Production of antimicrobial peptides and proteins is an important means of host defense in eukaryotes. The larger antimicrobial proteins, containing more than 100 amino acids, are often lytic enzymes, nutrient-binding proteins or contain sites that target specific microbial macromolecules. The smaller antimicrobial peptides act largely by disrupting the structure or function of microbial cell membranes. Hundreds of antimicrobial peptides have been found in the epithelial layers, phagocytic cells and body fluids of multicellular animals, from mollusks to humans. Some antimicrobial peptides are produced constitutively, others are induced in response to infection or inflammation. Studies of the regulation of antimicrobial peptide synthesis in Drosophila have been particularly fruitful, and have provided a new paradigm for the analysis of mammalian host defense responses. It now appears that the general patterns of antimicrobial responses of invertebrates have been preserved in vertebrates ("innate immunity") where they contribute to host defense both independently and in complex interplay with adaptive immunity.
Different tendons are (i) subject to very different stresses from their muscles and (ii) differ in their susceptibility to fatigue damage. The fatigue quality of each tendon is matched to the stress it experiences, so that, in life, all tendons are similarly prone to damage. On-going damage must be routinely repaired to maintain homeostasis and prevent damage from becoming symptomatic. The discovery of major differences in fatigue quality among tendons, which had previously seemed fairly similar in their mechanical properties, raises a wide range of new questions. (A) What structural and chemical differences underlie the variations in fatigue quality? (B) What molecular structure in the tendon is damaged and how is repair organised? (C) Is fatigue quality adaptable and if so what is the trigger for adaptation? Putting these questions into context leads to an integrated review of tendon, including structure and chemistry, the turnover of proteins, the cross-linking of collagen and the response of tenocytes to load on the tendon.
The leg tendons of certain avian species normally calcify. The gastrocnemius, or Achilles, tendon of the domestic turkey, Meleagris gallopavo, is one such example. Its structure and biomechanical properties have been studied to model the adaptive nature of this tendon to external forces, including the means by which mineral deposition occurs and the functional role mineralization may play in this tissue. Structurally, the distal rounded, thick gastrocnemius bifurcates into two smaller proximal segments that mineralize with time. Mineral deposition occurs at or near the bifurcation, proceeding in a distal-to-proximal direction along the segments toward caudal and medial muscle insertions of the bird hip. Mineral formation appears mediated first by extracellular matrix vesicles and later by type I collagen fibrils. Biomechanical analyses indicate lower tensile strength and moduli for the thick distal gastrocnemius compared to narrow, fan-shaped proximal segments. Tendon mineralization here appears to be strain-induced, the muscle forces causing matrix deformation leading conceptually to calcium binding through the exposure of charged groups on collagen, release of sequestered calcium by proteoglycans, and increased diffusion. Functionally, the mineralized tendons limit further tendon deformation, reduce tendon strain at a given stress, and provide greater load-bearing capacity to the tissue. They also serve as important and efficient elastic energy storage reservoirs, increasing the amount of stored elastic energy by preventing flexible type I collagen regions from stretching and preserving muscle energy during locomotion of the animals.
Two models have been proposed to describe the prey transport kinematics of terrestrial vertebrates (Bramble and Wake, 1985; Reilly and Lauder, 1990). The critical difference between the models is the presence or absence of a slow open-II phase (SO-II) in the gape profile during mouth opening. Each of these models has been applied to lizards, however to date, lizard feeding kinematics have not been adequately quantified to assess the utility of these models for this clade. Neither model has been sufficiently tested due to the lack of a methodology to assess the specific differences between the models. We describe a method that uses explicit mathematical criteria to define the kinematic phases in tetrapod feeding. This "slope analysis& is used to precisely quantify and compare the transport kinematics of seven lizard species. Lizard transport kinematics were highly variable both within and across taxa. However, several common gape cycle patterns were identified. The predominant patterns were slow-fast opening (37.3%), fast opening only (22.9%) and slow opening only (21.2%). The most common pattern explicitly fits the prediction of the Reilly and Lauder model while the other two are similar to patterns observed in salamanders. Thus, lizards possess both the slow opening-fast opening pattern predicted for amniotes and the more primitive, simple opening pattern characteristic of more basal tetrapods. Plateau phases were found in only 12.8% of the profiles and only a fourth of these (3.4% of the total) explicitly fit the Bramble and Wake model (slow opening, plateau, fast opening) and two species never exhibited plateaus in their gape cycles. Thus, it is clear that the Bramble and Wake model is not supported as a generalized model for lizards or generalized tetrapods.
Postinhibitory rebound (PIR) is an intrinsic property of many neurons but the underlying mechanism is not well understood. We studied PIR and its relationship to spike adaptation in B-cells isolated from the buccal ganglia of Aplysia. These neurons exhibit PIR following inhibitory synaptic input and following direct membrane hyperpolarization. Hyperpolarizing and depolarizing voltage clamp pulses from the resting potential evoke slow changes in membrane current that persist in the form of tail currents following the pulses. A subtraction method was used to isolate slow tail currents for study. Current-voltage measurements indicate that slow outward tail currents following depolarizing pulses result from increases in membrane conductance, while inward tail currents following hyperpolarizations to −50 and −60 mV result from conductance decreases. The reversal potential of both outward and inward tail current is between −60 and −70 mV. Tail currents activated by pulses more positive than −60 mV are sensitive to the external K+ concentration and blocked by injection of Cs+ and TEA. When Ca2+ influx is prevented by bathing cells in Ca2+ free saline or by adding Co2+ or Ni2+, the tail currents are reduced but a significant fraction of the current is insensitive to these treatments. More negative conditioning pulses activate a second component of inward tail current that is weakly sensitive to K+ but more strongly effected by substitution of N-methyl glucamine or Li+ for external Na+. We conclude that both PIR and adaptation result from slow changes in a voltage dependent, non-inactivating K+ conductance that is active at voltages near the resting potential and is not tightly coupled to Ca2+ influx. In addition, a second inward current is activated by large hyperpolarizing pulses that results from an increase in Na+ and K+ conductance. This second process is likely to contribute to PIR under particular circumstances.
