The impact of lianas on tree regeneration in tropical forest canopy gaps: evidence for an alternative pathway of gap‐phase regeneration

1 Regeneration in forest canopy gaps is thought to lead invariably to the rapid recruitment and growth of trees and the redevelopment of the canopy. Our observations, however, suggest that an alternate successional pathway is also likely, whereby gap‐phase regeneration is dominated by lianas and stalled in a low‐canopy state for many years. We investigated gap‐phase regeneration in an old‐growth tropical forest on Barro Colorado Island (BCI) in Panama to test the following two hypotheses: (i) many gaps follow a pathway in which they remain at a low canopy height and are dominated by lianas and (ii) the paucity of trees in this pathway is a function of liana density. 2 We surveyed a total of 428 gaps of varying ages (c. 5, c. 10, and 13+ years old) and identified those which followed the conventional pathway of regeneration and others that remained stalled in a low‐canopy state for many years and were dominated by either lianas or palms. Each of these pathways will likely have different successional trajectories that will favour the growth of a distinct suite of mature species and ultimately result in contrasting species composition. 3 The successional pathway of liana‐dominated, stalled gaps is common throughout the forest. We estimate conservatively that 7.5% of the gaps that form each year will follow this pathway, probably due to the suppression of tree regeneration by lianas, and that many of these stalled gaps will persist for much longer than 13 years. Consequently, a high proportion of gaps in the forest at any given time will be stalled. Furthermore, liana tangles, which persist in the tropical forest understorey for extended periods of time, almost certainly originate in these gaps. 4 Liana abundance was positively correlated with pioneer tree abundance and diversity while negatively correlated with non‐pioneer tree abundance and diversity. Thus, lianas appear to inhibit non‐pioneer tree survival while indirectly enhancing that of pioneer trees. 5 Lianas are abundant in many types of tropical and temperate forests and a successional pathway involving liana‐dominated, stalled gaps may therefore be frequent and widespread

Second-generation PLINK: rising to the challenge of larger and richer datasets

PLINK 1 is a widely used open-source C/C++ toolset for genome-wide association studies (GWAS) and research in population genetics. However, the steady accumulation of data from imputation and whole-genome sequencing studies has exposed a strong need for even faster and more scalable implementations of key functions. In addition, GWAS and population-genetic data now frequently contain probabilistic calls, phase information, and/or multiallelic variants, none of which can be represented by PLINK 1's primary data format. To address these issues, we are developing a second-generation codebase for PLINK. The first major release from this codebase, PLINK 1.9, introduces extensive use of bit-level parallelism, O(sqrt(n))-time/constant-space Hardy-Weinberg equilibrium and Fisher's exact tests, and many other algorithmic improvements. In combination, these changes accelerate most operations by 1-4 orders of magnitude, and allow the program to handle datasets too large to fit in RAM. This will be followed by PLINK 2.0, which will introduce (a) a new data format capable of efficiently representing probabilities, phase, and multiallelic variants, and (b) extensions of many functions to account for the new types of information. The second-generation versions of PLINK will offer dramatic improvements in performance and compatibility. For the first time, users without access to high-end computing resources can perform several essential analyses of the feature-rich and very large genetic datasets coming into use.Comment: 2 figures, 1 additional fil

Effect of irradiation on Akt signaling in atrophying skeletal muscle

Muscle irradiation (IRR) exposure can accompany unloading during spaceflight or cancer treatment, and this has been shown to be sufficient by itself to induce skeletal muscle signaling associated with a remodeling response. Although protein kinase B/Akt has an established role in the regulation of muscle growth and metabolism, there is a limited understanding of how Akt signaling in unloaded skeletal muscle is affected by IRR. Therefore, we examined the combined effects of acute IRR and short-term unloading on muscle Akt signaling. Female C57BL/6 mice were subjected to load bearing or hindlimb suspension (HS) for 5 days (n = 6/group). A single, unilateral hindlimb IRR dose (0.5 Gy X-ray) was administered on day 3. Gastrocnemius muscle protein expression was examined. HS resulted in decreased AktT308 phosphorylation, whereas HS+IRR resulted in increased AktT308 phosphorylation above baseline. HS resulted in reduced AktS473 phosphorylation, which was rescued by HS+IRR. Interestingly, IRR alone resulted in increased phosphorylation of AktS473, but not that of AktT308. HS resulted in decreased mTORC1 signaling, and this suppression was not altered by IRR. Both IRR and HS resulted in increased MuRF-1 expression, whereas atrogin-1 expression was not affected by either condition. These results demonstrate that either IRR alone or when combined with HS can differentially affect Akt phosphorylation, but IRR did not disrupt suppressed mTORC1 signaling by HS. Collectively, these findings highlight that a single IRR dose is sufficient to disrupt the regulation of Akt signaling in atrophying skeletal muscle

