Miracle-dz/UniFAR-FTUs huggingface dataset:
Trophy hunters’ willingness to pay for wildlife conservation and community benefits

In the face of fundamental land‐use changes, the potential for trophy hunting to contribute to conservation is increasingly recognized. Trophy hunting can, for example, provide economic incentives to protect wildlife populations and their habitat, but empirical studies on these relationships are few and tend to focus on the effects of benefit‐sharing schemes from an ex post perspective. We investigated the conditions under which trophy hunting could facilitate wildlife conservation in Ethiopia ex ante. We used a choice experiment approach to survey international trophy hunters’ (n = 224) preferences for trips to Ethiopia, here operationalized as trade‐offs between different attributes of a hunting package, as expressed through choices with an associated willingness to pay. Participants expressed strong preferences and, consequently, were willing to pay substantial premiums for hunting trips to areas with abundant nontarget wildlife where domestic livestock was absent and for arrangements that offered benefit sharing with local communities. For example, within the range of percentages considered in the survey, respondents were on average willing to pay an additional $3900 for every 10 percentage points of the revenue being given to local communities. By contrast, respondents were less supportive of hunting revenue being retained by governmental bodies: Willingness to pay decreased by $1900 for every 10 percentage points of the revenue given to government. Hunters’ preferences for such attributes of hunting trips differed depending on the degree to which they declared an interest in Ethiopian culture, nature conservation, or believed Ethiopia to be politically unstable. Overall, respondents thus expressly valued the outcomes of nature conservation activities—the presence of wildlife in hunting areas—and they were willing to pay for them. Our findings highlight the usefulness of insights from choice modeling for the design of wildlife management and conservation policies and suggest that trophy hunting in Ethiopia could generate substantially more financial support for conservation and be more in line with conservation objectives than is currently the case.
Mobile usability: An antecedent for influencing purchase intention moderated by omni-channel integration quality

The new concept of omni-channel has inspired researchers to develop a model of consumer confusion to increase purchase intention. Previous studies were tested that the omni-channel integration quality can improve customer satisfaction. As a novelty, this study introduced omni-channel integration as a moderating variable that influence consumer confusion to the intention of purchase. This paper constituted a hypothetical development about the proposed omni-channel integration as a part of the e-quality service. This proposed research aimed to explore the effect of consumer confusion towards purchase intention moderated by omni-channel integration. Three hypotheses were modeled in this research proposal. The future results of this research are expected to be a significant contribution towards business, science, and society.
Long-term mobility monitoring of older adults using accelerometers in a clinical environment

Objective: To assess the accuracy of accelerometer-based mobility monitoring during extended measurements on older adults in a clinical setting and to evaluate two different approaches to thresholding. Design: The monitoring device consisted of two Analog Devices ADXL202 accelerometers, an ambulatory data-logger and associated cabling. The monitoring system used custom-designed analysis software to detect activities of daily living, namely duration of sitting, standing, lying and moving during the period monitored. An investigator shadowed the subjects throughout the recording period. Subjects and setting: This study monitored five older adults, with varying degrees of mobility, resident in a rehabilitation clinic, over four days. Interventions: The accelerometer data were analysed using a MATLABÒ program that allowed trunk and thigh threshold angles to be set to distinguish between sitting, standing, lying and moving. Two different approaches to setting these thresholds were investigated: (1) using a midpoint tolerance value of 458 and (2) using a `best estimate' tolerance value. The analysis program generates a summary of activities, which is then compared line-by-line with the manual summary created by the observer. The result was a hit/miss ratio representative of the system's accuracy. Results: The detection accuracies for sitting and lying using a mid-point tolerance value were poor, with an average detection accuracy of 75% obtained. The `best estimate' approach improved the detection accuracies for sitting and lying by approximately 18% to an average value of 93%. Conclusion: In a population of older adults, the static activities of sitting, standing and lying and dynamic activities can be distinguished using the technique and threshold values outlined here to a degree of accuracy of 92% and higher.
Flavonoids and fatty acids of Camellia japonica leaves extract

