Strength, power and aerobic capacity of transgender athletes: a cross-sectional study.

OBJECTIVE: The primary objective of this cross-sectional study was to compare standard laboratory performance metrics of transgender athletes to cisgender athletes. METHODS: 19 cisgender men (CM) (mean±SD, age: 37±9 years), 12 transgender men (TM) (age: 34±7 years), 23 transgender women (TW) (age: 34±10 years) and 21 cisgender women (CW) (age: 30±9 years) underwent a series of standard laboratory performance tests, including body composition, lung function, cardiopulmonary exercise testing, strength and lower body power. Haemoglobin concentration in capillary blood and testosterone and oestradiol in serum were also measured. RESULTS: In this cohort of athletes, TW had similar testosterone concentration (TW 0.7±0.5 nmol/L, CW 0.9±0.4 nmol/), higher oestrogen (TW 742.4±801.9 pmol/L, CW 336.0±266.3 pmol/L, p=0.045), higher absolute handgrip strength (TW 40.7±6.8 kg, CW 34.2±3.7 kg, p=0.01), lower forced expiratory volume in 1 s:forced vital capacity ratio (TW 0.83±0.07, CW 0.88±0.04, p=0.04), lower relative jump height (TW 0.7±0.2 cm/kg; CW 1.0±0.2 cm/kg, p<0.001) and lower relative V̇O2max (TW 45.1±13.3 mL/kg/min/, CW 54.1±6.0 mL/kg/min, p<0.001) compared with CW athletes. TM had similar testosterone concentration (TM 20.5±5.8 nmol/L, CM 24.8±12.3 nmol/L), lower absolute hand grip strength (TM 38.8±7.5 kg, CM 45.7±6.9 kg, p=0.03) and lower absolute V̇O2max (TM 3635±644 mL/min, CM 4467±641 mL/min p=0.002) than CM. CONCLUSION: While longitudinal transitioning studies of transgender athletes are urgently needed, these results should caution against precautionary bans and sport eligibility exclusions that are not based on sport-specific (or sport-relevant) research.

The effects of physiological and injurious hydrostatic pressure on murine ex vivo articular and growth plate cartilage explants: an RNAseq study.

Introduction: Chondrocytes are continuously exposed to loads placed upon them. Physiological loads are pivotal to the maintenance of articular cartilage health, while abnormal loads contribute to pathological joint degradation. Similarly, the growth plate cartilage is subject to various loads during growth and development. Due to the high-water content of cartilage, hydrostatic pressure is considered one of the main biomechanical influencers on chondrocytes and has been shown to play an important role in the mechano-regulation of cartilage. Methods: Herein, we conducted RNAseq analysis of ex vivo hip cap (articular), and metatarsal (growth plate) cartilage cultures subjected to physiological (5 MPa) and injurious (50 MPa) hydrostatic pressure, using the Illumina platform (n = 4 replicates). Results: Several hundreds of genes were shown to be differentially modulated by hydrostatic pressure, with the majority of these changes evidenced in hip cap cartilage cultures (375 significantly upregulated and 322 downregulated in 5 MPa versus control; 1022 upregulated and 724 downregulated in 50 MPa versus control). Conversely, fewer genes were differentially affected by hydrostatic pressure in the metatarsal cultures (5 significantly upregulated and 23 downregulated in 5 MPa versus control; 7 significantly upregulated and 19 downregulated in 50 MPa versus control). Using Gene Ontology annotations for Biological Processes, in the hip cap data we identified a number of pathways that were modulated by both physiological and injurious hydrostatic pressure. Pathways upregulated in response to 50 MPa versus control, included those involved in the generation of precursor metabolites and cellular respiration. Biological processes that were downregulated in this tissue included ossification, connective tissue development, and chondrocyte differentiation. Discussion: Collectively our data highlights the divergent chondrocyte phenotypes in articular and growth plate cartilage. Further, we show that the magnitude of hydrostatic pressure application has distinct effects on gene expression and biological processes in hip cap cartilage explants. Finally, we identified differential expression of a number of genes that have previously been identified as osteoarthritis risk genes, including Ctsk, and Chadl. Together these data may provide potential genetic targets for future investigations in osteoarthritis research and novel therapeutics.