The Lyot Project Direct Imaging Survey of Substellar Companions: Statistical Analysis and Information from Nondetections

The Lyot project used an optimized Lyot coronagraph with Extreme Adaptive Optics at the 3.63m Advanced Electro-Optical System telescope (AEOS) to observe 86 stars from 2004 to 2007. In this paper we give an overview of the survey results and a statistical analysis of the observed nondetections around 58 of our targets to place constraints on the population of substellar companions to nearby stars. The observations did not detect any companion in the substellar regime. Since null results can be as important as detections, we analyzed each observation to determine the characteristics of the companions that can be ruled out. For this purpose we use a Monte Carlo approach to produce artificial companions, and determine their detectability by comparison with the sensitivity curve for each star. All the non-detection results are combined using a Bayesian approach and we provide upper limits on the population of giant exoplanets and brown dwarfs for this sample of stars. Our nondetections confirm the rarity of brown dwarfs around solar-like stars and we constrain the frequency of massive substellar companions (M>40Mjup) at orbital separation between and 10 and 50 AU to be <20%.Comment: 32 pages, 11 figures, 2 tables. Published in the Astrophysical Journa

Irrigating Alfalfa in South Dakota

Alfalfa performs admirably an irrigated crop in South Dakota-so well that it is often neglected. When given attention, it can realistically maintain irrigated yields of 6 to 7 TIA each year in most of South Dakota where 1 to 2 T are produced on dryland. Irrigated land that will produce 100-130 bu corn will produce 5-7 T alfalfa. On poorer irrigated land that produces 50-70 hu corn, one can expect 3-5 T alfalfa. Alfalfa has higher water requirements for peak yields than most other crops. It may not reach its full potential yield in any part of the stale without irrigation. Alfalfa is produced on 2.2 million acres dryland and irrigated land combined) in every county in South Dakota. By contrast, even when corn is irrigated, it is adapted to only about two thirds of the slate. If the marketing problems of transportation and fluctuating prices are overcome, alfalfa could become the state\u27s number one irrigated crop

The Regulation of Skeletal Muscle Protein Turnover During the Progression of Cancer Cachexia in the \u3cem\u3eApc\u3csup\u3eMin/+\u3c/sup\u3e\u3c/em\u3e Mouse

Muscle wasting that occurs with cancer cachexia is caused by an imbalance in the rates of muscle protein synthesis and degradation. The Apc(Min/+) mouse is a model of colorectal cancer that develops cachexia that is dependent on circulating IL-6. However, the IL-6 regulation of muscle protein turnover during the initiation and progression of cachexia in the Apc(Min/+) mouse is not known. Cachexia progression was studied in Apc(Min/+) mice that were either weight stable (WS) or had initial (≤5%), intermediate (6-19%), or extreme (≥20%) body weight loss. The initiation of cachexia reduced %MPS 19% and a further ∼50% with additional weight loss. Muscle IGF-1 mRNA expression and mTOR targets were suppressed with the progression of body weight loss, while muscle AMPK phosphorylation (Thr 172), AMPK activity, and raptor phosphorylation (Ser 792) were not increased with the initiation of weight loss, but were induced as cachexia progressed. ATP dependent protein degradation increased during the initiation and progression of cachexia. However, ATP independent protein degradation was not increased until cachexia had progressed beyond the initial phase. IL-6 receptor antibody administration prevented body weight loss and suppressed muscle protein degradation, without any effect on muscle %MPS or IGF-1 associated signaling. In summary, the %MPS reduction during the initiation of cachexia is associated with IGF-1/mTOR signaling repression, while muscle AMPK activation and activation of ATP independent protein degradation occur later in the progression of cachexia. IL-6 receptor antibody treatment blocked cachexia progression through the suppression of muscle protein degradation, while not rescuing the suppression of muscle protein synthesis. Attenuation of IL-6 signaling was effective in blocking the progression of cachexia, but not sufficient to reverse the process

The Acute Effects of 5 Fluorouracil on Skeletal Muscle Resident and Infiltrating Immune Cells in Mice