The ethanol extract from the leaves of Camellia japonica L. , Theaceae, showed antiradical potential in the DPPH test using TLC plates (SiO2). Aiming the isolation of active compounds, this extract was partitioned between BuOH:H2O (1:1) and the two obtained phases were also evaluated to detection of antiradical activity. The active BuOH phase was fractionated in Sephadex LH-20 and silica (normal or reverse phase) to afford three aglycone flavonoids (quercetin, kaempferol and apigenin), which have been described in the C. japonica at first time, two glycosilated flavonoids (rutin and quercetrin), and a mixture of saturated fatty acids. The structures of isolated compounds were defined by NMR and GC/MS analyses.
Connective tissue response to tubular implants for peripheral nerve regeneration: The role of myofibroblasts

The presence of contractile cells, their organization around regenerating nerve trunks, and the hypothetical effect of these organized structures on the extent of regeneration across a tubulated 10‐mm gap in the rat sciatic nerve were investigated. Collagen and silicone tubes were implanted both empty and filled with a collagen‐glycosaminoglycan (GAG) matrix. Nerves were retrieved at 6, 30, and 60 weeks postoperatively and time‐dependent values of the nerve trunk diameter along the tubulated length were recorded. The presence of myofibroblasts was identified immunohistochemically using a monoclonal antibody to α‐smooth muscle actin. Myofibroblasts were circumferentially arranged around the perimeter of regenerated nerve trunks, forming a capsule which was about 10 times thicker in silicone tubes than in collagen tubes. The nerve trunk diameter that formed inside collagen tubes was twice as large as that inside silicone tubes. In contrast, the collagen‐GAG matrix had a relatively small effect on capsule thickness or diameter of regenerate. It was hypothesized that the frequency of successful bridging by axons depends on the balance between two competitive forces: the axial forces generated by the outgrowth of axons and nonneuronal cells from the proximal stump and the constrictive, circumferential forces imposed by the contractile tissue capsule that promote closure of the wounded stumps and prevent axon elongation. Because the presence of the collagen‐GAG matrix has enhanced greatly the recovery of normal function of regenerates in silicone tubes, it was hypothesized that it accelerated axonal elongation sufficiently before the hypothetical forces constricting the nerve trunk in silicone tubes became sufficiently large. The combined data suggest a new mechanism for peripheral nerve regeneration along a tubulated gap. J. Comp. Neurol. 417:415–430, 2000. © 2000 Wiley‐Liss, Inc.
Implanted neonatal human dermal fibroblasts influence the recruitment of endothelial cells in mice

The vascularization of new tissue within a reasonable time is a crucial prerequisite for the success of different cell- and material-based strategies. Considering that angiogenesis is a multi-step process involving humoral and cellular regulatory components, only in vivo assays provide the adequate information about vessel formation and the recruitment of endothelial cells. The present study aimed to investigate if neonatal human dermal fibroblasts could influence in vivo neovascularization. Results obtained showed that fibroblasts were able to recruit endothelial cells to vascularize the implanted matrix, which was further colonized by murine functional blood vessels after one week. The vessels exhibited higher levels of hemoglobin, compared with the control matrix, implanted without fibroblasts, in which no vessel formation could be observed. No significant differences were detected in systemic inflammation. The presence of vessels originated from the host vasculature suggested that host vascular response was involved, which constitutes a fundamental aspect in the process of neovascularization. Fibroblasts implanted within matrigel increased the presence of endothelial cells with positive staining for CD31 and for CD34 and the production of collagen influencing the angiogenic process and promoting the formation of microvessels. New strategies in tissue engineering could be delineated with improved angiogenesis using neonatal fibroblasts.
Pathogenesis of Pancreatic Cancer

The past several decades have seen great effort devoted to mimicking the key features of pancreatic ductal adenocarcinoma (PDAC) in animals and have produced 2 robust models of this deadly cancer. Carcinogen-treated Syrian hamsters develop PDAC with genetic lesions, which reproduce those of human, including activation of the Kras oncogene, and early studies in this species validated nongenetic risk factors for PDAC including pancreatitis, obesity, and diabetes. More recently, PDAC research has been invigorated by the development of genetically engineered mouse models based on tissue-specific Kras activation and deletion of tumor suppressor genes. Surprisingly, mouse PDAC appears to arise from exocrine acinar rather than ductal cells, via a process of phenotypic reprogramming that is accelerated by inflammation. Studies in both models have uncovered molecular mechanisms by which inflammation promotes and sustains PDAC and identified targets for chemoprevention to suppress PDAC in high-risk individuals. The mouse model, in particular, has also been instrumental in developing new approaches to early detection as well as treatment of advanced disease. Together, animal models enable diverse approaches to basic and preclinical research on pancreatic cancer, the results of which will accelerate progress against this currently intractable cancer.
Adenovirus advances: new diagnostic and therapeutic options