Characterization of the extracellular vesicles, ultrastructural morphology, and intercellular interactions of multiple clinical isolates of the brain-eating amoeba, Naegleria fowleri.

Introduction: As global temperatures rise to unprecedented historic levels, so too do the latitudes of habitable niches for the pathogenic free-living amoeba, Naegleria fowleri. This opportunistic parasite causes a rare, but >97% fatal, neurological infection called primary amoebic meningoencephalitis. Despite its lethality, this parasite remains one of the most neglected and understudied parasitic protozoans. Methods: To better understand amoeboid intercellular communication, we elucidate the structure, proteome, and potential secretion mechanisms of amoeba-derived extracellular vesicles (EVs), which are membrane-bound communication apparatuses that relay messages and can be used as biomarkers for diagnostics in various diseases. Results and Discussion: Herein we propose that N. fowleri secretes EVs in clusters from the plasma membrane, from multivesicular bodies, and via beading of thin filaments extruding from the membrane. Uptake assays demonstrate that EVs are taken up by other amoebae and mammalian cells, and we observed a real-time increase in metabolic activity for mammalian cells exposed to EVs from amoebae. Proteomic analysis revealed >2,000 proteins within the N. fowleri-secreted EVs, providing targets for the development of diagnostics or therapeutics. Our work expands the knowledge of intercellular interactions among these amoebae and subsequently deepens the understanding of the mechanistic basis of PAM.

Heterogeneity in macrophages along the cochlear spiral in mice: insights from SEM and functional analyses.

The susceptibility of sensory cells to pathological conditions differs between the apical and basal regions of the cochlea, and the cochlear immune system may contribute to this location-dependent variability. Our previous study found morphological differences in basilar membrane macrophages between the apical and basal regions of the cochlea. However, the details of this site-dependent difference and its underlying structural and biological basis are not fully understood. In this study, we utilized scanning electron microscopy to examine the ultrastructure of macrophages and their surrounding supporting structures. Additionally, we examined the phagocytic activities of macrophages and the expression of immune molecules in both apical and basal regions of the cochlea. We employed two mouse strains (C57BL/6J and B6.129P-Cx3cr1tm1Litt/J) and evaluated three experimental conditions: young normal (1-4 months), aging (11-19 months), and noise-induced damage (120 dB SPL for 1 h). Using scanning electron microscopy, we revealed location-specific differences in basilar membrane macrophage morphology and surface texture, architecture in mesothelial cell layers, and spatial correlation between macrophages and mesothelial cells in both young and older mice. Observations of macrophage phagocytic activities demonstrated that basal macrophages exhibited greater phagocytic activities in aging and noise-damaged ears. Furthermore, we identified differences in the expression of immune molecules between the apical and basal cochlear tissues of young mice. Finally, our study demonstrated that as the cochlea ages, macrophages in the apical and basal regions undergo a transformation in their morphologies, with apical macrophages acquiring certain basal macrophage features and vice versa. Overall, our findings demonstrate apical and basal differences in macrophage phenotypes and functionality, which are related to distinct immune and structural differences in the macrophage surrounding tissues.

Turnover of Variant Surface Glycoprotein in Trypanosoma brucei Is Not Altered in Response to Specific Silencing.

African trypanosomes evade the immune system of the mammalian host by the antigenic variation of the predominant glycosylphosphatidylinositol (GPI)-anchored surface protein, variant surface glycoprotein (VSG). VSG is a very stable protein that is turned over from the cell surface with a long half-life (~26 h), allowing newly synthesized VSG to populate the surface. We have recently demonstrated that VSG turnover under normal growth is mediated by a combination of GPI hydrolysis and direct shedding with intact GPI anchors. VSG synthesis is tightly regulated in dividing trypanosomes, and when subjected to RNA interference (RNAi) silencing, cells display rapid cell cycle arrest in order to conserve VSG density on the cell surface (K. Sheader, S. Vaughan, J. Minchin, K. Hughes, et al., Proc Natl Acad Sci U S A 102:8716-8721, 2005, https://doi.org/10.1073/pnas.0501886102). Arrested cells also display an altered morphology of secretory organelles-engorgement of the trans-Golgi cisternae-that may reflect a disruption of post-Golgi secretory transport. We now ask whether trypanosomes under VSG silencing also reduce the rate of VSG turnover to further conserve coat density. Our data indicate that trypanosomes do not regulate VSG turnover according to VSG protein abundance, nor was there any effect on the post-Golgi transport of soluble or GPI-anchored secretory cargo. However, the surface morphology of silenced cells was altered from a typically rugose topology to a smoother profile, consistent with reduced overall membrane trafficking to the cell surface. IMPORTANCE African trypanosomes evade the host immune system by altering the expression of variant surface glycoproteins (VSGs) in a process called antigenic variation. VSG is essential, and when its synthesis is ablated by RNAi silencing, cells enter precytokinesis growth arrest as a means to maintain constant cell surface VSG levels. We have investigated whether arrested cells also alter the rate of natural VSG turnover as a means to conserve the surface coat. This work provides insights into the natural biology of the glycocalyx of this important human and veterinary parasite.

