Toward a physiological explanation of juvenile growth curves

Juvenile growth curves are generally sigmoid in shape: Growth is initially nearly exponential, but it slows to near zero as the animal approaches maturity. The drop‐off in growth rate is puzzling because, everything else being equal, selection favors growing as fast as possible. Existing theory posits sublinear scaling of resource acquisition with juvenile body mass and linear scaling of the requirement for maintenance, so the difference, fuel for growth, decreases as the juvenile increases in size. Experimental evidence, however, suggests that maintenance metabolism increases sublinearly not linearly with size. Here, we develop a new theory consistent with the experimental evidence. Our theory is based on the plausible assumption that there is a trade‐off in the capacity of capillaries to supply growing and developed cells. As the proportion of non‐growing cells increases, they take up more macromolecules from the capillaries, leaving fewer to support growing cells. The predicted growth curves are realistic and similar to those of previous models (Bertalanffy, Gompertz, and Logistic) but have the advantage of being derived from a plausible physiological model. We hope that our focus on resource delivery in capillaries will encourage new experimental work to identify the detailed physiological basis of the trade‐off underlying juvenile growth curves

(S)-6-Methyl-∊-caprolactone

The chiral title compound, C7H12O2, a lactone derivative, features a seven-membered ring that adopts a chair conformation. The crystal structure is stabilized by weak C—H⋯O inter­actions occurring in the (100) plane. The absolute configuration was assigned on the basis of the enantioselective synthesis

Critical turbulence revisited: The impact of submesoscale vertical mixing on plankton patchiness

By supplying nutrients to the ocean surface, submesoscale vertical motions can have a strong impact on phytoplankton growth and phytoplankton distributions. To study this impact, we model a phytoplankton population in a baroclinically unstable submesoscale eddy using a phytoplankton model coupled to a three-dimensional hydrodynamic model. In the eddy, strong vertical transports are generated as a consequence of baroclinic instability. The resulting plankton distributions turn out to depend strongly on the light intensity and local vertical transport. To analyze these distributions in detail, we use more idealized coupled hydrodynamic-biological models and we extend the critical turbulence concept to three dimensions

(4aS,5R,7R,8S,8aR)-8-(1,3-Dioxolan-2-yl)-7,8-dimethyl-5-(1-methyl­ethen­yl)perhydro­naphthalen-2-one

In the chiral title compound, C18H28O3, the two six-membered rings of the perhydronaphthalenone adopt a rigid chair–chair conformation and the five-membered dioxolanyl ring adopts an envelope conformation. The crystal structure is stabilized only by weak inter­actions

Modes of Growth in Dynamic Systems

Regardless of a system's complexity or scale, its growth can be considered to be a spontaneous thermodynamic response to a local convergence of down-gradient material flows. Here it is shown how growth can be constrained to a few distinct modes that depend on the availability of material and energetic resources. These modes include a law of diminishing returns, logistic behavior and, if resources are expanding very rapidly, super-exponential growth. For a case where a system has a resolved sink as well as a source, growth and decay can be characterized in terms of a slightly modified form of the predator-prey equations commonly employed in ecology, where the perturbation formulation of these equations is equivalent to a damped simple harmonic oscillator. Thus, the framework presented here suggests a common theoretical under-pinning for emergent behaviors in the physical and life sciences. Specific examples are described for phenomena as seemingly dissimilar as the development of rain and the evolution of fish stocks.Comment: 16 pages, 6 figures, including appendi

Neuroprotection by Insulin-like Growth Factor-1 in Rats with Ischemic Stroke is Associated with Microglial Changes and a Reduction in Neuroinflammation

We and others have shown that insulin-like growth factor-1 (IGF-1) is neuroprotective when administered systemically shortly following stroke. In the current study, we addressed the hypothesis that microglia mediate neuroprotection by IGF-1 following ischemic stroke. Furthermore, we investigated whether IGF-1 modulates pro- and anti-inflammatory mediators in ischemic brain with a special reference to microglia. Ischemic stroke was induced in normal conscious Wistar rats by infusing the vasoconstrictor, endothelin-1 (Et-1), next to middle cerebral artery (MCA). IGF-1 (300 μg) was injected subcutaneously (SC) at 30 and 120 min following stroke. Microglial inhibitor, minocycline, was injected intraperitoneally (IP) at 1 h before stroke (25 mg/kg) and 11 h after stroke (45 mg/kg). Post-stroke IGF-1 treatment reduced the infarct size and increased the sensorimotor function which coincided with an increase in the number of ameboid microglia in the ischemic cortex. Minocycline treatment abrogated the increase in ameboid microglia by IGF-1, while the effect of IGF-1 in the reduction of infarct size was only partially affected. IGF-1 suppressed mRNA expression of inducible nitric oxide synthase (iNOS) and interleukin (IL)-1β in the ischemic hemisphere, while in purified microglia, only iNOS expression levels were reduced. Our findings show that microglia are a target for IGF-1 and that neuroprotection by IGF-1 coincides with down-regulation of inflammatory mediators which could be instrumental to the beneficial effects