Purpose of review Adenoviral infection is common, can be severe, and may cause significant morbidity. Recent findings Ophthalmologists and optometrists are often guilty of spreading adenovirus because it is highly contagious and has 53 serotypes with variable morphology. Adenovirus is often difficult to diagnose based on clinical appearance and, in the early stages, is associated with a red eye or superficial keratitis common to herpes and other infections. This difficulty results in the indiscriminate use of antibiotics, which are expensive and of no established value in treating a viral infection. The difficulty of accurate diagnosis also makes the use of newer proposed treatments less valuable and even potentially hazardous. Summary New diagnostic tests such as the Rapid Pathogen Screening (RPS) Adeno Detector that are practical, rapid, and inexpensive to use in the office may obviate these problems.
The development of a serum-free derived bioengineered conjunctival epithelial equivalent using an ultrathin poly(epsilon-caprolactone) membrane substrate.

PURPOSE To evaluate the use of an ultrathin poly(epsilon-caprolactone) (PCL) membrane as a substrate for the development of a serum-free-derived conjunctival epithelial equivalent. METHODS Ultrathin PCL membranes 6 microm in thickness were prepared by solvent casting and biaxial stretching and analyzed by atomic force microscopy (AFM), scanning electron microscopy (SEM), tensile testing, and water-contact angle measurement. Rabbit conjunctival epithelial cells were cultivated on sodium hydroxide (NaOH)-treated PCL membranes and untreated PCL membranes in serum-free medium. The proliferative capacity of cultivated cells was analyzed with a bromodeoxyuridine (BrdU) ELISA proliferation assay. Conjunctival equivalents were xenografted into severe combined immune-deficient (SCID) mice. Immunostaining for tissue-specific and basement membrane-related proteins was performed. RESULTS After biaxial stretching, the tensile strength of PCL membranes increased from 21 to 42 MPa, with a Young's modulus of 225 MPa. AFM and SEM showed that biaxially stretched PCL membranes consisted of closely packed microfibrils. PCL membranes supported the attachment and proliferation of conjunctival epithelial cells to form confluent stratified epithelial sheets. Surface modification with NaOH resulted in greater hydrophilicity and cellular proliferation than that of untreated membranes. Transplanted conjunctival equivalents underwent greater proliferation and stratification in vivo. Cultivated conjunctival cells expressed K4, K19, MUC5AC, and Ki67, whereas collagen IV and integrin beta4 were detected at the basement membrane junction. CONCLUSIONS An ultrathin PCL membrane was shown to be biocompatible, mechanically strong enough to stand up to handling, and able to support conjunctival epithelial cell proliferation. This membrane may have potential for use as a scaffold matrix for tissue-engineered conjunctival equivalents.
Highly neurotoxic monomeric α-helical prion protein

Prion diseases are infectious and belong to the group of protein misfolding neurodegenerative diseases. In these diseases, neuronal dysfunction and death are caused by the neuronal toxicity of a particular misfolded form of their cognate protein. The ability to specifically target the toxic protein conformer or the neuronal death pathway would provide powerful therapeutic approaches to these diseases. The neurotoxic forms of the prion protein (PrP) have yet to be defined but there is evidence suggesting that at least some of them differ from infectious PrP (PrPSc). Herein, without making an assumption about size or conformation, we searched for toxic forms of recombinant PrP after dilution refolding, size fractionation, and systematic biological testing of all fractions. We found that the PrP species most neurotoxic in vitro and in vivo (toxic PrP, TPrP) is a monomeric, highly α-helical form of PrP. TPrP caused autophagy, apoptosis, and a molecular signature remarkably similar to that observed in the brains of prion-infected animals. Interestingly, highly α-helical intermediates have been described for other amyloidogenic proteins but their biological significance remains to be established. We provide unique experimental evidence that a monomeric α-helical form of an amyloidogenic protein represents a cytotoxic species. Although toxic PrP has yet to be purified from prion-infected brains, TPrP might be the equivalent of one highly neurotoxic PrP species generated during prion replication. Because TPrP is a misfolded, highly neurotoxic form of PrP reproducing several features of prion-induced neuronal death, it constitutes a useful model to study PrP-induced neurodegenerative mechanisms.
Relative mitochondrial membrane potential and [Ca2+]i in type I cells isolated from the rabbit carotid body.

