bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regional and organ-level responses to local lung irradiation in sheep
Authors: Collie David , Wright Steven H. , del-Pozo Jorge , Kay Elaine , Schwarz Tobias , Parys Magdalena , Lawrence Jessica 
Published: May 2021

AbstractLung is a dose-limiting organ in radiotherapy. This may limit tumour control when effort is made in planning to limit the likelihood of radiation-induced lung injury (RILI). Understanding the factors that dictate susceptibility to radiation-induced pulmonary fibrosis will aid in the prevention and management of RILI, and may lead to more effective personalized radiotherapy treatment. As the interaction of regional and organ-level responses may shape the chronic consequences of RILI, we sought to characterise both aspects of the response in an ovine model. A defined volume of left pulmonary parenchyma was prescribed 5 fractions of 6 Gy within 14 days while the contralateral lung dose was constrained. Radiographic changes via computed tomography (CT) were documented to define differences in radio-exposed lung relative to non-exposed lung at d21, d63 and d171 (n = 2), and at d21, d147 and d227 (n = 2). Gross and histologic lung changes were evaluated in samples derived at necropsy examination to define the chronic pulmonary response to radiation. Irradiated lung demonstrated reduced radio-density and increased homogeneity as evidenced from texture based radiomic feature analysis, relative to the control lung. At necropsy, the radiation field was readily defined by pallor on the pleural surface, which was also evident on the cut surface of fixed lung specimens. The degree and homogeneity of pallor reflected the sparse presence of erythrocytes in alveolar septal capillaries of radiation-exposed lung. These changes contrasted with dilated and congested microvasculature in the contralateral control lung. Referencing data to measurements made in control lung volumes of sheep experiencing acute RILI indicated that interstitial collagen continues to deposit in the radio-exposed lung field. Overall lung vascularity increased during the chronic response, as evidenced by increased expression of endothelial cell marker (CD31); however, vascularity was consistently decreased in irradiated lung and was negatively correlated with lung collagen. Other organ-level responses included increased expression of alpha smooth muscle actin (ASMA), increased numbers of proliferating cells (Ki67 positive), and cells expressing the dendritic cell-lysosomal associated membrane protein (DC-LAMP) antigen. The chronic response to RILI in this model is effected at both the whole organ and local lung level. Whilst the long-term consequences of exposure to radiation involved the continued deposition of collagen in the radiation field, organ-level responses also included increased vascularization and increased expression of ASMA, Ki67 and DC-LAMP. Interrupting the interplay between these aspects may influence susceptibility to pulmonary fibrosis after radiotherapy. We advocate for the importance of large animal model systems in pursuing these opportunities to target local, organ-level and systemic mechanisms in parallel within the same subject over time.
Amplification of weak magnetic field effects on oscillating reactions
Authors: Player Thomas C. , Baxter Edward D. A. , Allatt Sarah , Hore P. J. 
Published: May 2021

AbstractWe explore the possibility that chemical feedback and autocatalysis in oscillating chemical reactions could amplify weak magnetic field effects on the rate constant of one of the constituent reactions, assumed to proceed via a radical pair mechanism. Using the Brusselator model oscillator, we find that the amplitude of limit cycle oscillations in the concentrations of reaction intermediates can be extraordinarily sensitive to minute changes in the rate constant of the initiation step. The relevance of such amplification to biological effects of 50/60 Hz electromagnetic fields is discussed.
Dynamical determinants enabling two different types of flight in cheetah gallop to enhance speed through spine movement
Authors: Kamimura Tomoya , Aoi Shinya , Higurashi Yasuo , Wada Naomi , Tsuchiya Kazuo , Matsuno Fumitoshi 
Published: May 2021

