Native and nonnative plant species can exhibit differences in the timing of their reproductive phenology and their phenological sensitivity to climate. These contrasts may influence species' interactions and the invasion potential of nonnative species; however, a limited number of phenology studies expressly consider phenological mismatches among native and nonnative species over broad spatial or temporal scales. To fill this knowledge gap, we used two complementary approaches: First, we quantified the flowering phenology of native and nonnative plants at five old‐field sites across a spatially extensive range of eastern North America. Second, we used herbarium records to compare the sensitivity of flowering and fruiting phenology to climate across a 114‐yr time period in a subset of common old‐field species in southwestern Pennsylvania. Across the study region, nonnatives reproduced substantially earlier in the growing season than natives, suggesting that nonnatives occupy a unique phenological niche (0.55 months earlier flowering across the North American study sites; 50.1 d earlier flowering and 17.5 d earlier fruiting in southwestern Pennsylvania). Both natives and nonnatives advanced their reproductive phenology between 1900 and 2014 but exhibited contrasting phenological sensitivity to climate factors. During the flowering stage of phenology, nonnatives were more sensitive to changes in precipitation than natives and generally delayed flowering in wetter years. Nonnative plants had greater sensitivity and advanced fruiting when the month preceding fruiting was warmer, while native plants had greater sensitivity and advanced fruiting when the three‐month period preceding fruiting was warmer. Our findings suggest that nonnative old‐field species occupy an earlier phenological niche relative to native species, which may facilitate their invasion into old‐field communities. However, given the different sensitivities of native and nonnative plants to climate factors, present‐day patterns of phenology are likely to shift with future climate changes, potentially leading to novel species interactions that may influence the outcomes of invasion.

The effects of two training and two surgical procedures on the recovery of a visual pattern discrimination were compared in rats with visual cortex damage (areas 17, 18, and 18a). Normal control subjects and rats with serial or simultaneous visual cortex lesions were first trained on a brightness (black vs. white) discrimination task and then on a pattern (horizontal vs. vertical stripes) discrimination task by either classical or fading procedures. The rats' performance in the preoperative, interoperative, and postoperative stages of training were compared. Rats with serial lesions showed postoperative savings in the brightness task and relearned the pattern discrimination task when trained by either the fading or the classical method. Serially lesioned subjects presented fewer errors to criterion when trained by the fading procedure than when trained by the classical procedure. Rats with simultaneous lesions showed no savings on the brightness discrimination task and all of the subjects in this group relearned the pattern discrimination task when trained by the fading procedure. Simultaneously lesioned subjects trained to a maximum of 750 trials using the classical method did not relearn the pattern discrimination task, except for one subject. Interaction between the surgical and training variables is discussed.It has long been known that, after simultaneous bilateral removal of the visual cortex (areas 17, 18, and 18a, as defined by Krieg, 1946aKrieg, , 1946b or all the posterior half of the cortex, rats are able to relearn a black vs. white (B-W) brightness discrimination task

<p>Supplementary Figure S1. Phosphorylated-Akt staining in human vascular tumors. Immunohistochemical stains for phospho-Akt (S473) in normal human skin and human vascular tumors. Representative areas of "low" and "high" levels of staining within a tumor are shown. Arrows in normal skin indicate immuno-reactive blood vessels. Scale bar, 100 μm. Supplementary Figure S2. Isolation of primary infantile hemangioma endothelial cells, and effects of Akt1 knockdown on vascular tumor cell apoptosis. Supplementary Figure S3. Expression levels of Akt1, Akt2 and Akt3 in double transgenic myrAkt1 mice, and the development of hemangioma in myrAkt1 skin grafts in syngeneic immunocompetent FVB recipients. Supplementary Figure S4. Akt1, Akt2 and Akt3 expression in human vascular tumors. Supplementary Figure S5. Akt3 expression in vascular tumor cell lines. Supplementary Figure S6. Knockdown of Akt1, Akt2 and Akt3 in tumor cells, and the effects of loss of Akt1, Akt2 and Akt3 on vascular tumor growth in vivo. Supplementary Figure S7. Loss of S6-Kinase rescues the effects of Akt3 on tumor cell migration. Supplementary Figure S8. Loss of Rictor increases S6K pathway activation. Supplementary Table S1. In vitro properties of the S6K inhibitor LY2584702. *Kinases related to p70 S6K. Supplementary Table S2. Sequences of lentiviral short-hairpin RNA (shRNA) constructs.</p>

<p>Supplementary Figure S1. Phosphorylated-Akt staining in human vascular tumors. Immunohistochemical stains for phospho-Akt (S473) in normal human skin and human vascular tumors. Representative areas of "low" and "high" levels of staining within a tumor are shown. Arrows in normal skin indicate immuno-reactive blood vessels. Scale bar, 100 μm. Supplementary Figure S2. Isolation of primary infantile hemangioma endothelial cells, and effects of Akt1 knockdown on vascular tumor cell apoptosis. Supplementary Figure S3. Expression levels of Akt1, Akt2 and Akt3 in double transgenic myrAkt1 mice, and the development of hemangioma in myrAkt1 skin grafts in syngeneic immunocompetent FVB recipients. Supplementary Figure S4. Akt1, Akt2 and Akt3 expression in human vascular tumors. Supplementary Figure S5. Akt3 expression in vascular tumor cell lines. Supplementary Figure S6. Knockdown of Akt1, Akt2 and Akt3 in tumor cells, and the effects of loss of Akt1, Akt2 and Akt3 on vascular tumor growth in vivo. Supplementary Figure S7. Loss of S6-Kinase rescues the effects of Akt3 on tumor cell migration. Supplementary Figure S8. Loss of Rictor increases S6K pathway activation. Supplementary Table S1. In vitro properties of the S6K inhibitor LY2584702. *Kinases related to p70 S6K. Supplementary Table S2. Sequences of lentiviral short-hairpin RNA (shRNA) constructs.</p>