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Abstract Helicopter-based shooting is an effective management tool for large vertebrate pest animals. However, animals in low-density populations and/or dense habitat can be difficult to locate visually. Thermal-imaging technology can increase detections in these conditions. We used thermal-imaging equipment with a specific helicopter crew configuration to assist in aerial culling for feral pigs (Sus scrofa) and fallow deer (Dama dama) in South Australia in 2021. Seventy-two percent of pigs and 53% of deer were first detected in dense canopy/tall forest habitat. Median time from the first impact shot to incapacitation was

The extent of increasing anthropogenic impacts on large marine vertebrates partly depends on the animals' movement patterns. Effective conservation requires identification of the key drivers of movement including intrinsic properties and extrinsic constraints associated with the dynamic nature of the environments the animals inhabit. However, the relative importance of intrinsic versus extrinsic factors remains elusive. We analyze a global dataset of ∼2.8 million locations from >2,600 tracked individuals across 50 marine vertebrates evolutionarily separated by millions of years and using different locomotion modes (fly, swim, walk/paddle). Strikingly, movement patterns show a remarkable convergence, being strongly conserved across species and independent of body length and mass, despite these traits ranging over 10 orders of magnitude among the species studied. This represents a fundamental difference between marine and terrestrial vertebrates not previously identified, likely linked to the reduced costs of locomotion in water. Movement patterns were primarily explained by the interaction between species-specific traits and the habitat(s) they move through, resulting in complex movement patterns when moving close to coasts compared with more predictable patterns when moving in open oceans. This distinct difference may be associated with greater complexity within coastal microhabitats, highlighting a critical role of preferred habitat in shaping marine vertebrate global movements. Efforts to develop understanding of the characteristics of vertebrate movement should consider the habitat(s) through which they move to identify how movement patterns will alter with forecasted severe ocean changes, such as reduced Arctic sea ice cover, sea level rise, and declining oxygen content.

Background: There is some evidence that the epithelial cell rests of Malassez partition the root surface from the periodontal ligament blood vessels, and may protect the root from resorption.

This paper reports on changes in mandibular condylar growth in sheep fitted with experimental functional appliances. The paper also addresses the similarities of mandibular condylar growth in sheep and humans. Experimental functional appliances were developed, constructed and applied to four, four-month old, male sheep. Another four sheep served as matched controls. All animals received fluorochrome bone labels during the study and their weight gain also was recorded. Fifteen weeks later, all animals were sacrificed and each temporo-mandibular joint and left metacarpus were removed. Undecalcified mid-sagittal sections of the joint and metacarpus were prepared for fluorescence microscopy. The mandibular condylar growth vector in sheep was found to be in a postero-superior direction. Condylar growth in the control sheep during the experimental period varied from 8.8 to 11.9 mm, with the mean being 10.6 mm, which is quantitatively similar to two years of condylar growth in human adolescents. In the experimental sheep, the condylar growth varied from 8.5 to 13.3 mm, with the mean being 11.4 mm. When metacarpal growth and weight gain were taken into consideration using multivariant analysis, the coefficients for growth in the postero-superior and posterior direction were found to be high, with adjusted r2 as 0.84 and 0.82 respectively. The induced condylar growth was estimated to be largest in the posterior direction (2.30 mm), which is also similar to previous reports in humans. These findings suggest the appropriateness of using sheep as a model for quantitative histological analysis when investigating the mechanisms of functional appliance treatment.

The purpose of this study was to undertake preliminary analyses of the extracel- lular proteoglycans in carcinogen [4-nitroquinoline N-oxide (4NQO)]-treated rat tongue mucosa. Experimental rats were exposed to twice-weekly applications of 4NQO in propylene glycol for six months, after which the animals were killed. Control and 4NQO-treated tissues were subjected to sequential aqueous extractions of proteoglycans under associative and dissociative conditions, followed by alkaline cleavage of protein-glycosaminoglycan linkages to yield a glycosaminoglycan residue. Tissues subjected to 4NQO applications contained smaller proportions of proteoglycans which were readily soluble under associative and dissociative conditions. Proportionately more proteoglycan remained strongly associated with other intercellular tissue components, being released only by alkaline cleavage. These biochemical alterations in preinvasive 4NQO-treated epithelium and connective tissues, together with an observed associated change in water retention by the connective tissue, occurred prior to actual neoplastic invasion and suggest differences in macromolecular conformation and orderliness. We hypothesize that these changes are related to the phenomenon of neoplastic epithelial invasion. [ABSTRACT FROM AUTHOR]