Turnover of Variant Surface Glycoprotein in Trypanosoma brucei Is a Bimodal Process.

African trypanosomes utilize glycosylphosphatidylinositol (GPI)-anchored variant surface glycoprotein (VSG) to evade the host immune system. VSG turnover is thought to be mediated via cleavage of the GPI anchor by endogenous GPI-specific phospholipase C (GPI-PLC). However, GPI-PLC is topologically sequestered from VSG substrates in intact cells. Recently, A. J. Szempruch, S. E. Sykes, R. Kieft, L. Dennison, et al. (Cell 164:246-257, 2016, https://doi.org/10.1016/j.cell.2015.11.051) demonstrated the release of nanotubes that septate to form free VSG+ extracellular vesicles (EVs). Here, we evaluated the relative contributions of GPI hydrolysis and EV formation to VSG turnover in wild-type (WT) and GPI-PLC null cells. The turnover rate of VSG was consistent with prior measurements (half-life [t1/2] of ∼26 h) but dropped significantly in the absence of GPI-PLC (t1/2 of ∼36 h). Ectopic complementation restored normal turnover rates, confirming the role of GPI-PLC in turnover. However, physical characterization of shed VSG in WT cells indicated that at least 50% is released directly from cell membranes with intact GPI anchors. Shedding of EVs plays an insignificant role in total VSG turnover in both WT and null cells. In additional studies, GPI-PLC was found to have no role in biosynthetic and endocytic trafficking to the lysosome but did influence the rate of receptor-mediated endocytosis. These results indicate that VSG turnover is a bimodal process involving both direct shedding and GPI hydrolysis. IMPORTANCE African trypanosomes, the protozoan agent of human African trypanosomaisis, avoid the host immune system by switching expression of the variant surface glycoprotein (VSG). VSG is a long-lived protein that has long been thought to be turned over by hydrolysis of its glycolipid membrane anchor. Recent work demonstrating the shedding of VSG-containing extracellular vesicles has led us to reinvestigate the mode of VSG turnover. We found that VSG is shed in part by glycolipid hydrolysis but also in approximately equal part by direct shedding of protein with intact lipid anchors. Shedding of exocytic vesicles made a very minor contribution to overall VSG turnover. These results indicate that VSG turnover is a bimodal process and significantly alter our understanding of the "life cycle" of this critical virulence factor.

Publisher Correction: Metabolic reprogramming of stromal fibroblasts by melanoma exosome microRNA favours a pre-metastatic microenvironment.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.

An in vitro comparison of ultraviolet versus white light in the detection of adhesive remnants during orthodontic debonding.

OBJECTIVES: To assess the effectiveness and efficiency of ultraviolet (UV) illumination compared to conventional white light in the detection of fluorescent-tagged adhesive remnants during orthodontic debonding. MATERIALS AND METHODS: Orthodontic brackets were bonded to extracted human premolars using one of two bonding resins having fluorescent properties (Pad Lock, Reliance Orthodontics, Itasca, Ill; Opal Bond MV, Opal Orthodontics, South Jordan, Utah; n = 40 each). The brackets were then debonded and, in each adhesive group, half the teeth had the remaining adhesive resin removed under illumination using the operatory light and the other half using a UV (395 nm) light emitting diode (LED) flashlight (n = 20/group). Time for teeth cleanup was recorded. Follow-up images were obtained under a dissecting microscope using UV illumination, and the surface area of adhesive remnants was calculated. Effectiveness of adhesive removal was also assessed using scanning electron microscopy imaging. Analysis of variance and Kruskal-Wallis tests were used to analyze time and adhesive remnants, respectively. RESULTS: Assessment using the dissecting microscope found groups using UV light during adhesive removal had statistically significantly lower amounts of adhesive remnants than groups using white light (P ≤ .01). Time for adhesive removal was significantly lower with Opal Bond MV adhesive using UV light when compared with the white light (P ≤ .01). Assessment by scanning electron microscopy showed that thin remnants of adhesive (<2 µm) remained undetected by UV illumination. CONCLUSIONS: UV light is more effective and tends to be more efficient than white light in the detection of fluorescent adhesive during orthodontic debonding. Although there are limitations, the use of UV LED lighting is a practical tool that aids in adhesive detection.

