Role of gestation delay in a plankton-fish model under stochastic fluctuations

The present paper studies a minimal prey-predator model in the context of marine plankton interaction together with predation by planktivorous fish. The time lag required for gestation of the predator is incorporated and the resulting delayed model is analyzed for stability and bifurcation phenomena. A stochastic extension of the model is considered by perturbing the growth process of phytoplankton using colored noise process known to be more appropriate for the marine environment. The stochastic models with and without gestation delay are analyzed for stability aspects and a threshold value of gestation delay is obtained; this threshold is then compared with that of the deterministic model.     

一类含分布时滞革新传播模型的稳定性

建立了一类含分布时滞的革新传播模型dU（t）/dt=-（α＋βA（t））U（t）-pU（t）＋p,dA（t）/dt=∫＋∞ 0 αE（τ）U（t-τ）dτ＋βU（t）A（t）-（p＋k）A（t）。研究了分布时滞对传播过程的影响,讨论了正平衡点的存在性和唯一性及其局部与全局的渐近稳定性,当分布时滞的核函数取δe^-δτ时,证明了正平衡点是绝对渐近稳定的。     

Oxidant-induced cell-cycle delay in Saccharomyces cerevisiae: the involvement of the SWI6 transcription factor

Cells treated with low doses of linoleic acid hydroperoxide (LoaOOH) exhibit a cell-cycle delay that may provide a mechanism to overcome oxidative stress. Strains sensitive to LoaOOH from the genome-wide deletion collection were screened to identify deletants in which the cell-cycle delay phenotype was reduced. Forty-seven deletants were identified that were unable to mount the normal delay response, implicating the product of the deleted gene in the oxidant-mediated cell-cycle delay of the wild-type. Of these genes, SWI6 was of particular interest due to its role in cell-cycle progression through Start. The swi6 deletant strain was delayed on entry into the cell cycle in the absence of an oxidant, and oxidant addition caused no further delay. Transforming the swi6 deletant with SWI6 on a plasmid restored the G1 arrest in response to LoaOOH, indicating that Swi6p is involved in oxidant sensing leading to cell division delay. Micro-array studies identified genes whose expression in response to LoaOOH depended on SWI6. The screening identified 77 genes that were upregulated in the wild-type strain and concurrently downregulated in the swi6 deletant treated with LoaOOH. These data show that functions such as heat shock response, and glucose transport are involved in the response.     

Identification of the Nucleotidase Responsible for the AMP Hydrolysing Hyperactivity Associated with Neurological and Developmental Disorders

Nucleoside monophosphate phosphohydrolases comprise a family of enzymes dephosphorylating nucleotides both in intracellular and extracellular compartments. Members of this family exhibit different sequence, location, substrate specificity and regulation. Besides the ectosolic 5′-nucleotidase, several cytosolic and one mitochondrial enzymes have been described. Nevertheless, researchers refer any AMP-dephosphorylating activity to as 5′-nucleotidase, lacking a more accurate identification. Increase of AMP hydrolysing activity has been associated with neurological and developmental disorders. The identification of the specific enzyme involved in these pathologies would be fundamental for the comprehension of the linkage between the enzyme activity alteration and brain functions. We demonstrate that the described neurological symptoms are associated with increased ectosolic 5′-nucleotidase activity on the basis of radiochemical assays and immunoblotting analysis. Furthermore, present data evidence that the assay conditions normally applied for the determination of cytosolic 5′-nucleotidases activity in crude extracts are affected by the presence of solubilised ectosolic nucleotidase.     

The Precautionary Principle,Epidemiology and the Ethics of Delay

Ethics tells us: do good and do no harm and invokes the norms of justice, equity and respect for autonomy in protecting and promoting health and well-being. The Precautionary Principle, a contemporary re-definition of Bradford Hill's case for action, gives us a common sense rule for doing good by preventing harm to public health from delay: when in doubt about the presence of a hazard, there should be no doubt about its prevention or removal. It shifts the burden of proof from showing presence of risk to showing absence of risk, aims to do good by preventing harm, and subsumes the upstream strategies of the DPSEEA (Driving Forces Pressure Stress Exposure Effect Action) model and downstream strategies from molecular epidemiology for detection and prevention of risk. The Precautionary Principle has emerged because of the ethical import of delays in detection of risks to human health and the environment. Ethical principles, the Precautionary Principle, the DPSEEA model and molecular epidemiology all imply re-emphasizing epidemiology's classic rôle for early detection and prevention. Delays in recognizing risks from past exposures and acting on the findings (e.g., cigarette smoking and lung cancer, asbestos, organochlorines and endocrine disruption, radiofrequency, raised travel speeds) were examples of failures that were not only scientific, but ethical, since they resulted in preventable harm to exposed populations. These may delay results from, among other things, external and internal determinants of epidemiologic investigations of hazard and risk, including misuse of tests of statistical significance. Furthermore, applying the Precautionary Principle to ensure justice, equity, and respect for autonomy raises questions concerning the short-term costs of implementation to achieve long-term goals and the principles that guide compensation.     