Life-history characteristics of six tropical Lethrinus species sampled from the Great Barrier Reef World Heritage Area were compared. Two species groups were identified based on fork length ( LF): large species with maximum LF > 640 mm (longface emperor Lethrinus olivaceus, yellowlip emperor Lethrinus xanthochilus and spangled emperor Lethrinus nebulosus) and small species with maximum LF < 480 mm (Pacific yellowtail emperor Lethrinus atkinsoni, pink ear emperor Lethrinus lentjan and ornate emperor Lethrinus ornatus). Lifespan was not correlated with LF. Early growth for all species was rapid and similar during the first few years of life, but coefficients of the von Bertalanffy growth function varied considerably among species. Growth also differed between sexes for L. atkinsoni. Reproductive characteristics varied among species, with peak periods of spawning occurring in November to December for L. atkinsoni, July to August for L. nebulous, September to October for L. olivaceus and a protracted season for L. lentjan, although fewer samples were available for the last two species. Sex-specific LF and age distributions and gonad histology of L. lentjan were suggestive of a functional protogynous reproductive pattern, as observed in other lethrinids. Gonad histology indicated non-functional protogynous hermaphroditism for L. atkinsoni and L. nebulosus. The diversity of life histories among these closely related species emphasizes the difficulty in devising single management strategies appropriate for multi-species fisheries and illustrates the importance of understanding species-specific life histories to infer responses to exploitation. [ABSTRACT FROM AUTHOR]

Surgicel®, a local haemostatic gauze, is claimed to consist of oxidised regenerated cellulose. It is a polyanion, the functional unit of which is termed polyanhydroglucuronic acid. The ability of tissues to absorb Surgicel® and its inherent haemostatic properties have been extensively investigated. This study was undertaken a) to determine the time required for absorption of Surgicel® from implantation sites in the chest wall muscles of rats. and b) to establish mechanisms for its rcmoval. Data derived from sequential uronic acid assays, histochemistry using the stain alcian bluc, and transmission electron microscopy of implanted Surgicel® were interpreted to reveal that Surgicel® consists of at least two active components. These are a soluble uronic acid component which is lost after 6 h, and a fibrous component which persists. The latter material resembles Surgicel® in the electron microscope and is still evident at the implantation site at 48 h post-implantation. Moreover. Surgicel® can be characterized /n vitro into at least two components according to its solubility under dissocialive salt conditions (4M guanidinium chloride). A residual fibrous material could then be hydrolysed with 0.3N sodium hydroxide. We postulate that the absorption of the former salt soluble uronate in vivo is by early degradation and/or systemic clearance, whilst removal of the fibrous material requires phagocytosis. [ABSTRACT FROM AUTHOR]

Experimentally-induced external inflammatory tooth-root resorption can be inhibited by therapeutic doses of calcitonin. Such doses can be delivered by an intrinsically slow diffusion pathway, from a reservoir in endodontically-debrided root canals, via the dentinal tubules. While the kinetics of this journey have been followed in an earlier report, the binding characteristics of calcitonin to the tooth mineral, which will be responsible, in part, for these kinetics, have not been reported before. The current study examines the binding potential of calcitonin to root mineral and addresses the potential role of non-specific binding proteins. A modified Scatchard plot indicated that a simple non-reactive type of ligand binding exists between calcitonin and root mineral, represented by a small number of identical binding sites. This interaction is both strong and reversible. Furthermore, it appears to be time-dependent with more time being required for the residual ligands to interact with the diminishing numbers of free calcitonin-binding sites. While preloaded [125I]-calcitonin could be incompletely (75-91%) displaced from dental-root material by non-radioactive calcitonin, its release was slow over 23 h. Calcitonin was four times as effective as bovine-serum albumin in competing for common "calcitonin binding sites" on macerated dental-root material. Thus, even in the presence of extraneous protein, calcitonin will bind tightly but reversibly to tooth-root material, making it a good candidate for therapeutically protracted delivery to external root surfaces from root canals. [ABSTRACT FROM AUTHOR]