1. In the accompanying paper (Duchen & Biscoe, 1992) we have described graded changes in autofluorescence derived from mitochondrial NAD(P)H in type I cells of the carotid body in response to changes of PO2 over a physiologically significant range. These observations suggest that mitochondrial function in these cells is unusually sensitive to oxygen and could play a role in oxygen sensing. We have now explored further the relationships between hypoxia, mitochondrial membrane potential (delta psi m) and [Ca2+]i. 2. The fluorescence of Rhodamine 123 (Rh 123) accumulated within mitochondria is quenched by delta psi m. Mitochondrial depolarization thus increases the fluorescence signal. Blockade of electron transport (CN‐, anoxia, rotenone) and uncoupling agents (e.g. carbonyl cyanide p‐trifluoromethoxy‐phenylhydrazone; FCCP) increased fluorescence by up to 80‐120%, while fluorescence was reduced by blockade of the F0 proton channel of the mitochondrial ATP synthase complex (oligomycin). 3. delta psi m depolarized rapidly with anoxia, and was usually completely dissipated within 1‐2 min. The depolarization of delta psi m with anoxia (or CN‐) and repolarization on reoxygenation both followed a time course well characterized as the sum of two exponential processes. Oligomycin (0.2‐2 micrograms/ml) hyperpolarized delta psi m and abolished the slower components of both the depolarization with anoxia and of the subsequent repolarization. These data (i) illustrate the role of the F1‐F0 ATP synthetase in slowing the rate of dissipation of delta psi m on cessation of electron transport, (ii) confirm blockade of the ATP synthetase by oligomycin at these concentrations, and (iii) indicate significant accumulation of intramitochondrial ADP during 1‐2 min of anoxia. 4. Depolarization of delta psi m was graded with graded changes in PO2 below about 60 mmHg. The stimulus‐response curves thus constructed strongly resemble those for [Ca2+]i and NAD(P)H with PO2. The change in delta psi m closely followed changes in PO2 with time. 5. The rate of rise of [Ca2+]i in response to anoxia is strongly temperature sensitive. The rate of depolarization of delta psi m with anoxia similarly increased at least two‐ to fivefold on warming from 22 to 36 degrees C. The change with FCCP was not significantly altered by temperature. 6. These data show that the mitochondrial membrane potential changes over a physiological range of PO2 values in type I cells. This contrasts with the behaviour in dissociated chromaffin cells and sensory neurons, in which no change was measurable until the PO2 fell close to zero. (ABSTRACT TRUNCATED AT 400 WORDS)
The Reliability and Validity of a Four-Minute Running Time-Trial in Assessing V˙O2max and Performance

Introduction: Traditional graded-exercise tests to volitional exhaustion (GXTs) are limited by the need to establish starting workloads, stage durations, and step increments. Short-duration time-trials (TTs) may be easier to implement and more ecologically valid in terms of real-world athletic events. The purpose of the current study was to assess the reliability and validity of maximal oxygen uptake (V˙O2max) and performance measured during a traditional GXT (STEP) and a four-minute running time-trial (RunTT). Methods: Ten recreational runners (age: 32 ± 7 years; body mass: 69 ± 10 kg) completed five STEP tests with a verification phase (VER) and five self-paced RunTTs on a treadmill. The order of the STEP/VER and RunTT trials was alternated and counter-balanced. Performance was measured as time to exhaustion (TTE) for STEP and VER and distance covered for RunTT. Results: The coefficient of variation (CV) for V˙O2max was similar between STEP, VER, and RunTT (1.9 ± 1.0, 2.2 ± 1.1, and 1.8 ± 0.8%, respectively), but varied for performance between the three types of test (4.5 ± 1.9, 9.7 ± 3.5, and 1.8 ± 0.7% for STEP, VER, and RunTT, respectively). Bland-Altman limits of agreement (bias ± 95%) showed V˙O2max to be 1.6 ± 3.6 mL·kg−1·min−1 higher for STEP vs. RunTT. Peak HR was also significantly higher during STEP compared with RunTT (P = 0.019). Conclusion: A four-minute running time-trial appears to provide more reliable performance data in comparison to an incremental test to exhaustion, but may underestimate V˙O2max.
MicroRNA‐138 and MicroRNA‐25 Down‐regulate Mitochondrial Calcium Uniporter, Causing the Pulmonary Arterial Hypertension Cancer Phenotype

