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91.
M. Colter Chitwood Marcus A. Lashley John C. Kilgo Kenneth H. Pollock Christopher E. Moorman Christopher S. DePerno 《PloS one》2015,10(3)
Coyotes recently expanded into the eastern U.S. and potentially have caused localized white-tailed deer population declines. Research has focused on quantifying coyote predation on neonates, but little research has addressed the potential influence of bedsite characteristics on survival. In 2011 and 2012, we radiocollared 65 neonates, monitored them intensively for 16 weeks, and assigned mortality causes. We used Program MARK to estimate survival to 16 weeks and included biological covariates (i.e., sex, sibling status [whether or not it had a sibling], birth weight, and Julian date of birth). Survival to 16 weeks was 0.141 (95% CI = 0.075-0.249) and the top model included only sibling status, which indicated survival was lower for neonates that had a sibling. Predation was the leading cause of mortality (35 of 55; 64%) and coyotes were responsible for the majority of depredations (30 of 35; 86%). Additionally, we relocated neonates for the first 10 days of life and measured distance to firebreak, visual obstruction, and plant diversity at bedsites. Survival of predation to 10 days (0.726; 95% CI = 0.586-0.833) was weakly associated with plant diversity at bedsites but not related to visual obstruction. Our results indicate that neonate survival was low and coyote predation was an important source of mortality, which corroborates several recent studies from the region. Additionally, we detected only weak support for bedsite cover as a covariate to neonate survival, which indicates that mitigating effects of coyote predation on neonates may be more complicated than simply managing for increased hiding cover. 相似文献
92.
Chamber formation and morphogenesis in the developing mammalian heart 总被引:23,自引:0,他引:23
93.
Ni L Ma CJ Zhang Y Nandakumar S Zhang CL Wu XY Borthwick T Hamati A Chen XY Kumaraguru U Moorman JP Yao ZQ 《Immunology and cell biology》2011,89(4):535-539
T regulatory (T(R)) cells suppress T-cell responses that are critical in the development of chronic viral infection and associated malignancies. Programmed death-1 (PD-1) also has a pivotal role in regulation of T-cell functions during chronic viral infection. To examine the role of PD-1 pathway in regulating T(R)-cell functions that inhibit T-cell responses during virus-associated malignancy, T(R) cells were investigated in the setting of hepatitis C virus-associated lymphoma (HCV-L), non-HCV-associated lymphoma (non-HCV-L), HCV infection alone and healthy subjects (HS). Relatively high numbers of CD4(+)CD25(+) and CD8(+)CD25(+) T(R) cells, as well as high levels of PD-1 expressions on these T(R) cells were found in the peripheral blood of subjects with HCV-L compared with those from non-HCV-L or HCV alone or HS. T(R) cells from the HCV-L subjects were capable of suppressing the autogeneic lymphocyte response, and depletion of T(R) cells in peripheral blood mononuclear cells from HCV-L improved T-cell proliferation. Additionally, the suppressed T-cell activation and proliferation in HCV-L was partially restored by blocking the PD-1 pathway ex vivo, resulting in both a reduction in T(R)-cell number and the ability of T(R) to suppress the activity of effector T cells. This study suggests that the PD-1 pathway is involved in regulating T(R) cells that suppress T-cell functions in the setting of HCV-associated B-cell lymphoma. 相似文献
94.
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96.
Hamstring muscle strain injury is one of the most commonly seen injuries in sports such as track and field, soccer, football, and rugby. The purpose of this study was to advance our understanding of the mechanisms of hamstring muscle strain injuries during over ground sprinting by investigating hamstring muscle-tendon kinematics and muscle activation. Three-dimensional videographic and electromyographic (EMG) data were collected for 20 male runners, soccer or lacrosse players performing overground sprinting at their maximum effort. Hamstring muscle-tendon lengths, elongation velocities, and linear envelop EMG data were analyzed for a running gait cycle of the dominant leg. Hamstring muscles exhibited eccentric contractions during the late stance phase as well as during the late swing phase of overground sprinting. The peak eccentric contraction speeds of the hamstring muscles were significantly greater during the late swing phase than during the late stance phase (p=0.001) while the hamstring muscle-tendon lengths at the peak eccentric contraction speeds were significantly greater during the late stance phase than during the late swing phase (p=0.001). No significant differences existed in the maximum hamstring muscle-tendon lengths between the two eccentric contractions. The potential for hamstring muscle strain injury exists during the late stance phase as well as during the late swing phases of overground sprinting. 相似文献
97.