Insertion of calcitonin into root canals of monkey teeth has been shown to inhibit external inflammatory root resorption and suppress inflammation. Regulation of this therapeutic event depends upon the rate of arrival (diffusion) of the hormone at sites of resorptive activity. In the present study, the diffusion characteristics of calcitonin through the dental root in an extracted human-tooth model are described, and the role of cementum in the diffusion process is also addressed. Root-canals were endodontically prepared to form a reservoir for [125I]-calcitonin, and macerated to remove organic material from dentinal tubules. In teeth with intact cementum, an initial period of delay (4-5 h) prior to the detection of calcitonin at the external tooth-root surface was followed by a rapid release of the calcitonin during the first 10.5 h (rate peaks at 6 h). Slower, sustained releases of calcitonin through intact cementum were measured for the following 9 days. Removal of cementum, to expose "smear-free" dentine, resulted in an earlier efflux of calcitonin (2 h) at external tooth surfaces and increased amounts of calcitonin release over 9 days. Biphasic delivery of calcitonin by such internal diffusion mechanisms suggests that loss of cementum will enhance therapeutic availability, while prolonged delivery to intact external dental-root surfaces following early intra-canal placement may also be useful for the therapeutic prevention of external inflammatory root resorption. [ABSTRACT FROM AUTHOR]

The NADPH-dependent microsomal metabolism of [C]procarbazine, labeled on the terminal N-methyl group, resulted in the covalent binding of the drug to exogenously added DNA; this reaction was inhibited by metyrapone. Procarbazine metabolism was also shown to result in covalent binding of the methyl group of the drug to microsomal protein upon metabolism, but the extent of protein binding was at least an order of magnitude smaller than that seen with its primary oxidative metabolite. N-isopropyl-α-(2-methylazo)--toluamide. The characteristics of the reactions leading to the covalent binding of the N-methyl group of the azo derivative to microsomal protein and its metabolism to form the hydrocarbon, methane, possessed a number of similarities in the apparent kinetic parameters ( and ), induction, and inhibition patterns indicating a common pathway of metabolism to form a reactive intermediate and the involvement of cytochrome P-450. Reduced glutathione stimulated methane formation and inhibited covalent binding to protein. One azoxy derivative, N-isopropyl-α-(2-methyl-ONN-azoxy)--toluamide, was chemically unstable and its decomposition was shown to lead to covalent binding to microsomal protein. A diazene intermediate and a methyl radical are proposed to be intermediates in the formation of methane during the oxidative metabolism of the azo derivative of procarbazine and a common intermediate in the activation of procarbazine may result in both covalent binding to cellular macromolecules and methane production. In addition, chemical decomposition of the azoxy metabolites may also contribute to a small portion of the covalent binding, but not to methane formation. [ABSTRACT FROM PUBLISHER]

Utilizing the technique of alkaline elution analysis, the ability of N-nitrosomethyl(2-oxopropyl)amine (MOP), a potent pancreatic carcinogen, to damage pancreatic DNA in rats and hamsters was examined. Pancreatic DNA isolated from hamsters exposed for 1 h to MOP given i.p. at doses of 7–60 mg/kg showed dose-related DNA damage. A similar dose-response was observed in the pancreas of rats receiving 20 — 180 mg MOP/kg, suggesting that hamsters were 2–3 times more sensitive than rats. In contrast to the results obtained , functionally viable acinar cells from both rat and hamster pancreas, when exposed to levels of MOP comparable to those (20–180 μ/ml), failed to show dose-related DNA damage. Acinar cells from hamsters pretreated with 5, 6-benzoflavone, an inducer of cytochrome P-450 activity, showed greatly enhanced drug-metabolizing capability, but again no DNA damage was observed upon exposure to MOP. Minced hamster or rat pancreas also failed to show DNA damage in response to MOP treatment. When hamsters in which hepatic blood supply was interrupted by ligation were given 60 mg/kg MOP i.v. and sacrificed 15 min later, damage to pancreatic and liver DNA was comparable to that observed in ligated controls which had received saline only. Administration of MOP to sham-operated animals led to extensive DNA damage in both pancreas and liver at 15 min. Analysis by h.p.l.c. showed an almost Mold increase in the amount of MOP present in the pancreases of the liver-ligated animals as compared to the sham-operated unligated animals. MOP was absent from the liver of the ligated animals. These experiments strongly suggest that DNA damage by MOP to the pancreatic acinar cells and probably to other pancreatic cell types, as well, requires metabolic activation by the liver. [ABSTRACT FROM PUBLISHER]

