DR and the mean fluorescent intensity for the cell population was significantly diminished. By performing these experiments at 37 and at 4 degrees C we concluded that a factor or factors present in RP bind onto and mask class II major histocompatibility (MHC) antigen expression.

Mechanisms of macrophage activation in rheumatoid arthritis: the role of gamma-interferon.

Gamma-interferon (gamma-IFN) is a potent inducer of surface expression of class II MHC molecules in vitro. Enhanced HLA-DR expression is a characteristic immuno-histological feature of rheumatoid joints. To assess the possible relevance of gamma-IFN to macrophage (M phi) activation in rheumatoid arthritis (RA) we investigated the spontaneous and mitogen-induced production of gamma-IFN by RA lymphocytes using a sensitive radioimmunoassay. Synovial fluids (SF) from a variety of inflammatory and non-inflammatory rheumatic diseases did not contain measurable amounts of IFN. RA lymphocytes from peripheral blood (PBL) and joints failed to show spontaneous gamma-IFN production. RA and control PBL were equally responsive to both mitogen stimulation and to the addition of exogenous interleukin 2 (IL-2) as control PBL. SF lymphocytes from RA patients showed a significantly decreased PHA-stimulated gamma-IFN production and this was in contrast to the SF lymphocytes from patients with other inflammatory joint diseases who showed significantly increased gamma-IFN production compared with matched PB lymphocytes. These results show that gamma-IFN production by peripheral blood and joint cells from patients with RA is normal and it remains to be established whether gamma-IFN is the factor responsible for the macrophage activation seen in the disease.

Inhibition of interleukin-2 production by retroplacental sera: a possible mechanism for human fetal allograft survival.

Fetal tolerance may be a consequence of a local nonspecific serum factor(s) having immunomodulatory activity on maternal cellular effector responses. Paired peripheral and retroplacental sera were collected from 15 healthy patients having elective caesarean section and the sera were studied for their abilities to inhibit the uptake of tritiated thymidine by activated lymphocytes in the mixed lymphocyte reaction (MLR). We found that: Twenty-eight percent of peripheral blood (PB) and all retroplacental sera (RP) could inhibit the MLR. Conditioned medium (MLRS) could completely overcome the inhibition by RP sera. Ultrapure interleukin-1 (IL-1) could not reverse the inhibitory effect. Recombinant interleukin-2 (IL-2) (100 units/culture) completely reversed the inhibition. Inhibition by RP sera occurred between 0 and 24 hours of cell-cell interactions in the MLR and, The inhibition was both on stimulator and responder cells. Thus, factor(s) in RP sera may act to inhibit IL-2 production at the fetomaternal interface. These findings are discussed in the context of fetal allograft rejection.

Human pregnancy serum inhibits interleukin-2 production.

Cell-mediated immunity may be depressed during pregnancy. We used the two way mixed lymphocyte reaction as an in vitro model of cell mediated immunity and studied the effect of pregnancy sera on this system by the amount of tritiated thymidine taken up by activated lymphocytes. We found that: (1) pregnancy sera contain a factor inhibiting the mixed lymphocyte reaction; (2) the inhibition of the mixed lymphocyte reaction induced by sera could be reversed by the addition of the supernatant from allogeneic mixed lymphocyte reaction; (3) pure interleukin-1 could not reverse the inhibitory effect and (4) recombinant interleukin-2 (IL-2) completely reversed the inhibitory effect of pregnancy sera on the mixed lymphocyte reaction. We conclude that a factor (or factors) present in serum from pregnant women is capable of inhibiting the generation of IL-2 during lymphocyte activation.