分布时滞竞争模型的周期解

研究了分布时滞竞争模型周期解,利用Gaines与Mawhin的重合度理论,通过构造恰当的Lyapunov函数得到模型正周期解的存在性、唯一性及全局稳定性。     

Echo delay versus spectral cues for temporal hyperacuity in the big brown bat,Eptesicus fuscus

Big brown bats can discriminate between echoes that alternate in delay (jitter) by as little as 10–15 ns and echoes that are stationary in delay. This delay hyperacuity seems so extreme that it has been rejected in favor of an explanation in terms of artifacts in echoes, most likely spectral in nature, that presumably are correlated with delay. Using different combinations of digital, analog, and cable delays, we dissociated the overall delay of jittering echoes from the size of the analog component of delay, which alone is presumed to determine the strength of the apparatus artifact. The bats' performance remains invariant with respect to the overall delay of the jittering echoes, not with respect to the amount of analog delay. This result is not consistent with the possible use of delay-related artifacts produced by the analog delay devices. Moreover, both electronic and acoustic measurements disclose no spectral cues or impedance-mismatch reflections in delayed signals, just time-delays. The absence of artifacts from the apparatus and the failure of overlap and interference from reverberation to account for the 10-ns result means that closing the gap between the level of temporal accuracy plausibly explained from physiology and the level observed in behavior may require a better understanding of the physiology.Abbreviations FM frequency-modulated - XCR cross-correlation function     

Enhancement of the steady-state magnetization in TROSY experiments

Under the condition that the longitudinal relaxation time of spin I is shorter than the longitudinal relaxation time of spin S the steady-state magnetization in [S,I]-TROSY-type experiments can be enhanced by intermediate storage of a part of the steady-state magnetization of spin I on spin S with a pulse sequence element during the relaxation delay. It is demonstrated with samples ranging in size from the 1 kDa cyclosporin to the 110 kDa ¹⁵N,²H-labeled dihydroneopterin Aldolase that intermediate storage of steady-state magnetization in a [¹⁵N,¹H]-TROSY experiment yields a signal gain of 10–25%. The method proposed here for intermediate storage of steady-state magnetization can be implemented in any [¹⁵N,¹H]-TROSY-type experiments.     

Adjusting for reporting delay in cancer incidence when combining different sets of cancer registries

Cancer registries collect cancer incidence data that can be used to calculate incidence rates in a population and track changes over time. For incidence rates to be accurate, it is critical that diagnosed cases be reported in a timely manner. Registries typically allow a fixed amount of time (e.g. two years) for diagnosed cases to be reported before releasing the initial case counts for a particular diagnosis year. Inevitably, however, additional cases are reported after the initial counts are released; these extra cases are included in subsequent releases that become more complete over time, while incidence rates based on earlier releases will underestimate the true rates. Statistical methods have been developed to estimate the distribution of reporting delay (the amount of time until a diagnosed case is reported) and to correct incidence rates for underestimation due to reporting delay. Since the observed reporting delays must be less than the length of time the registry has been collecting data, most methods estimate a truncated delay distribution. These methods can be applied to a group of registries that began collecting data in the same diagnosis year. In this paper, we extend the methods to two groups of registries that began collecting data in two different diagnosis years (so that the delay distributions are truncated at different times). We apply the proposed method to data from the National Cancer Institute's Surveillance Epidemiology and End Results (SEER) program, a consortium of U.S. cancer registries that includes nine registries with data collection beginning in 1981 and four registries with data collection beginning in 1992. We use the method to obtain delay‐adjusted incidence rates for melanoma, liver cancer, and Hodgkin lymphoma.