Preparative chromatographic fractions of human umbilical cord hyaluronic acid (HA) of a molecular weight of 10(6) were subjected to graded oxygen-derived free radical (oxy radical) fluxes produced by: (a) the autoxidation of ferrous ions; (b) the action of xanthine oxidase (XO) on hypoxanthine (HX); and (c) by peripheral blood polymorphonuclear leucocytes that had been stimulated by phorbol myristate acetate (PMA). Analysis by gel chromatography of the products obtained with each of the oxy radical generating systems showed polydispersity in size. The smallest molecules detected had a molecular weight of 10(4). This limiting size was not reduced further by exposure to a second oxy radical flux. The relative proportions of large, medium, and small degradation products were established for various levels of oxy radical flux. Consistently a relatively rapid transition from large to small material was seen on Sepharose 2B chromatography, suggesting an ordered element to the breakdown process. Although the decrease in molecular weight after oxy radical exposure was confirmed by analytical ultracentrifugation, this procedure showed that those samples of lowest viscosity did not have the lowest sedimentation values, possibly reflecting oxy radical-induced repolymerisation. If the size and possibly the conformational characteristics of HA are altered, oxy radical exposure might be expected to alter its biological properties. [ABSTRACT FROM PUBLISHER]

Synthesis of sulphated proteoglycans by cell lines derived from explants of 7 rheumatoid and 9 normal specimens of synovial tissue, as well as by 7 lines of skin fibroblasts from non-rheumatoid patients, was examined. Cells of all 3 types were cultured as monolayers. They were then disaggregated and their capacity to synthesise proteoglycan estimated in cell suspensions by the incorporation of [35S]-sulphate into CPC-precipitable material during 2 hours of incubation. Cell suspensions incorporated somewhat more [35S]-sulphate than corresponding duplicate monolayers. Synovial cells from rheumatoid patients incorporated 2 to 3 times as much [35S]-sulphate as synovial cells from normals. Skin fibroblasts, however, incorporated less [35S]-sulphate than rheumatoid or normal synovial cells up to the fifth passage. Thereafter their incorporation gradually increased to overtake that of synovial cells. About one-half to one-third of the total [35S]-sulphate labelled material was closely associated with cells from synovial tissues and fibroblasts respectively. [ABSTRACT FROM PUBLISHER]

The effect of a chemically induced oxygen-derived free radical flux has been studied on extracted porcine gingival hyaluronic acid and proteoglycans as well as on cryostat sections of porcine gingivae. The result of the free radical producing system on hyaluronic acid and the proteoglycans was one of reduction of specific viscosity and molecular size. When frozen sections were subjected to the same oxygen-derived free radical flux and subsequently stained with Alcian blue, a noticeable decrease in staining intensity was observed when compared to control sections. These results are considered to reflect the in vitro capacity of oxygen-derived free radicals to depolymerize the two major non-fibrous extracellular macromolecules of gingivae. It is postulated that such a mechanism may be responsible, at least in part, for the destruction of gingival proteoglycans and hyaluronic acid observed in inflammatory periodontal disease. [ABSTRACT FROM AUTHOR]

he sequential extractability of uronic acid containing macromolecules, proteoglycans (mucopolysaccharides), from pig gingivae under associative and dissociative aqueous conditions has been investigated. Some of the macromolecular material thus extracted formed highly insoluble precipitates following dialysis against 0.1 M-sodium acetate. Both soluble and insoluble fractions from associative and dissociative extraction regimes were assayed for uronic acid. The residual glycosaminoglycan in the tissue was assayed following papain digestion of the tissue. The limitation of assay reproducibility for various sized source tissue indicates that at least 100 mg dry weight of gingivae is required. When epithelium was removed from the underlying gingival connective tissue, the reproducibility of hydroxyproline estimation was improved. These data emphasize that the epithelium contributes an uncontrollable variable to the basic dry weights of gingivae as a whole against which such measurements as collagen content may be assessed. Furthermore, the data generated from sequential extraction of macromolecular uronates from pig gingivae indicated that there was less susceptibility of intercellular material to dissolution under associative conditions than previously reported for human gingivae. This resistance to salt extraction implies a greater degree of macromolecular organization. In consequence, the different macromolecular structure of the pig gingival intercellular matrix may be less susceptible to degradative processes, a suggestion which is supported by the low incidence of periodontal inflammation observed in these pigs. [ABSTRACT FROM AUTHOR]

