Predicting the population viability of an endangered amphibian under environmental and demographic uncertainty

Population viability analyses (PVAs) represent a key component of many recovery plans for threatened and endangered species. Demography links the processes that affect individuals to population-level patterns, and hence projections constructed from demographic data are the most common tools for PVAs. We constructed a size-structured integral projection model (IPM) for the United States federally endangered Reticulated Flatwoods Salamander, Ambystoma bishopi, to evaluate demographic influences on population growth and predict the efficacy of future management actions. Flatwoods salamanders breed in ephemeral wetlands in the Southeastern United States. The ephemeral nature of breeding sites can result in complete recruitment failure in drought years when wetlands fail to fill, or dry before metamorphosis occurs. As a result, this species exhibits marked temporal variability in vital rates that must be accounted for in projection models. We constructed a stochastic IPM using 13 years of mark-recapture data (2010–2023) from two breeding wetlands. Variable survival rates exhibited by flatwoods salamanders, coupled with a high probability of recruitment failure, result in a low predicted probability of population persistence. Sensitivity analyses revealed age at maturity and the frequency of recruitment exerted the greatest influence on population growth, and thus managers should prioritize conservation efforts that target these demographic processes. Additional management should consider strategies to dampen temporal variability in larval survival, something that could be achieved through emergency salvage operations, captive rearing efforts, and manipulation of wetland hydroperiods

Entangled state preparation via dissipation-assisted adiabatic passages

The main obstacle for coherent control of open quantum systems is decoherence due to different dissipation channels and the inability to precisely control experimental parameters. To overcome these problems we propose to use dissipation-assisted adiabatic passages. These are relatively fast processes where the presence of spontaneous decay rates corrects for errors due to non-adiabaticity while the system remains in a decoherence-free state and behaves as predicted for an adiabatic passage. As a concrete example we present a scheme to entangle atoms by moving them in and out of an optical cavity.Comment: 11 pages, 7 figures, minor changes, accepted for publication in Phys. Rev.

Changes in rat n-3 and n-6 fatty acid composition during pregnancy are associated with progesterone concentrations and hepatic FADS2 expression

The mechanisms responsible for changes to long-chain polyunsaturated fatty acid (LC PUFA) status during pregnancy have not been fully elucidated. Tissue samples were collected from virgin and pregnant (day 12 and 20) female rats. LC PUFA status, sex hormone concentrations and hepatic mRNA expression of FADS1, FADS2 and elongase were assessed. Day 20 gestation females had higher plasma and liver docosahexaenoic acid and lower arachidonic acid content than virgin females (P<0.05). There was higher FADS2 mRNA expression during pregnancy (P=0.051). Progesterone and oestradiol concentrations positively correlated with hepatic FADS2 mRNA expression (P=0.043, P=0.004). Progesterone concentration positively correlated with hepatic n-6 docosapentaenoic acid content (P=0.006), and inversely correlated with intermediates in LC PUFA synthesis including n-3 docosapentaenoic acid, ?-linolenic acid and 20:2n-6 (P<0.05). Changes in progesterone and oestradiol during pregnancy may promote the synthesis of LC PUFA via increased FADS2 expression

Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan

Cellular senescence, a stress-induced irreversible growth arrest often characterized by expression of p16(Ink4a) (encoded by the Ink4a/Arf locus, also known as Cdkn2a) and a distinctive secretory phenotype, prevents the proliferation of preneoplastic cells and has beneficial roles in tissue remodelling during embryogenesis and wound healing. Senescent cells accumulate in various tissues and organs over time, and have been speculated to have a role in ageing. To explore the physiological relevance and consequences of naturally occurring senescent cells, here we use a previously established transgene, INK-ATTAC, to induce apoptosis in p16(Ink4a)-expressing cells of wild-type mice by injection of AP20187 twice a week starting at one year of age. We show that compared to vehicle alone, AP20187 treatment extended median lifespan in both male and female mice of two distinct genetic backgrounds. The clearance of p16(Ink4a)-positive cells delayed tumorigenesis and attenuated age-related deterioration of several organs without apparent side effects, including kidney, heart and fat, where clearance preserved the functionality of glomeruli, cardio-protective KATP channels and adipocytes, respectively. Thus, p16(Ink4a)-positive cells that accumulate during adulthood negatively influence lifespan and promote age-dependent changes in several organs, and their therapeutic removal may be an attractive approach to extend healthy lifespan

Phosphorylation of caldesmon by myosin light chain kinase increases its binding affinity for phosphorylated myosin filaments

Phosphorylation of myosin by myosin light chain kinase (MLCK) is essential for smooth muscle contraction. In this study we show that caldesmon (CaD) is also phosphorylated in vitro by MLCK. The phosphorylation is calcium- and calmodulin (CaM)-dependent and requires a MLCK concentration close to that found in vivo. On average, approximately 2 mol Pi per mol of CaD are incorporated at Thr-626 and Thr-693, with additional partial phosphorylation at Ser-658 and Ser-702. The phosphorylation rate for CaD is 20- to 50-fold slower than that for filamentous myosin; faster relative rates were obtained with CaD added to purified actomyosin or myosin preparations containing endogenous MLCK/CaM complex. Addition of CaM also augmented CaD phosphorylation. We further demonstrate that [32P] labeled CaD binds much more readily to phosphorylated filamentous myosin than to unphosphorylated myosin. For actomyosin, CaD binding affinity doubles after myosin phosphorylation, without a significant change in binding stoichiometry (approx. one CaD per myosin molecule). Unphosphorylated CaD is ineffective in competing with the phosphorylated protein for the binding site(s) on myosin filaments. The ATPase activity of reconstituted actomyosin is inhibited by unphosphorylated CaD, and this inhibition was removed by CaD phosphorylation. Our results suggest that CaD phosphorylation plays a role in modifying actomyosin interaction in vivo, particularly during prolonged muscle activation