AbstractCheetahs use a galloping gait in their fastest speed range. It has been reported that cheetahs achieve high-speed galloping by performing two types of flight through spine movement (gathered and extended). However, the dynamic factors that enable cheetahs to incorporate two types of flight while galloping remain unclear. To elucidate this issue from a dynamical viewpoint, we developed a simple analytical model. We derived possible periodic solutions with two different flight types (like cheetah galloping), and others with only one flight type (unlike cheetah galloping). The periodic solutions provided two criteria to determine the flight type, related to the position and magnitude of ground reaction forces entering the body. The periodic solutions and criteria were verified using measured cheetah data, and provided a dynamical mechanism by which galloping with two flight types enhances speed. These findings extend current understanding of the dynamical mechanisms underlying high-speed locomotion in cheetahs.
Human infants can override possessive tendencies to share valued items with others
Authors: Barragan Rodolfo Cortes , Meltzoff Andrew N. 
Published: May 2021

AbstractPossessiveness toward objects and sharing are competing tendencies that influence dyadic and group interactions within the primate lineage. A distinctive form of sharing in adultHomo sapiensinvolves active giving of high-valued possessions to others, without an immediate reciprocal benefit. In two Experiments with 19-month-old human infants (N = 96), we found that despite measurable possessive behavior toward their own personal objects (favorite toy, bottle), infants spontaneously gave these items to a begging stranger. Moreover, human infants exhibited this behavior across different types of objects that are relevant to theory (personal objects, sweet food, and common objects)—showing flexible generalizability not evidenced in non-human primates. We combined these data with a previous dataset, yielding a large sample of infants (N = 192), and identified sociocultural factors that may calibrate young infants’ sharing of objects with others. The current findings show a proclivity that is rare or absent in our closest living relatives—the capacity to override possessive behavior toward personally valued objects by sharing those same desired objects with others.
Palliative radiotherapy for gross hematuria in patients with advanced cancer
Authors: Ogita Mami , Kawamori Jiro , Yamashita Hideomi , Nakagawa Keiichi 
Published: May 2021

AbstractThis study assessed the efficacy of palliative radiotherapy for gross hematuria caused by advanced cancer. Patients who received palliative radiotherapy to control gross hematuria in two hospitals between October 2006 and May 2020 were retrospectively reviewed. We evaluated the gross hematuria response, gross hematuria control duration, blood transfusion rate, blood transfusion-free duration, and overall survival. Cox multivariate analysis was performed to examine factors associated with hematuria control duration. Fifty-three consecutive patients were included. The most frequently used dose fractionation regimen was 30 Gy in 10 fractions (BED10 = 39 Gy), followed by 20 Gy in 5 fractions (BED10 = 20 Gy). Forty patients (76%) became gross hematuria free. The median hematuria control duration was 4.3 months (95% confidence interval 1.9–6.6). Twenty-six patients received blood transfusion 3 months before radiotherapy; 17 of them (65%) were free from blood transfusion 1 month after radiotherapy. A high BED10 (≥ 36 Gy) was a statistically significant factor for hematuria control duration in the multivariate analysis (P = 0.02). Palliative radiotherapy can effectively relieve gross hematuria irrespective of the primary tumor site. A high BED10 may be recommended for a prolonged hematuria control duration if patients have a good prognosis.
Cortisol modulates calcium release-activated calcium channel gating in fish hepatocytes
Authors: Das Chinmayee , Rout Manoj K. , Wildering Willem C. , Vijayan Mathilakath M. 
Published: May 2021

AbstractGlucocorticoids (GCs) are rapidly released in response to stress and play an important role in the physiological adjustments to re-establish homeostasis. The mode of action of GCs for stress coping is mediated largely by the steroid binding to the glucocorticoid receptor (GR), a ligand-bound transcription factor, and modulating the expression of target genes. However, GCs also exert rapid actions that are independent of transcriptional regulation by modulating second messenger signaling. However, a membrane-specific protein that transduces rapid GCs signal is yet to be characterized. Here, using freshly isolated hepatocytes from rainbow trout (Oncorhynchus mykiss) and fura2 fluorescence microscopy, we report that stressed levels of cortisol rapidly stimulate the rise in cytosolic free calcium ([Ca2+]i). Pharmacological manipulations using specific extra- and intra-cellular calcium chelators, plasma membrane and endoplasmic reticulum channel blockers and receptors, indicated extracellular Ca2+ entry is required for the cortisol-mediated rise in ([Ca2+]i). Particularly, the calcium release-activated calcium (CRAC) channel gating appears to be a key target for the rapid action of cortisol in the ([Ca2+]i) rise in trout hepatocytes. To test this further, we carried out in silico molecular docking studies using the Drosophila CRAC channel modulator 1 (ORAI1) protein, the pore forming subunit of CRAC channel that is highly conserved. The result predicts a putative binding site on CRAC for cortisol to modulate channel gating, suggesting a direct, as well as an indirect regulation (by other membrane receptors) of CRAC channel gating by cortisol. Altogether, CRAC channel may be a novel cortisol-gated Ca2+ channel transducing rapid nongenomic signalling in hepatocytes during acute stress.
Evaluation of antibiotic-induced taste and smell disorders using the FDA adverse event reporting system database
Authors: Kan Yusuke , Nagai Junko , Uesawa Yoshihiro 
Published: May 2021