In contrast to lower vertebrates, the mammalian heart has a very limited regenerative capacity. Cardiomyocytes, lost after ischemia, are replaced by fibroblasts. Although the human heart is able to form new cardiomyocytes throughout its lifespan, the efficiency of this phenomenon is not enough to substitute sufficient myocardial mass after an infarction. In contrast, zebrafish hearts regenerate through epicardial activation and initiation of myocardial proliferation. With this study we obtain insights into the activation and cellular contribution of the mammalian epicardium in response to ischemia. In a mouse myocardial infarction model we analyzed the spatio-temporal changes in expression of embryonic epicardial, EMT, and stem cell markers and the contribution of cells of the Wt1-lineage to the infarcted area. Though the integrity of the epicardial layer overlaying the infarct is lost immediately after the induction of the ischemia, it was found to be regenerated at three days post infarction. In this regenerated epicardium, the embryonic gene program is transiently re-expressed as well as proliferation. Concomitant with this activation, Wt1-lineage positive subepicardial mesenchyme is formed until two weeks post-infarction. These mesenchymal cells replace the cardiomyocytes lost due to the ischemia and contribute to the fibroblast population, myofibroblasts and coronary endothelium in the infarct, and later also to the cardiomyocyte population. We show that in mice, as in lower vertebrates, an endogenous, epicardium-dependent regenerative response to injury is induced. Although this regenerative response leads to the formation of new cardiomyocytes, their number is insufficient in mice but sufficient in lower vertebrates to replace lost cardiomyocytes. These molecular and cellular analyses provide basic knowledge essential for investigations on the regeneration of the mammalian heart aiming at epicardium-derived cells. 相似文献
98.
Bell JR Kennington E Fuller W Dighe K Donoghue P Clark JE Jia LG Tucker AL Moorman JR Marber MS Eaton P Dunn MJ Shattock MJ 《American journal of physiology. Heart and circulatory physiology》2008,294(2):H613-H621
Phospholemman (PLM, FXYD1), abundantly expressed in the heart, is the primary cardiac sarcolemmal substrate for PKA and PKC. Evidence supports the hypothesis that PLM is part of the cardiac Na-K pump complex and provides the link between kinase activity and pump modulation. PLM has also been proposed to modulate Na/Ca exchanger activity and may be involved in cell volume regulation. This study characterized the phenotype of the PLM knockout (KO) mouse heart to further our understanding of PLM function in the heart. PLM KO mice were bred on a congenic C57/BL6 background. In vivo conductance catheter measurements exhibited a mildly depressed cardiac contractile function in PLM KO mice, which was exacerbated when hearts were isolated and Langendorff perfused. There were no significant differences in action potential morphology in paced Langendorff-perfused hearts. Depressed contractile function was associated with a mild cardiac hypertrophy in PLM KO mice. Biochemical analysis of crude ventricular homogenates showed a significant increase in Na-K-ATPase activity in PLM KO hearts compared with wild-type controls. SDS-PAGE and Western blot analysis of ventricular homogenates revealed small, nonsignificant changes in Na- K-ATPase subunit expression, with two-dimensional gel (isoelectric focusing, SDS-PAGE) analysis revealing minimal changes in ventricular protein expression, indicating that deletion of PLM was the primary reason for the observed PLM KO phenotype. These studies demonstrate that PLM plays an important role in the contractile function of the normoxic mouse heart. Data are consistent with the hypothesis that PLM modulates Na-K-ATPase activity, indirectly affecting intracellular Ca and hence contractile function. 相似文献
99.
M. Colter Chitwood Marcus A. Lashley Christopher E. Moorman Christopher S. DePerno 《Journal of Ethology》2017,35(3):251-257
An evolutionary trap occurs when an organism makes a formerly adaptive decision that now results in a maladaptive outcome. Such traps can be induced by anthropogenic environmental changes, with nonnative species introductions being a leading cause. The recent establishment of coyotes (Canis latrans) into the southeastern USA has the potential to change white-tailed deer (Odocoileus virginianus) population dynamics through direct predation and behavioral adaptation. We used movement rate and bedsite characteristics of radiocollared neonates to evaluate their antipredator strategies in the context of novel predation risk in a structurally homogeneous, fire-maintained ecosystem. Neonate bedsites had greater plant cover values compared with random sites (t = 30.136; p < 0.001), indicating bedsite selection was consistent with the hider strategy used to avoid predation. We determined selection gradients of coyote predation on neonate movement rate and plant cover and diversity at bedsites during the first 10 days of life. Interestingly, neonates that moved less and bedded in denser cover were more likely to be depredated by coyotes, meaning that greater neonate movement rate and bedsites located in less dense cover were favored by natural selection. These results are counter to expected antipredator strategies in white-tailed deer and exemplify how an adaptive response could be maladaptive in novel contexts. 相似文献
100.
Keeley EC Moorman JR Liu L Gimple LW Lipson LC Ragosta M Taylor AM Lake DE Burdick MD Mehrad B Strieter RM 《PloS one》2011,6(6):e21174