Investigating the effect of sterilisation methods on the physical properties and cytocompatibility of methyl cellulose used in combination with alginate for 3D-bioplotting of chondrocytes.

For both the incorporation of cells and future therapeutic applications the sterility of a biomaterial must be ensured. However, common sterilisation techniques are intense and often negatively impact on material physicochemical attributes, which can affect its suitability for tissue engineering and 3D printing. In the present study four sterilisation methods, autoclave, supercritical CO2 (scCO2) treatment, UV- and gamma (γ) irradiation were evaluated regarding their impact on material properties and cellular responses. The investigations were performed on methyl cellulose (MC) as a component of an alginate/methyl cellulose (alg/MC) bioink, used for bioprinting embedded bovine primary chondrocytes (BPCs). In contrast to the autoclave, scCO2 and UV-treatments, the γ-irradiated MC resulted in a strong reduction in alg/MC viscosity and stability after extrusion which made this method unsuitable for precise bioprinting. Gel permeation chromatography analysis revealed a significant reduction in MC molecular mass only after γ-irradiation, which influenced MC chain mobility in the Ca2+-crosslinked alginate network as well as gel composition and microstructure. With regard to cell survival and proteoglycan matrix production, the results determined UV-irradiation and autoclaving as the best candidates for sterilisation. The scCO2-treatment of MC resulted in an unfavourable cell response indicating that this method needs careful optimisation prior to application for cell encapsulation. As proven by consistent FT-IR spectra, chemical alterations could be excluded as a cause for the differences seen between MC treatments on alg/MC behaviour. This investigation provides knowledge for the development of a clinically appropriate 3D-printing-based fabrication process to produce bioengineered tissue for cartilage regeneration.

Engineering of TIMP-3 as a LAP-fusion protein for targeting to sites of inflammation.

Tissue inhibitor of metalloproteinase (TIMP)-3 is a natural inhibitor of a range of enzymes that degrade connective tissue and are involved in the pathogenesis of conditions such as arthritis and cancer. We describe here the engineering of TIMP-3 using a novel drug-delivery system known as the 'LAP technology'. This involves creating therapeutic proteins in fusion with the latency-associated peptide (LAP) from the cytokine TGF-? to generate proteins that are biologically inactive until cleavage of the LAP to release the therapy. LAP-TIMP-3 was successfully expressed in mammalian cells and the presence of the LAP resulted in a 14-fold increase in the quantity of recombinant TIMP-3 produced. LAP-TIMP-3 was latent until release from the LAP by treatment with matrix metalloproteinase when it could inhibit proteases of the adamalysins and adamalysins with thrombospondin motifs families, but not matrix metalloproteinases, indicating that this version of TIMP-3 is a more specific inhibitor than the native protein. There was sufficient protease activity in synovial fluid from human joints with osteoarthritis to release TIMP-3 from the LAP fusion. These results demonstrate the potential for development of TIMP-3 as a novel therapy for conditions where upregulation of catabolic enzymes are part of the pathology.

Metabolic reprogramming of stromal fibroblasts by melanoma exosome microRNA favours a pre-metastatic microenvironment.