The effect of extraneous hyaluronidase, trypsin, hyaluronic acid, chrondroitin sulphate, and commercial heparin on the synthesis and secretion of proteoglycans (mucopolysaccharides) by gingival epithelium in short term incubations was investigated by autoradiography. Small pieces of human gingivae were incubated at 37° C in tissue culture medium (T.C. 199) for 75 min. The first 15 min incubation included a "pulse' of (35S)-sulphate, after which the radioactive incorporation was "chased" in radioactive free medium. Cryostat sections of these pieces were cut, air dried, slide fixed with cetylpyridinium chloride, and prepared for autoradiography. The effect of the various additives in the "pulse" or the "chase" incubations on the autoradiographic localization of incorporated (35S)-sulphate in the epithelium was noted. The responses by the epithelium to the enzymes hyaluronidase and trypsin were different. The former caused marked tissue disruption, probably due in part to degradation of the ground substance. Synthesis and secretion of sulphated macromolecules were evident when the lower concentrations of hyaluronidase were used. Tissue disruption appeared to be less severe. Trypsin in the medium of the gingival incubations appeared to cause both metabolic and secretory disruption. Both the sulphated polyanions, chrondroitin sulphate and heparin, when added to gingival incubations, showed inhibition of localization of (35S)-sulphate label intercellularly. Chrondroitin sulphate included in the "chase" incubations alone resulted in the inhibition, while only low concentrations of heparin caused any inhibition. These latter data were curious. The interpretations of a comparison of the data from "pulse" and "chase'' additions of the non-sulphated hyaluronic acid imply that there was an initial inhibitory effect on secretion which in turn resulted in a subsequent regulation of synthesis of the intercellular sulphated macromolecules. These data and those derived from other tissues such as endothelium, cartilage, and chondrocyte cultures are briefly contrasted. [ABSTRACT FROM AUTHOR]

Short incubations, at 37°C, of small freshly excised pieces of healthy human gingivae incorporated [35S]-sulphate and [³H]-acetate into macromolecular material which could be precipitated intercellularly in the epithelium. Following radioactively pulse-chased incubations, such localization was observed by autoradiography on cryostat histological sections fixed in cetylpyridinium chloride. Critical electrolyte salt concentration elution indicated that most of the intercellular material was soluble in 0.63M-MgCl2, and any material which remained was intracellular. In vitro and in vivo incorporation studies were compared. These data corroborate biochemical studies (Wiebkin, Bartold & Thonard 1979) together with other histochemical observations that proteoglycans (mucopolysaccharides) are a major intercellular component of human gingival epithelium. Molecular conformation and the relatively rapid synthesis and secretion rate for this class of epithelial macromolecule may explain the lack of susceptibility of this material in the intercellular site, both to degradation by some specific enzymes previously reported and to elution with critical salt concentrations from cationic detergent precipitates. The method described, together with in vivo incorporation studies, provides a useful technique for studying direct effects of some microenvironmental influences on gingival epithelium. [ABSTRACT FROM AUTHOR]