Rationale: Pulmonary arterial hypertension (PAH) is an obstructive vasculopathy characterized by excessive pulmonary artery smooth muscle cell (PASMC) proliferation, migration, and apoptosis resistance. This cancer‐like phenotype is promoted by increased cytosolic calcium ([Ca2+]cyto), aerobic glycolysis, and mitochondrial fission. Objectives: To determine how changes in mitochondrial calcium uniporter (MCU) complex (MCUC) function influence mitochondrial dynamics and contribute to PAH's cancer‐like phenotype. Methods: PASMCs were isolated from patients with PAH and healthy control subjects and assessed for expression of MCUC subunits. Manipulation of the pore‐forming subunit, MCU, in PASMCs was achieved through small interfering RNA knockdown or MCU plasmid‐mediated up‐regulation, as well as through modulation of the upstream microRNAs (miRs) miR‐138 and miR‐25. In vivo, nebulized anti‐miRs were administered to rats with monocrotaline‐induced PAH. Measurements and Main Results: Impaired MCUC function, resulting from down‐regulation of MCU and up‐regulation of an inhibitory subunit, mitochondrial calcium uptake protein 1, is central to PAH's pathogenesis. MCUC dysfunction decreases intramitochondrial calcium ([Ca2+]mito), inhibiting pyruvate dehydrogenase activity and glucose oxidation, while increasing [Ca2+]cyto, promoting proliferation, migration, and fission. In PAH PASMCs, increasing MCU decreases cell migration, proliferation, and apoptosis resistance by lowering [Ca2+]cyto, raising [Ca2+]mito, and inhibiting fission. In normal PASMCs, MCUC inhibition recapitulates the PAH phenotype. In PAH, elevated miRs (notably miR‐138) down‐regulate MCU directly and also by decreasing MCU's transcriptional regulator cAMP response element‐binding protein 1. Nebulized anti‐miRs against miR‐25 and miR‐138 restore MCU expression, reduce cell proliferation, and regress established PAH in the monocrotaline model. Conclusions: These results highlight miR‐mediated MCUC dysfunction as a unifying mechanism in PAH that can be therapeutically targeted.
Characterization of skin inflammation induced by repeated exposure of toluene, xylene, and formaldehyde in mice

Volatile organic compounds (VOCs) are considered the main cause of sick building syndrome and they are likely to irritate the skin, eyes, and mucous membrane; however, the toxic threshold and the mechanisms of cutaneous reaction induced by long‐time VOC exposure have not been clarified. In the present study, we investigated the effect of repeated painting of VOCs onto mouse skin. Various concentrations of toluene, xylene, and formaldehyde (FA) were applied once a week for 5 weeks. While FA solution (2–10%) induced remarkable ear swelling and caused evident infiltration of inflammatory cells, high concentrations of toluene and xylene (50 or 100%) evoked mild ear swelling and marginal inflammatory cell invasion. In addition, FA exposure markedly increased the expression of interleukin‐4 (IL‐4), brain‐derived neurotrophic factor (BDNF), neurotrophin‐3 (NT‐3), and transient receptor potential vanilloid‐1 (TRPV‐1) mRNAs in the ears and IL‐4 and NT‐3 mRNAs in the cervical lymph nodes. Furthermore, capsazepine, a TRPV‐1 antagonist, significantly suppressed ear swelling caused by repeated painting of 5% FA. These findings demonstrate that FA has more potent irritancy against skin than toluene or xylene and suggest that the Th2 response, neurotrophins and TRPV‐1 play important roles in FA‐induced skin inflammation. © 2009 Wiley Periodicals, Inc. Environ Toxicol, 2011.