Local acidification of stroma is proposed to favour pre-metastatic niche formation but the mechanism of initiation is unclear. We investigated whether Human Melanoma-derived exosomes (HMEX) could reprogram human adult dermal fibroblasts (HADF) and cause extracellular acidification. HMEX were isolated from supernatants of six melanoma cell lines (3 BRAF V600E mutant cell lines and 3 BRAF wild-type cell lines) using ultracentrifugation or Size Exclusion Chromatography (SEC). Rapid uptake of exosomes by HADF was demonstrated following 18 hours co-incubation. Exposure of HDAF to HMEX leads to an increase in aerobic glycolysis and decrease in oxidative phosphorylation (OXPHOS) in HADF, consequently increasing extracellular acidification. Using a novel immuno-biochip, exosomal miR-155 and miR-210 were detected in HMEX. These miRNAs were present in HMEX from all six melanoma cell lines and were instrumental in promoting glycolysis and inhibiting OXPHOS in tumour cells. Inhibition of miR-155 and miR-210 activity by transfection of miRNA inhibitors into HMEX reversed the exosome-induced metabolic reprogramming of HADF. The data indicate that melanoma-derived exosomes modulate stromal cell metabolism and may contribute to the creation of a pre-metastatic niche that promotes the development of metastasis.

Rab11 mediates selective recycling and endocytic trafficking in Trypanosoma brucei.

Trypanosoma brucei possesses a streamlined secretory system that guarantees efficient delivery to the cell surface of the critical glycosyl-phosphatidylinositol (GPI)-anchored virulence factors, variant surface glycoprotein (VSG) and transferrin receptor (TfR). Both are thought to be constitutively endocytosed and returned to the flagellar pocket via TbRab11+ recycling endosomes. We use conditional knockdown with established reporters to investigate the role of TbRab11 in specific endomembrane trafficking pathways in bloodstream trypanosomes. TbRab11 is essential. Ablation has a modest negative effect on general endocytosis, but does not affect turnover, steady state levels or surface localization of TfR. Nor are biosynthetic delivery to the cell surface and recycling of VSG affected. TbRab11 depletion also causes increased shedding of VSG into the media by formation of nanotubes and extracellular vesicles. In contrast to GPI-anchored cargo, TbRab11 depletion reduces recycling of the transmembrane invariant surface protein, ISG65, leading to increased lysosomal turnover. Thus, TbRab11 plays a critical role in recycling of transmembrane, but not GPI-anchored surface proteins. We proposed a two-step model for VSG turnover involving release of VSG-containing vesicles followed by GPI hydrolysis. Collectively, our results indicate a critical role of TbRab11 in the homeostatic maintenance of the secretory/endocytic system of bloodstream T. brucei.

Controlling transferrin receptor trafficking with GPI-valence in bloodstream stage African trypanosomes.

Bloodstream-form African trypanosomes encode two structurally related glycosylphosphatidylinositol (GPI)-anchored proteins that are critical virulence factors, variant surface glycoprotein (VSG) for antigenic variation and transferrin receptor (TfR) for iron acquisition. Both are transcribed from the active telomeric expression site. VSG is a GPI2 homodimer; TfR is a GPI1 heterodimer of GPI-anchored ESAG6 and ESAG7. GPI-valence correlates with secretory progression and fate in bloodstream trypanosomes: VSG (GPI2) is a surface protein; truncated VSG (GPI0) is degraded in the lysosome; and native TfR (GPI1) localizes in the flagellar pocket. Tf:Fe starvation results in up-regulation and redistribution of TfR to the plasma membrane suggesting a saturable mechanism for flagellar pocket retention. However, because such surface TfR is non-functional for ligand binding we proposed that it represents GPI2 ESAG6 homodimers that are unable to bind transferrin-thereby mimicking native VSG. We now exploit a novel RNAi system for simultaneous lethal silencing of all native TfR subunits and exclusive in-situ expression of RNAi-resistant TfR variants with valences of GPI0-2. Our results conform to the valence model: GPI0 ESAG7 homodimers traffick to the lysosome and GPI2 ESAG6 homodimers to the cell surface. However, when expressed alone ESAG6 is up-regulated ~7-fold, leaving the issue of saturable retention in the flagellar pocket in question. Therefore, we created an RNAi-resistant GPI2 TfR heterodimer by fusing the C-terminal domain of ESAG6 to ESAG7. Co-expression with ESAG6 generates a functional heterodimeric GPI2 TfR that restores Tf uptake and cell viability, and localizes to the cell surface, without overexpression. These results resolve the longstanding issue of TfR trafficking under over-expression and confirm GPI valence as a critical determinant of intracellular sorting in trypanosomes.