An in-vitro biotoxicity test system, suitable for the assessment of endodontic filling materials, has been developed and used to test cell responses to Hydron, AH26 and Tubliseal. A robust, well-characterized and stable cell line (L-cells) which was grown as uniform cultures on Millipore filters, has been used as indicator cells. As they approached confluence they were exposed to test substances for 24 h and biosynthetic activities were measured. The test system is a modification of that described by Wennberg et al. (1979). By inverting the cultures on organ-culture rafts, cells were separated from the test material, which was placed on top of the Millipore liken. Freshly mixed polymerizing Hydron and prepolymerized Hydron were tested. The cell responses were compared with those of cultures exposed to freshly mixed AH26 and Tubliseal. Polymerizing and prepolymerized Hydron depressed both cell division, assessed by 3H-thymidine incorporation, and the synthesis and secretion of matrix material as measured by precipitable 35S-sulphate. Prepolymerized Hydron decreased cell functions by 59% and 56% of live cell controls, respectively, while the freshly mixed polymerizing Hydron inhibited biosynthesis by 89% and 94%, respectively. The data for polymerizing Hydron were compared with results for other root-filling materials and showed similar values to those for Tubliseal (92% and 95%), but greater inhibition of biosynthesis than for AH26 (53% and 5 0%). The AH26 values were similar to those obtained from cultures exposed to the prepolymerized Hydron. Recovery of biosynthetic capacity by these cultures after removal of all endodontic material was also assessed. Partial biosynthetic recovery of cell cultures was observed 24 h after removal of prepolymerized Hydron. The unpolymerized Hydron continued to yield a soluble component which substantially depressed biosynthetic activity of the experimental cultures up to 14 days. In general, the results indicated that Hydron, particularly in its freshly mixed state, when not in actual cell contact, depressed cell division and extracellular-matrix synthesis. Data derived from similar in-vitro testing with AH26 and Tubliseal revealed that they both inhibited cell division and matrix synthesis. Tubliseal inhibited these cell responses to the same extent as polymerizing Hydron. Polymerizing Hydron was significantly more toxic than AH26, while there were no significant differences in the levels of toxicity of polymerized Hydron and AH26. [ABSTRACT FROM AUTHOR]

To directly demonstrate both the presence and in vivo activity of tissue collagenase (EC 3.4.24.7) during gingival inflammation, tissue extracts from 54 specimens of variously inflamed human gingiva were analyzed individually for: a) collagenase- specific collagen degradation products, and b) collagen-bound collagenase. The TC collagen degradation product, identified using SDS-PAGE, was shown in 13/19 (68.4%) of insoluble tissue-residue fractions extracted from moderate-to-severely inflamed gingiva, but in only 2/21 (9.6%) slight-to-mildly inflamed gingival specimens, suggesting differences in the in vivo collagenase activity between the two groups. Using in vitro collagenase assays, gingival collagenase (as bound to insoluble collagen) was demonstrated in 92.8% of the moderate-to-severely inflamed gingival specimens and in 50% of the slight-to-mildly inflamed gingival specimens. A relationship was established between the active and latent forms of the enzyme and the degree of inflammation. Active enzyme was present in 78% of the moderate-to-severely inflamed specimens and in 14% of the slight- to-mildly inflamed gingiva. In contrast, latent collagenase was predominant in the slight-to-mildly inflamed group (86% of coliagenase-positive samples) compared with 46% of collagenase-positive moderate-to-severely inflamed gingival samples. The collagen-bound gingival collagenase was inhibited by metal ion chelators, sulphydryl reagents and 10% FBS, but not by serine- nor thiol-proteinase inhibitors and is therefore a neutral metalloproteinase. [ABSTRACT FROM AUTHOR]

Previous studies demonstrating mucopolysaccharides (MPS) in tissue cultured epithelial cells did not eliminate the possibility that some of the reported staining could be attributed to acidic lipids, nucleic acids and substrate movement, although these possibilities were deemed minimal due to the employment of generally accepted techniques. Human amnion cells were grown on coverslips in tissue culture. Some coverslips were treated to remove MPS, lipid or nucleic acids before fixation and staining, whilst others were merely fixed and stained. Fixatives included 10% formalin. 10% formalin in 80 % ethanol, 1% cetylpyridinium chloride and 1% cetylpyridinium chloride in 80% ethanol. Stains employed were the Hale colloidal iron, alcian blue, toluidine blue at pH 6.0 and 2.5 and sudan black. Substrate extractions were effected with testicular hyaluronidase, ribonuclease, KOH and pyridine. The present report confirms earlier results and provides evidence that human epithelial-like cells produce MPS in vitro the staining specificity of which eliminates lipids and nucleic acids as the source of the observed reactions. It is claimed that the MPS is mainly confined to the cell surface and therefore is more discernible as a MPS stainable moiety in contiguous cell cultures than when cells are dispersed singly. [ABSTRACT FROM AUTHOR]