AbstractAdverse effects can occur owing to anorexia, which can reduce treatment compliance and worsen the patients overall condition. One such side effect, namely drug-induced taste and smell disorders, reduces patients quality of life. Although antibiotics can cause taste and smell disorders, a few studies have examined antibiotic-induced taste and smell disorders. Therefore, this study comprehensively analyzed the relationship between taste and smell disorders and antibiotic usage. The side effects of antibiotics were investigated using the FDA Adverse Event Reporting System database (FAERS). The reporting odds ratios between the listed drugs and taste and smell disorders P values were comprehensively calculated. Adjusted odds ratios were calculated to account for patient background. Furthermore, to clarify the feature of this adverse effect, shape parameters indicating the expression pattern were calculated. Signals that induced taste and smell disorders were detected for six antibiotics, including drugs for which this event is not described in the package insert in Japan. Multiple logistic regression analysis suggested an association of taste and smell disorders with gender, hypertension, mental disorder, and cancer. The median time to onset of antibiotic-induced taste and smell disorders was 2–5 days. Six antibiotics could be analyzed, and four of these drugs matched those with detected signals. Our study supported previous findings on gender and age. Furthermore, antibiotic-induced taste and smell disorders are likely to develop in the early stage of treatment. For these reasons, it is important to remember the risk of developing of taste and smell disorders when administering antibiotics. In addition, it is recommended that the patient be monitored carefully for at least 1 week before initiating treatment, and the patients course should be followed for at least 2 months.
Emergence of fluoroquinolone resistance and possible mechanisms in clinical isolates of Stenotrophomonas maltophilia from Iran
Authors: Azimi Akram , Rezaei Farhad , Yaseri Mehdi , Jafari Sirus , Rahbar Mohammad , Douraghi Masoumeh 
Published: May 2021

AbstractStenotrophomonas maltophilia exhibits wide spectrum of fluoroquinolone resistance using different mechanisms as multidrug efflux pumps and Smqnr alleles. Here, the role of smeDEF, smeVWX efflux genes and contribution of Smqnr alleles in the development of fluoroquinolone resistance was assessed. Ciprofloxacin, levofloxacin and moxifloxacin resistance were found in 10.9%, 3.5%, and 1.6% of isolates, respectively. More than four-fold differences in ciprofloxacin MICs were detected in the presence of reserpine and smeD, F, V expression was significantly associated with ciprofloxacin resistance (p = 0.017 for smeD, 0.003 for smeF, and 0.001 for smeV). Smqnr gene was found in 52% of the ciprofloxacin-resistant isolates and Smqnr8 was the most common allele detected. Fluoroquinolone resistance in S. maltophilia clinical isolates was significantly associated with active efflux pumps. There was no correlation between the Smqnr alleles and ciprofloxacin resistance; however, contribution of the Smqnr genes in low-level levofloxacin resistance was revealed.
Homoarginine and methylarginines independently predict long-term outcome in patients presenting with suspicion of venous thromboembolism
Authors: Rodionov Roman N. , Beyer-Westendorf Jan , Bode-Böger Stefanie M. , Eggebrecht Lisa , Konstantinides Stavros , Martens-Lobenhoffer Jens , Nagler Markus , Prochaska Jürgen , Wild Philipp 
Published: May 2021

