Nesting of Northern Bobwhites on Rangeland Versus Conservation Reserve Program Habitats in the Rolling Plains of Texas

Conservation Reserve Program (CRP) contracts account for about 1.7 million ha in Texas, and are often touted as habitat for upland game birds. We compared nest site locations, hatch rates, and arthropod abundance for northern bobwhites (Colinus virginianus) on CRP versus rangeland habitats at the Rolling Plains Quail Research Ranch (RPQRR), Fisher County, Texas from 2008 to 2011. Nest sites were monitored via radio-marked females. Simulated nests (n 1⁄4 144/yr) were used to evaluate hatch rates between the 2 habitat types. Arthropod abundance (as an indicator of brood habitat) was measured annually in August using sweep nets and pitfall traps. We documented 103 nest sites, 14% were in CRP while the remaining 86% were in rangeland; bobwhites neither selected nor avoided CRP as nesting habitat. ‘Survival’ of simulated nests (i.e., percent intact at 28 days exposure) across the 4 years averaged 63.2% for CRP and 74.4% on rangelands. Arthropod availability was greater in rangeland in 3 of the 4 years studied. CRP pastures dominated by kleingrass (Panicum coloratum) were used for nesting in proportion to their availability, but rangeland provided better brood habitat

Evaluation of Survey Indices for Scaled Quail in West Texas

Wildlife biologists and land managers require information on population demographics to effectively plan harvest schedules and evaluate habitat modifications. Population indices can potentially provide an efficient way to gather reliable information on wildlife populations as long as they reflect population behavior. We evaluated the relationships among standard survey indices used to monitor scaled quail (Callipepla squamata) across 6 sites in west Texas from 2007 to 2010. We collected data on spring cock call counts, simulated nest survival, roadside counts, and helicopter counts. The mean difference between methods was 2.4 quail/1.6 km on the Andrews County sites, and 4 quail/1.6 km at the Upton/Reagan County sites. Roadside counts and helicopter counts had similar numerical trends in relative abundance with a correlation coefficient of (0.67). Simulated nest fate (i.e., dummy nests) tended to track trends in population abundance. Our survey indices also followed annual fluctuations in scaled quail abundance as estimated from Texas Parks and Wildlife Department’s annual roadside surveys

BRAF V600E-Positive Multisite Langerhans Cell Histiocytosis in a Preterm Neonate

Hemorrhagic pustules with a “blueberry muffin” appearance accompanied by respiratory failure in a neonate present a challenging differential diagnosis that includes infections and neoplasms. We present a case of multiorgan, multisite Langerhans cell histiocytosis (LCH), positive for the oncogenic BRAF V600E mutation, in a preterm neonate. Infants with LCH pose a diagnostic challenge due to their heterogeneous presentations. This case is unusual in that the newborn presented with severe multiorgan involvement. Due to the rare incidence, wide spectrum of clinical manifestations, and high mortality rate, clinicians must maintain a high index of suspicion for LCH

Monocyte chemoattractant protein-1 promotes macrophage-mediated tubular injury, but not glomerular injury, in nephrotoxic serum nephritis

Monocyte chemoattractant protein-1 (MCP-1) is upregulated in renal parenchymal cells during kidney disease. To investigate whether MCP-1 promotes tubular and/or glomerular injury, we induced nephrotoxic serum nephritis (NSN) in MCP-1 genetically deficient mice. Mice were analyzed when tubules and glomeruli were severely damaged in the MCP-1–intact strain (day 7). MCP-1 transcripts increased fivefold in MCP-1–intact mice. MCP-1 was predominantly localized within cortical tubules (90%), and most cortical tubules were damaged, whereas few glomerular cells expressed MCP-1 (10%). By comparison, there was a marked reduction (>40%) in tubular injury in MCP-1–deficient mice (histopathology, apoptosis). MCP-1–deficient mice were not protected from glomerular injury (histopathology, proteinuria, macrophage influx). Macrophage accumulation increased adjacent to tubules in MCP-1–intact mice compared with MCP-1–deficient mice (70%, P < 0.005), indicating that macrophages recruited by MCP-1 induce tubular epithelial cell (TEC) damage. Lipopolysaccharide-activated bone marrow macrophages released molecules that induced TEC death that was not dependent on MCP-1 expression by macrophages or TEC. In conclusion, MCP-1 is predominantly expressed by TEC and not glomeruli, promotes TEC and not glomerular damage, and increases activated macrophages adjacent to TEC that damage TEC during NSN. Therefore, we suggest that blockage of TEC MCP-1 expression is a therapeutic strategy for some forms of kidney disease.published_or_final_versio

Differential roles of CCL2 and CCR2 in host defense to coronavirus infection.

The CC chemokine ligand 2 (CCL2, monocyte chemoattractant protein-1) is important in coordinating the immune response following microbial infection by regulating T cell polarization as well as leukocyte migration and accumulation within infected tissues. The present study examines the consequences of mouse hepatitis virus (MHV) infection in mice lacking CCL2 (CCL2(-/-)) in order to determine if signaling by this chemokine is relevant in host defense. Intracerebral infection of CCL2(-/-) mice with MHV did not result in increased morbidity or mortality as compared to either wild type or CCR2(-/-) mice and CCL2(-/-) mice cleared replicating virus from the brain. In contrast, CCR2(-/-) mice displayed an impaired ability to clear virus from the brain that was accompanied by a reduction in the numbers of antigen-specific T cells as compared to both CCL2(-/-) and wild-type mice. The paucity in T cell accumulation within the central nervous system (CNS) of MHV-infected CCR2(-/-) mice was not the result of either a deficiency in antigen-presenting cell (APC) accumulation within draining cervical lymph nodes (CLN) or the generation of virus-specific T cells within this compartment. A similar reduction in macrophage infiltration into the CNS was observed in both CCL2(-/-) and CCR2(-/-) mice when compared to wild-type mice, indicating that both CCL2 and CC chemokine receptor 2 (CCR2) contribute to macrophage migration and accumulation within the CNS following MHV infection. Together, these data demonstrate that CCR2, but not CCL2, is important in host defense following viral infection of the CNS, and CCR2 ligand(s), other than CCL2, participates in generating a protective response

Novel Tumor Suppressor Function of Glucocorticoid-Induced TNF Receptor GITR in Multiple Myeloma

Glucocorticoid-induced TNF receptor (GITR) plays a crucial role in modulating immune response and inflammation, however the role of GITR in human cancers is poorly understood. In this study, we demonstrated that GITR is inactivated during tumor progression in Multiple Myeloma (MM) through promoter CpG island methylation, mediating gene silencing in primary MM plasma cells and MM cell lines. Restoration of GITR expression in GITR deficient MM cells led to inhibition of MM proliferation in vitro and in vivo and induction of apoptosis. These findings were supported by the presence of induction of p21 and PUMA, two direct downstream targets of p53, together with modulation of NF-κB in GITR-overexpressing MM cells. Moreover, the unbalanced expression of GITR in clonal plasma cells correlated with MM disease progression, poor prognosis and survival. These findings provide novel insights into the pivotal role of GITR in MM pathogenesis and disease progression