Multi-scale habitat selection affects offspring survival in a precocial species.

In theory, habitat preferences should be adaptive. Accordingly, fitness is often assumed to be greater in preferred habitats; however, this assumption is rarely tested and, when it is, the results are often equivocal. Habitat preferences may not directly convey fitness advantages if animals are constrained by tradeoffs with other selective pressures like predation or food availability. We address unresolved questions about the survival consequences of habitat choices made during brood-rearing in a precocial species with exclusive maternal care (mallard Anas platyrhynchos, n = 582 radio-marked females on 27 sites over 8 years). We directly linked duckling survival with habitat selection patterns at two spatial scales using logistic regression and model selection techniques. At the landscape scale (55-80 km(2)), females that demonstrated stronger selection of areas with more cover type 4 wetlands and greater total cover type 3 wetland area (wetlands with large expanses of open water surrounded by either a narrow or wide peripheral band of vegetation, respectively) had lower duckling survival rates than did females that demonstrated weaker selection of these habitats. At finer scales (0.32-7.16 km(2)), females selected brood-rearing areas with a greater proportion of wetland habitat with no consequences for duckling survival. However, females that avoided woody perennial habitats composed of trees and shrubs fledged more ducklings. The relationship between habitat selection and survival depended on both spatial scale and habitats considered. Females did not consistently select brood-rearing habitats that conferred the greatest benefits, an unexpected finding, although one that has also been reported in other recent studies of breeding birds.

Autoimmune pancytopenia. Lymphocyte inhibition of autologous but not allogenic bone marrow growth in vitro.

A patient with autoimmune renal failure, cavitary lung lesions and arthritis experienced pancytopenia while prednisone therapy was being tapered. Utilizing semisolid culture techniques, a population of nonadherent peripheral blood mononuclear cells was demonstrated, which inhibited autologous but not allogeneic bone marrow erythroid colony-forming units (CFU-E) and myeloid colony-forming units (CFU-c) in vitro. No inhibition of CFU-E or CFU-c colony formation was seen when patient's serum or immunoglobulin G (IgG) was added to cultures. Reinstitution of prednisone therapy resulted in normalization of peripheral blood counts, which was accompanied by the loss of the hemopoietic inhibitor cell activity in the patient's peripheral blood. These results demonstrate the need for testing autologous marrow samples when looking for possible immune-mediated inhibition of hematopoiesis.

Asymptomatic IgA nephropathy associated with pulmonary hemosiderosis.

A glomerular lesion identical to that of IgA nephropathy was demonstrated unexpectedly in a 17 year old boy who presented with clinical manifestations of pulmonary hemosiderosis and with no evidence of renal disease. This subclinical glomerular lesion would have remained undetected in this patient unless kidney tissue was obtained and examined by immunofluorescence or electron microscopy. It is unknown if the glomerular lesion in this case is causally related to pulmonary hemosiderosis.

Acute graft rejection in the late survivors of renal transplantation. Clinical and histological observations in the second decade.

The clinical and histological spectrum of renal allograft rejection occurring in the early posttransplant period is well described, but there is not much information with regard to the nature of graft rejection occurring in the long-term survivors of renal transplantation. In this study, we analyzed the incidence, clinical and histological data, and outcome of graft rejection in 69 patients who survived with a functioning kidney for 10 years or longer. In this second decade, during a mean follow-up of 3 years (0.1-9.7 years), 15 patients (22%) developed 20 late rejections. Two of them received living-donor transplants and 13 received cadaver kidneys. Only 8 of these rejections (40%) were associated with abnormal clinical findings; the other 12 (60%) were asymptomatic and were detected on the basis of an unexplained deterioration in graft function. The diagnosis was made on clinical grounds in 10 cases and the other 10 were confirmed by renal histology: acute cellular rejection 1, acute cellular rejection superimposed on chronic rejection 4, and chronic rejection only 5. Thirteen acute rejections in 8 patients were treated with high-dose steroids. Of these, 6 (46%) responded fully, 4 (31%) responded partially, and 3 (23%) did not respond. Seven patients with chronic rejection were not treated. Of these, 5 have returned to dialysis within a mean period of 8 months and one patient died of hepatic failure. Our data suggest that acute reversible graft rejections can occur even after 10 years following renal transplantation. It is therefore essential to continue the maintenance immunosuppressive therapy and monitor the clinical and renal functional data at regular intervals in long-term survivors of renal transplantation.

Immune complex nephritis in nude mice.

To examine the effect of T lymphocyte deficiency on the course of immune complex nephritis, we studied renal function and structure in Swiss albino nude and non-nude mice following injection of heterologous protein. Four groups of 22 mice each (two nude and two non-nude) received either apoferritin 2 mg or saline daily for 10 weeks. Nude mice were maintained in a gnotobiotic environment. Non-nude mice receiving apoferritin developed proteinuria and had increased cellularity within glomeruli compared to either nude mice receiving apoferritin or to control groups (p less than 0.05). Of 22 non-nude mice receiving apoferritin, 16 had glomerular immune deposits by electron and immunofluorescent microscopy while 9 of 22 counterpart nude mice receiving apoferritin had such deposits. Non-nude mice more commonly showed membraneous deposits. Nude and non-nude mice receiving saline had no glomerular deposits. These preliminary data suggest that T lymphocytes may play a significant role in the development of immune complex nephritis.

Ferritin- and apoferritin-induced immune complex glomerulonephritis in mice.

In order to study the effects of the protein moiety independent of the protein-iron complex in the development of ferritin-induced glomerulonephritis, we compared the effects of ferritin, equimolar amounts of apoferritin, and equimolar amounts of iron dextran in Swiss albino mice. The results were compared to both saline-injected and non-injected controls. Ferritin resulted in a glomerulonephritis associated with predominantly mesangial deposition of immune complexes. Tubulo-interstitial changes occurred as well. Iron dextran resulted in similar but less severe tubulo-interstitial changes and evoked no glomerular alterations. Apoferritin resulted in an immune complex glomerulonephritis usually associated with membranous deposits. No tubular or interstitial changes occurred. Proteinuria developed in animals receiving apoferritin. Since the protein-iron complex caused tubular and interstitial damage, apoferritin may provide a more suitable model of immune-complex-mediated glomerulonephritis.