AbstractEndogenous arginine derivatives homoarginine, asymmetric dimethylarginine (ADMA) and symmetric dimethyarginine (SDMA) are independent mortality predictors in atherosclerotic cardiovascular disease (CVD). Our study reports the first analysis, whether homoarginine, ADMA and SDMA predict venous thromboembolism (VTE) recurrence and overall mortality in patients with suspected acute VTE. We assessed serum levels of homoarginine, ADMA and SDMA by LC–MS/MS in 865 individuals from a prospective consecutive cohort of patients with clinical suspicion of VTE. The median follow-up time for mortality was 1196 days. VTE was confirmed by imaging in 418 patients and excluded in 447 patients. Low levels of homoarginine and high levels of ADMA or SDMA independently predicted all-cause mortality after adjustment for sex, age, oral anticoagulants, body mass index, arterial hypertension, diabetes mellitus, smoking, dyslipidemia, chronic heart failure, history of stroke, creatinine and cancer both in patients with VTE and without VTE. Interestingly, none of those parameters was predictive for VTE recurrence. We provide the first report that low circulating levels of homoarginine and high circulating levels of ADMA and SDMA independently predict all-cause mortality in patients with suspected VTE. These parameters might serve as markers of “frailty” and should be considered for future risk stratification approaches in this clinical population. Taking into account that homoarginine supplementation is protective in animal models of CVD and safe in healthy human volunteers, our study provides the basis for future homoarginine supplementation studies in patients with suspected VTE to investigate possible direct protective effects of homoarginine in this population.
Study on attractors during organism evolution
Authors: Kasperski Andrzej , Kasperska Renata 
Published: May 2021

AbstractThe important question that arises during determining the evolution of organisms is whether evolution should be treated as a continuous process or whether groups of organisms fall into 'local' attractors during evolution. A similar question arises during considering the development of cells after cancer transformation. Answers to these questions can provide a better understanding of how normal and transformed organisms evolve. So far, no satisfactory answers have been found to these questions. To find the answers and demonstrate that organisms during evolution get trapped in 'local' attractors, an artificial neural network supported by a semihomologous approach and unified cell bioenergetics concept have been used in this work. A new universal model of cancer transformation and cancer development has been established and presented to highlight the differences between the development of transformed cells and normal organisms. An unequivocal explanation of cancer initialization and development has not been discovered so far, thus the proposed model should shed new light on the evolution of transformed cells.
Tailoring grain sizes of the biodegradable iron-based alloys by pre-additive manufacturing microalloying
Authors: Huang Chih-Chieh , Lam Tu-Ngoc , Amalia Lia , Chen Kuan-Hung , Yang Kuo-Yi , Muslih M. Rifai , Singh Sudhanshu Shekhar , Tsai Pei-I. , Lee Yuan-Tzu , Jain Jayant , Lee Soo Yeol , Lai Hong-Jen , Huang Wei-Chin , Chen San-Yuan , Huang E-Wen 
Published: May 2021

AbstractWe demonstrated the design of pre-additive manufacturing microalloying elements in tuning the microstructure of iron (Fe)-based alloys for their tunable mechanical properties. We tailored the microalloying stoichiometry of the feedstock to control the grain sizes of the metallic alloy systems. Two specific microalloying stoichiometries were reported, namely biodegradable iron powder with 99.5% purity (BDFe) and that with 98.5% (BDFe-Mo). Compared with the BDFe, the BDFe-Mo powder was found to have lower coefficient of thermal expansion (CTE) value and better oxidation resistance during consecutive heating and cooling cycles. The selective laser melting (SLM)-built BDFe-Mo exhibited high ultimate tensile strength (UTS) of 1200 MPa and fair elongation of 13.5%, while the SLM-built BDFe alloy revealed a much lower UTS of 495 MPa and a relatively better elongation of 17.5%, indicating the strength enhancement compared with the other biodegradable systems. Such an enhanced mechanical behavior in the BDFe-Mo was assigned to the dominant mechanism of ferrite grain refinement coupled with precipitate strengthening. Our findings suggest the tunability of outstanding strength-ductility combination by tailoring the pre-additive manufacturing microalloying elements with their proper concentrations.
Long pentraxin PTX3 is upregulated systemically and centrally after experimental neurotrauma, but its depletion leaves unaltered sensorimotor deficits or histopathology
Authors: Oggioni Marco , Mercurio Domenico , Minuta Denise , Fumagalli Stefano , Popiolek-Barczyk Katarzyna , Sironi Marina , Ciechanowska Agata , Ippati Stefania , De Blasio Daiana , Perego Carlo , Mika Joanna , Garlanda Cecilia , De Simoni Maria-Grazia 
Published: May 2021

