Alternation of sleeping groves by yellow baboons (Papio cynocephalus) as a strategy for parasite avoidance

The primary locus of contact between free-living yellow baboons (Papio cynocephalus) in the Amboseli National Park of Kenya and the infective stages of their intestinal parasites is believed to be soil beneath sleeping trees contaminated by the baboons' own fecal emissions. In this report, we present evidence both that infective ova and larvae of intestinal parasites are found at very high densities in the soil beneath sleeping groves and that Amboseli baboons substantially reduce their contact with this reservoir of parasites by alternating periods of a few consecutive nights' use of any particular grove with much longer periods of avoidance of that grove. Although many factors other than the presence of parasite larvae also influence choice of sleeping groves, we propose as a working hypothesis that the temporal pattern of sleeping grove alternation shown by Amboseli baboons reflects a subtle behavioral strategy for parasite avoidance.     

Inhibition of thermolysin and human alpha-thrombin by cobalt(III) Schiff base complexes.

Cobalt(III) Schiff base complexes have been shown to inhibit the replication of the ocular herpes virus. It is well known that these complexes have a high affinity for nitrogenous donors such as histidine residues, and it is possible that they bind to (and inhibit) an enzyme that is crucial to viral replication. In model studies, we have found that [Co(acacen)(NH3)2]+ is an effective irreversible inhibitor of thermolysin at millimolar concentrations; it also inhibits human alpha-thrombin. Axial ligand exchange with an active-site histidine is the proposed mechanism of inhibition. The activity of thermolysin and thrombin can be protected by binding a reversible inhibitor to the active site before addition of the cobalt(III) complex.     

Effect of genetic background on glycosylation heterogeneity in human antithrombin produced in the mammary gland of transgenic goats

Glycosylation is involved in the correct folding, targeting, bioactivity and clearance of therapeutic glycoproteins. With the development of transgenic animals as expression systems it is important to understand the impact of different genetic backgrounds and lactations on glycosylation. We have evaluated the glycosylation of recombinant antithrombin produced in several transgenic goat lines, from cloned animals and from different types of lactation including induced lactations. Our results show glycosylation patterns from the protein expressed in animals, derived from the same founder goat, are mostly comparable. Furthermore, the protein expressed in two cloned goats had highly consistent oligosaccharide profiles and similar carbohydrate composition. However, there were significantly different oligosaccharide profiles from the proteins derived from different founder goats. Artificial induction of lactation did not have significant effects on overall carbohydrate structures when compared to natural lactation. The only major difference was that recombinant antithrombin from induced lactations contained a slightly higher ratio of N-acetylneuraminic acid to N-glycolylneuraminic acid and less amount of oligosaccharides containing N-glycolylneuraminic acid. The oligosaccharides from all animals were a mixture of high mannose-, hybrid- and complex-type oligosaccharides. Sialic acid was present as alpha-2,6-linkage and no alpha-1,3-linked galactose was observed. These results indicate that transgenic animals with closely related genetic backgrounds express recombinant protein with comparable glycosylation.     

Why do asthmatic subjects respond so strongly to inhaled adenosine?

Bronchospasm induced by adenosine is blocked by representatives of all the major classes of drugs used in the treatment of asthma. Understanding the mechanism of this bronchospasm may help understand the way these drugs work. Clinical studies have suggested involvement of neural pathways, mast-like cells and mediators such as histamine, serotonin and lipoxygenase products. There is a strong link between responsiveness to adenosine and eosinophilia. In different animal models A1, A2b and A3 adenosine receptor subclasses have all been implicated in inducing bronchospasm. whilst occupation of the A2a receptor generally has no, or the opposite effect. At least two different mechanisms, both involving neural pathways, exist. One, involving the adenosine A1 receptor, functions in mast cell depleted animals; the other requires interaction with a population of mast-like cells activated over A2b or A3 receptors. Not only histamine but also serotonin and lipoxygenase products released from the mast-like cells are potential mediators. In animal models good reactivity to adenosine receptor agonists is generally only found when the animals are first sensitized and exposed to allergen in ways likely to induce an allergic inflammation. An exception is the BDE rat, which reacts to adenosine receptor agonists such as APNEA or NECA even without allergen exposure. This rat strain does however show evidence of spontaneous eosinophilic inflammation in the lung even without immunization. As mast cells both release adenosine and respond to adenosine, adenosine provides a non-specific method of amplifying specific signals resulting from IgE/antigen interaction. This mechanism may not only have a pathological significance in asthma; it may be part of a normal bodily defense response that in asthmatic subjects is inappropriately activated.     

Comparison of carpal canal pressure in paraplegic and nonparaplegic subjects: clinical implications

The purpose of this study was to evaluate the pressure within the carpal tunnel that was generated with certain tasks in paraplegic versus nonparaplegic subjects. Four groups of subjects were evaluated: 10 wrists in six paraplegic subjects with carpal tunnel syndrome, 11 wrists in six paraplegics without the syndrome, 12 wrists in nine nonparaplegics with the syndrome, and 17 wrists in 11 nonparaplegics without the syndrome. Carpal canal pressures were measured in the wrists in three positions (neutral, 45-degree flexion, 45-degree extension) and during two dynamic tasks [wheelchair propulsion and RAISE (relief of anatomic ischial skin embarrassment) maneuver]. External force resistors were placed over the carpal canal and correlated with internal tunnel pressures. At each wrist position, paraplegics with carpal tunnel syndrome consistently had higher carpal canal pressure than did the other groups at the corresponding wrist position; statistical significance was evident with regard to the neutral wrist position (p < 0.05). Within each group of subjects, wrist extension and wrist flexion produced a statistically significant increase in carpal canal pressure (p < 0.05), compared with the neutral wrist position. Dynamic tasks (wheelchair propulsion and the RAISE maneuver) significantly elevated the carpal canal pressure in paraplegics with carpal tunnel syndrome, compared with the other groups (p < 0.05). Lastly, there is a linear positive correlation between carpal canal pressure and external force resistance.