69 research outputs found
The winter habits of plants
Citation: Bergman, Herbert F. The winter habits of plants. Senior thesis, Kansas State Agricultural College, 1905.Morse Department of Special CollectionsIntroduction: In climates there is a period at some time of the year when plants cannot continue to live in an active state, but are required, by environmental conditions, to assume a form that will enable them to live through the unfavorable period. Whether a plant must pass through a period of cold, unfavorable to plant activity, or through a periodic drouth, the methods of meeting both these adverse conditions are the same. Since, in the temperate zone, it is the cold against which the plants must protect themselves, the forms assumed by them for protection during the winter are called their winter habits. If one should take a stroll through the fields or woods in the fall, he would notice that all plants do not succumb to the cold at the same time. Some plants cease activity at the "first suggestion of cold, while others continue through a. long succession of frosts before they perish. For example, such trees as the Maple, Boxelder, and Ash shed their leaves early, while cottonwood, elms and oaks cone somewhat later; many oaks retaining their leaves throughout the winter, shedding them early the following spring. Other plants yet, such as conifers, mosses, liver-orts and lichens, live through the winter with no apparent change. Between the group of plants which are killed by the winter, and the group which survive without apparent change in outward forms, stand the deciduous plants which cast their leaves and the herbaceous plants with thickened underground stems or roots wherein the living substance, withdrawn from the leaves and stems, is able to survive the winter. The degree of cold necessary to cruse the death of any plant depends upon the nature of the protoplasm, i, e. the ability of the protoplasts of that kind of plant to withstand adverse conditions, and also upon the stage of development or activity of the plant at the time it is subjected to the cold
Increased searching and handling effort in tall swards lead to a Type IV functional response in small grazing herbivores
Understanding the functional response of species is important in comprehending the species’ population dynamics and the functioning of multi-species assemblages. A Type II functional response, where instantaneous intake rate increases asymptotically with sward biomass, is thought to be common in grazers. However, at tall, dense swards, food intake might decline due to mechanical limitations or if animals selectively forage on the most nutritious parts of a sward, leading to a Type IV functional response, especially for smaller herbivores. We tested the predictions that bite mass, cropping time, swallowing time and searching time increase, and bite rate decreases with increasing grass biomass for different-sized Canada geese (Branta canadensis) foraging on grass swards. Bite mass indeed showed an increasing asymptotic relationship with grass biomass. At high biomass, difficulties in handling long leaves and in locating bites were responsible for increasing cropping, swallowing, and searching times. Constant bite mass and decreasing bite rate caused the intake rate to decrease at high sward biomass after reaching an optimum, leading to a Type IV functional response. Grazer body mass affected maximum bite mass and intake rate, but did not change the shape of the functional response. As grass nutrient contents are usually highest in short swards, this Type IV functional response in geese leads to an intake rate that is maximised in these swards. The lower grass biomass at which intake rate was maximised allows resource partitioning between different-sized grazers. We argue that this Type IV functional response is of more importance than previously thought
The uncoupling protein 1 gene, UCP1, is expressed in mammalian islet cells and associated with acute insulin response to glucose in African American families from the IRAS Family Study
BACKGROUND: Variants of uncoupling protein genes UCP1 and UCP2 have been associated with a range of traits. We wished to evaluate contributions of known UCP1 and UCP2 variants to metabolic traits in the Insulin Resistance and Atherosclerosis (IRAS) Family Study. METHODS: We genotyped five promoter or coding single nucleotide polymorphisms (SNPs) in 239 African American (AA) participants and 583 Hispanic participants from San Antonio (SA) and San Luis Valley. Generalized estimating equations using a sandwich estimator of the variance and exchangeable correlation to account for familial correlation were computed for the test of genotypic association, and dominant, additive and recessive models. Tests were adjusted for age, gender and BMI (glucose homeostasis and lipid traits), or age and gender (obesity traits), and empirical P-values estimated using a gene dropping approach. RESULTS: UCP1 A-3826G was associated with AIR(g )in AA (P = 0.006) and approached significance in Hispanic families (P = 0.054); and with HDL-C levels in SA families (P = 0.0004). Although UCP1 expression is reported to be restricted to adipose tissue, RT-PCR indicated that UCP1 is expressed in human pancreas and MIN-6 cells, and immunohistochemistry demonstrated co-localization of UCP1 protein with insulin in human islets. UCP2 A55V was associated with waist circumference (P = 0.045) in AA, and BMI in SA (P = 0.018); and UCP2 G-866A with waist-to-hip ratio in AA (P = 0.016). CONCLUSION: This study suggests a functional variant of UCP1 contributes to the variance of AIR(g )in an AA population; the plausibility of this unexpected association is supported by the novel finding that UCP1 is expressed in islets