Practical Considerations in Trace Element Analysis of Bone by Portable X-ray Fluorescence.

Forensic anthropologists are more often turning to nondestructive methods to assist with skeletal analyses, specifically for trace elemental analyses. Portable XRF (pXRF) instruments are versatile and are able to be used in diverse settings or for specimens of a shape and size that cannot be accommodated by laboratory-based instruments. Use of XRF requires knowledge of analysis parameters such as X-ray penetration and exit depth. Analysis depth was determined by examining pure elements through known thicknesses of equine bone slices. Correlation between the element's X-ray emission energy and the depth of reading was observed. Bone surfaces from a small unknown historic cemetery were analyzed before and after sanding of the periosteal surface to observe possible changes in XRF readings based on potential diagenesis. Results validate the pXRF device as a powerful and convenient instrument for nondestructive analysis, while highlighting limitations and considerations for the analysis of osseous materials.

Forensic bitemark identification: weak foundations, exaggerated claims.

Several forensic sciences, especially of the pattern-matching kind, are increasingly seen to lack the scientific foundation needed to justify continuing admission as trial evidence. Indeed, several have been abolished in the recent past. A likely next candidate for elimination is bitemark identification. A number of DNA exonerations have occurred in recent years for individuals convicted based on erroneous bitemark identifications. Intense scientific and legal scrutiny has resulted. An important National Academies review found little scientific support for the field. The Texas Forensic Science Commission recently recommended a moratorium on the admission of bitemark expert testimony. The California Supreme Court has a case before it that could start a national dismantling of forensic odontology. This article describes the (legal) basis for the rise of bitemark identification and the (scientific) basis for its impending fall. The article explains the general logic of forensic identification, the claims of bitemark identification, and reviews relevant empirical research on bitemark identification-highlighting both the lack of research and the lack of support provided by what research does exist. The rise and possible fall of bitemark identification evidence has broader implications-highlighting the weak scientific culture of forensic science and the law's difficulty in evaluating and responding to unreliable and unscientific evidence.

Complex layered dental restorations: Are they recognizable and do they survive extreme conditions?

Recent research has shown that restorative dental materials can be recognized by microscopy and elemental analysis (scanning electron microscopy/energy dispersive X-ray spectroscopy and X-ray fluorescence; SEM/EDS and XRF) and that this is possible even in extreme conditions, such as cremation. These analytical methods and databases of dental materials properties have proven useful in DVI (disaster victim identification) of a commercial plane crash in 2009, and in a number of other victim identification cases. Dental materials appear on the market with ever expanding frequency. With their advent, newer methods of restoration have been proposed and adopted in the dental office. Methods might include placing multiple layers of dental materials, where they have different properties including adhesion, viscosity, or working time. These different dental materials include filled adhesives, flowable resins, glass ionomer cements, composite resins, liners and sealants. With possible combinations of different materials in these restorations, the forensic odontologist is now confronted with a new difficulty; how to recognize each individual material. The question might be posed if it is even possible to perform this task. Furthermore, an odontologist might be called upon to identify a victim under difficult circumstances, such as when presented with fragmented or incinerated remains. In these circumstances the ability to identify specific dental materials could assist in the identification of the deceased. Key to use of this information is whether these new materials and methods are detailed in the dental chart. Visual or radiographic inspection may not reveal the presence of a restoration, let alone the possible complex nature of that restoration. This study demonstrates another scientific method in forensic dental identification.

Distortion in fingerprints: a statistical investigation using shape measurement tools.

Friction ridge impression appearance can be affected due to the type of surface touched and pressure exerted during deposition. Understanding the magnitude of alterations, regions affected, and systematic/detectable changes occurring would provide useful information. Geometric morphometric techniques were used to statistically characterize these changes. One hundred and fourteen prints were obtained from a single volunteer and impressed with heavy, normal, and light pressure on computer paper, soft gloss paper, 10-print card stock, and retabs. Six hundred prints from 10 volunteers were rolled with heavy, normal, and light pressure on soft gloss paper and 10-print card stock. Results indicate that while different substrates/pressure levels produced small systematic changes in fingerprints, the changes were small in magnitude: roughly the width of one ridge. There were no detectable changes in the degree of random variability of prints associated with either pressure or substrate. In conclusion, the prints transferred reliably regardless of pressure or substrate.