5 fluorouracil (5FU) has been a first-choice chemotherapy drug for several cancer types (e.g., colon, breast, head, and neck); however, its efficacy is diminished by patient acquired resistance and pervasive side effects. Leukopenia is a hallmark of 5FU; however, the impact of 5FU-induced leukopenia on healthy tissue is only becoming unearthed. Recently, skeletal muscle has been shown to be impacted by 5FU in clinical and preclinical settings and weakness and fatigue remain among the most consistent complaints in cancer patients undergoing chemotherapy. Monocytes, or more specifically macrophages, are the predominate immune cell in skeletal muscle which regulate turnover and homeostasis through removal of damaged or old materials as well as coordinate skeletal muscle repair and remodeling. Whether 5FU-induced leukopenia extends beyond circulation to impact resident and infiltrating skeletal muscle immune cells has not been examined. The purpose of the study was to examine the acute effects of 5FU on resident and infiltrating skeletal muscle monocytes and inflammatory mediators. Male C57BL/6 mice were given a physiologically translatable dose (35 mg/kg) of 5FU, or PBS, i.p. once daily for 5 days to recapitulate 1 dosing cycle. Our results demonstrate that 5FU reduced circulating leukocytes, erythrocytes, and thrombocytes while inducing significant body weight loss (\u3e5%). Flow cytometry analysis of the skeletal muscle indicated a reduction in total CD45+ immune cells with a corresponding decrease in total CD45+CD11b+ monocytes. There was a strong relationship between circulating leukocytes and skeletal muscle CD45+ immune cells. Skeletal muscle Ly6cHigh activated monocytes and M1-like macrophages were reduced with 5FU treatment while total M2-like CD206+CD11c- macrophages were unchanged. Interestingly, 5FU reduced bone marrow CD45+ immune cells and CD45+CD11b+ monocytes. Our results demonstrate that 5FU induced body weight loss and decreased skeletal muscle CD45+ immune cells in association with a reduction in infiltrating Ly6cHigh monocytes. Interestingly, the loss of skeletal muscle immune cells occurred with bone marrow cell cycle arrest. Together our results highlight that skeletal muscle is sensitive to 5FU’s off-target effects which disrupts both circulating and skeletal muscle immune cells

Multisphalerons in the Weinberg-Salam Theory

We construct multisphaleron solutions in the Weinberg-Salam theory. The multisphaleron solutions carry Chern-Simons charge $n/2$, where $n$ is an integer, counting the winding of the fields in the azimuthal angle. The well-known sphaleron has $n=1$. The multisphalerons possess axial symmetry and parity reflection symmetry. We vary the Higgs mass and the mixing angle. For small $n$ the energies of the multisphalerons are on the order of $n$ times the energy of the sphaleron and their magnetic dipole moments are on the order of $n$ times the magnetic dipole moment of the sphaleron.Comment: 18 pages, latex, 17 figures in uuencoded postscript files. THU-94/1

IL-6 Regulation on Skeletal Muscle Mitochondrial Remodeling During Cancer Cachexia in the \u3cem\u3eApc\u3csup\u3eMin/+\u3c/sup\u3e\u3c/em\u3e Mouse

BACKGROUND: Muscle protein turnover regulation during cancer cachexia is being rapidly defined, and skeletal muscle mitochondria function appears coupled to processes regulating muscle wasting. Skeletal muscle oxidative capacity and the expression of proteins regulating mitochondrial biogenesis and dynamics are disrupted in severely cachectic ApcMin/+ mice. It has not been determined if these changes occur at the onset of cachexia and are necessary for the progression of muscle wasting. Exercise and anti-cytokine therapies have proven effective in preventing cachexia development in tumor bearing mice, while their effect on mitochondrial content, biogenesis and dynamics is not well understood. The purposes of this study were to 1) determine IL-6 regulation on mitochondrial remodeling/dysfunction during the progression of cancer cachexia and 2) to determine if exercise training can attenuate mitochondrial dysfunction and the induction of proteolytic pathways during IL-6 induced cancer cachexia. METHODS: ApcMin/+ mice were examined during the progression of cachexia, after systemic interleukin (IL)-6r antibody treatment, or after IL-6 over-expression with or without exercise. Direct effects of IL-6 on mitochondrial remodeling were examined in cultured C2C12 myoblasts. RESULTS: Mitochondrial content was not reduced during the initial development of cachexia, while muscle PGC-1α and fusion (Mfn1, Mfn2) protein expression was repressed. With progressive weight loss mitochondrial content decreased, PGC-1α and fusion proteins were further suppressed, and fission protein (FIS1) was induced. IL-6 receptor antibody administration after the onset of cachexia improved mitochondrial content, PGC-1α, Mfn1/Mfn2 and FIS1 protein expression. IL-6 over-expression in pre-cachectic mice accelerated body weight loss and muscle wasting, without reducing mitochondrial content, while PGC-1α and Mfn1/Mfn2 protein expression was suppressed and FIS1 protein expression induced. Exercise normalized these IL-6 induced effects. C2C12 myotubes administered IL-6 had increased FIS1 protein expression, increased oxidative stress, and reduced PGC-1α gene expression without altered mitochondrial protein expression. CONCLUSIONS: Altered expression of proteins regulating mitochondrial biogenesis and fusion are early events in the initiation of cachexia regulated by IL-6, which precede the loss of muscle mitochondrial content. Furthermore, IL-6 induced mitochondrial remodeling and proteolysis can be rescued with moderate exercise training even in the presence of high circulating IL-6 levels