Filovirus RefSeq Entries: Evaluation and Selection of Filovirus Type Variants, Type Sequences, and Names
Sequence determination of complete or coding-complete genomes of viruses is becoming common practice for supporting the work of epidemiologists, ecologists, virologists, and taxonomists. Sequencing duration and costs are rapidly decreasing, sequencing hardware is under modification for use by non-experts, and software is constantly being improved to simplify sequence data management and analysis. Thus, analysis of virus disease outbreaks on the molecular level is now feasible, including characterization of the evolution of individual virus populations in single patients over time. The increasing accumulation of sequencing data creates a management problem for the curators of commonly used sequence databases and an entry retrieval problem for end users. Therefore, utilizing the data to their fullest potential will require setting nomenclature and annotation standards for virus isolates and associated genomic sequences. The National Center for Biotechnology Information’s (NCBI’s) RefSeq is a non-redundant, curated database for reference (or type) nucleotide sequence records that supplies source data to numerous other databases. Building on recently proposed templates for filovirus variant naming [ ()////-], we report consensus decisions from a majority of past and currently active filovirus experts on the eight filovirus type variants and isolates to be represented in RefSeq, their final designations, and their associated sequences
Cationic Amino Acid Transporter-2 Regulates Immunity by Modulating Arginase Activity
Cationic amino acid transporters (CAT) are important regulators of NOS2 and ARG1 activity because they regulate L-arginine availability. However, their role in the development of Th1/Th2 effector functions following infection has not been investigated. Here we dissect the function of CAT2 by studying two infectious disease models characterized by the development of polarized Th1 or Th2-type responses. We show that CAT2−/− mice are significantly more susceptible to the Th1-inducing pathogen Toxoplasma gondii. Although T. gondii infected CAT2−/− mice developed stronger IFN-γ responses, nitric oxide (NO) production was significantly impaired, which contributed to their enhanced susceptibility. In contrast, CAT2−/− mice infected with the Th2-inducing pathogen Schistosoma mansoni displayed no change in susceptibility to infection, although they succumbed to schistosomiasis at an accelerated rate. Granuloma formation and fibrosis, pathological features regulated by Th2 cytokines, were also exacerbated even though their Th2 response was reduced. Finally, while IL-13 blockade was highly efficacious in wild-type mice, the development of fibrosis in CAT2−/− mice was largely IL-13-independent. Instead, the exacerbated pathology was associated with increased arginase activity in fibroblasts and alternatively activated macrophages, both in vitro and in vivo. Thus, by controlling NOS2 and arginase activity, CAT2 functions as a potent regulator of immunity
Rule-Based Cell Systems Model of Aging using Feedback Loop Motifs Mediated by Stress Responses
Investigating the complex systems dynamics of the aging process requires integration of a broad range of cellular processes describing damage and functional decline co-existing with adaptive and protective regulatory mechanisms. We evolve an integrated generic cell network to represent the connectivity of key cellular mechanisms structured into positive and negative feedback loop motifs centrally important for aging. The conceptual network is casted into a fuzzy-logic, hybrid-intelligent framework based on interaction rules assembled from a priori knowledge. Based upon a classical homeostatic representation of cellular energy metabolism, we first demonstrate how positive-feedback loops accelerate damage and decline consistent with a vicious cycle. This model is iteratively extended towards an adaptive response model by incorporating protective negative-feedback loop circuits. Time-lapse simulations of the adaptive response model uncover how transcriptional and translational changes, mediated by stress sensors NF-κB and mTOR, counteract accumulating damage and dysfunction by modulating mitochondrial respiration, metabolic fluxes, biosynthesis, and autophagy, crucial for cellular survival. The model allows consideration of lifespan optimization scenarios with respect to fitness criteria using a sensitivity analysis. Our work establishes a novel extendable and scalable computational approach capable to connect tractable molecular mechanisms with cellular network dynamics underlying the emerging aging phenotype
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