Shape measurement tools in footwear analysis: a statistical investigation of accidental characteristics over time.

Presence of accidental characteristics on footwear strengthens the linkage of a given piece of footwear to a footwear impression left at a crime-scene. Thus an understanding of rate of appearance and disappearance of these characteristics is of importance. Artificial cut-marks, 1-3mm in depth, were cut into outsoles of 11 pairs of athletic shoes. Loss of these cut-marks and acquisition of new accidental characteristics/wear patterns were monitored over a seven-week time-span. Feature-vector methods were used to acquire multivariate data on wear/acquisition rates. A repeatability study indicated the feature vector method could detect small differences among shoes relative to measurement uncertainty. The shoes displayed a strong retention of artificial cut-marks over the study interval. Net rate of wear was 0.1% of the textured area of the shoe per week, predominantly in the heel and ball area. Results indicate accidental characteristics can reasonably be expected to persist over time.

Environmental manipulations alter age differences in attribution of incentive salience to reward-paired cues.

Cues repeatedly paired with rewards often themselves become imbued with enhanced motivational value, or incentive salience. During Pavlovian conditioned approach procedures, a cue repeatedly preceding reward delivery often elicits conditioned responses at either the reward delivery location ("goal-tracking") or the cue itself ("sign-tracking"). Sign-tracking behavior is thought to reflect the individual differences in attribution of incentive salience to reward-paired cues that may contribute to addiction vulnerability. Adolescent rats typically demonstrate less sign-tracking behavior than adult rats, a surprising finding given that adolescence is hypothesized to be a time of heightened addiction vulnerability. Given evidence that adult sign-tracking behavior can be influenced by environmental conditions, the present study compared the effects of isolate housing and food deprivation on expression of sign-tacking and goal-tracking behavior in adolescent and adult male rats across eight days of a Pavlovian conditioned approach procedure. Pair-housed adults exhibited more sign-tracking behavior than pair-housed adolescents; however, this age difference was not apparent in isolate-housed subjects. Adolescents often appeared more sensitive than adults to both food restriction- and isolate housing-induced changes in behavior, with food restriction promoting an increase in sign-tracking among isolate-housed adolescents and an increase in goal-tracking among pair-housed adolescents. For adults, food restriction resulted in a modest increase in overall expression of both sign- and goal-tracking behavior. To the extent that sign-tracking behavior reflects attribution of incentive salience to reward-paired cues, results from the present study provide evidence that reactivity to rewards during adolescence is strongly related to the nature of the surrounding environment.

Effect of systematic dental shape modification in bitemarks.

Studies on human cadaver models have reported significant levels of distortion of bitemarks in skin, indicating that tooth characteristics are not reliably transferred and recorded in the bitten subject. Moreover, matches among the anterior biting dentition in open population studies have been found. This prompts the question as to what degree of difference in shape will distinguish one dentition from another as reflected in a bitemark. In order to understand how these variables appear on skin, 10 dental casts with systematic variations in tooth positions were produced. The height of the lateral incisors was systematically altered in 1mm increments up to 3mm and lateral incisor/canines were altered in facial/lingual displacement in 1mm increments up to 5mm. Each of the models was used to produce a series of 10 repeated bites, distributed over arms and legs of un-embalmed cadavers. Landmark-based geometric morphometrics were used for analysis of digital images of the bitemarks. Results indicate that alterations of height and displacement of particular teeth affected the position of impressions created by the adjacent teeth. Displacement of one lateral incisor/canine led to a relative shift in impressions of the central incisors and unaltered canines, while height alteration of the lateral incisors led to a shift in relative position of central incisors as recorded in the bitemark. The prominence of displacements was more pronounced in the bitemarks than in images of the dentition used to make the bites, thus the bitemarks tended to exaggerate the differences. It was found that a displacement of 5mm between teeth allowed for reliable distinction between bitemarks. No such threshold of distinction could be established for differences in height of teeth under these experimental conditions. The effect of distortion was more significant in the mandibular than maxillary arch, suggesting that the mandible exhibits higher variation than the maxilla, as impressed in skin. Numerous bitemarks also exhibited arch flattening, consistent with recent studies showing arch width as the principal variable in a bitemark.