AbstractLong pentraxin PTX3, a pattern recognition molecule involved in innate immune responses, is upregulated by pro-inflammatory stimuli, contributors to secondary damage in traumatic brain injury (TBI). We analyzed PTX3 involvement in mice subjected to controlled cortical impact, a clinically relevant TBI mouse model. We measured PTX3 mRNA and protein in the brain and its circulating levels at different time point post-injury, and assessed behavioral deficits and brain damage progression in PTX3 KO mice. PTX3 circulating levels significantly increased 1–3 weeks after injury. In the brain, PTX3 mRNA was upregulated in different brain areas starting from 24 h and up to 5 weeks post-injury. PTX3 protein significantly increased in the brain cortex up to 3 weeks post-injury. Immunohistochemical analysis showed that, 48 h after TBI, PTX3 was localized in proximity of neutrophils, likely on neutrophils extracellular traps (NETs), while 1- and 2- weeks post-injury PTX3 co-localized with fibrin deposits. Genetic depletion of PTX3 did not affect sensorimotor deficits up to 5 weeks post-injury. At this time-point lesion volume and neuronal count, axonal damage, collagen deposition, astrogliosis, microglia activation and phagocytosis were not different in KO compared to WT mice. Members of the long pentraxin family, neuronal pentraxin 1 (nPTX1) and pentraxin 4 (PTX4) were also over-expressed in the traumatized brain, but not neuronal pentraxin 2 (nPTX2) or short pentraxins C-reactive protein (CRP) and serum amyloid P-component (SAP). The long-lasting pattern of activation of PTX3 in brain and blood supports its specific involvement in TBI. The lack of a clear-cut phenotype in PTX3 KO mice may depend on the different roles of this protein, possibly involved in inflammation early after injury and in repair processes later on, suggesting distinct functions in acute phases versus sub-acute or chronic phases. Brain long pentraxins, such as PTX4—shown here to be overexpressed in the brain after TBI—may compensate for PTX3 absence.
Association of urinary ketamine and APOA1 levels with bladder dysfunction in ketamine abusers revealed via proteomics and targeted metabolite analyses
Authors: Liu Jo-Chuan , Chen Yi-Ting , Hsieh Ya-Ju , Wu Chia-Chun , Huang Ming-Chyi , Hsu Yu-Chao , Wu Chun-Te , Chen Chih-Ken , Dash Srinivas , Yu Jau-Song 
Published: May 2021

AbstractChronic ketamine abuse is associated with bladder dysfunction and cystitis. However, the effects of ketamine abuse on the urinary proteome profile and the correlations among urinary proteins, urinary ketamine (and metabolites) and clinicopathological features of ketamine-induced bladder dysfunction remain to be established. Here, we recruited 56 ketamine abusers (KA) and 40 age-matched healthy controls (HC) and applied the iTRAQ-based proteomics approach to unravel quantitative changes in the urine proteome profile between the two groups. Many of the differentially regulated proteins are involved in the complement and coagulation cascades and/or fibrotic disease. Among them, a significant increase in APOA1 levels in KA relative to control samples (392.1 ± 59.9 ng/ml vs. 13.7 ± 32.6 ng/ml, p < 0.0001) was detected via ELISA. Moreover, urinary ketamine, norketamine and dehydronorketamine contents (measured via LC-SRM-MS) were found to be positively correlated with overactive bladder syndrome score (OABSS) and APOA1 levels with urinary RBC, WBC, OABSS and numeric pain rating scale in KA. Collectively, our results may aid in developing new molecular tool(s) for management of ketamine-induced bladder dysfunction. Moreover, information regarding the differentially regulated proteins in urine of KA provides valuable clues to establish the molecular mechanisms underlying ketamine-induced cystitis.