bluuebunny/crossref_metadata_2025_split huggingface dataset:
Musculoskeletal anatomy knowledge in Australian chiropractors
Authors: Giuriato Rosemary , Štrkalj Goran , Prvan Tania , Hulme Anneliese , Pather Nalini 
Published: July 2021

AbstractAnatomy is a key knowledge area in chiropractic and is formally offered in the undergraduate component of chiropractic education. There is the potential for loss of anatomy knowledge before the opportunity to apply it in a clinical setting. This study aimed to determine whether chiropractic clinicians retain a level of anatomy knowledge comparable to that of chiropractic students and to compare chiropractors' self‐rating of their anatomical knowledge against an objective knowledge assessment tool. A previously validated multiple‐choice test was utilized to measure retention of limb musculoskeletal (MSK) knowledge in Australian chiropractors. One hundred and one registered chiropractors completed the questionnaire and responses were scored, analyzed, and compared to scores attained by undergraduate and postgraduate chiropractic students who had previously completed the same questionnaire. The results indicated that practitioners retained their anatomy knowledge, with a significantly higher total mean score than the undergraduate group [total mean score = 36.5% (±SD 13.6%); P < 0.01] but not significantly different to the postgraduate group [total mean score = 52.2% (±SD 14.1%); P = 0.74]. There was a weak positive correlation between chiropractors' self‐rated knowledge and test performance scores indicating the effectiveness of this Australian chiropractic group in self‐assessing their anatomy knowledge. This study found that Australian chiropractors' knowledge of MSK anatomy was retained during the transition from university to clinical practice and they accurately evaluated their own test performance.
Breaking barriers: The landscape of human and veterinary medical anatomy education and the potential for collaboration
Authors: McNulty Margaret A. , Mussell Jason C. , Lufler Rebecca S. 
Published: July 2021

AbstractDespite human (HUM) and veterinary (VET) medical institutions sharing the goal of educating future clinicians, there is little collaboration between them regarding curricular and pedagogical practices during the preclinical/basic science training years. This may be, at least in part, due to a lack of understanding of each type of curriculum. This study presents data about curricula, student populations, pedagogical methodologies applied, and anatomy educators' training at both HUM and VET institutions. Preclinical curricula, admissions criteria, and student demographics were analyzed for 21 institutions in the United States having both HUM and VET schools. This dataset was augmented by a questionnaire sent to anatomists internationally, detailing anatomy curricula, pedagogies applied, and anatomy educators' training. Many curricular similarities between both training programs were identified, including anatomy education experiences. However, VET programs were found to include more preclinical coursework than HUM programs. Students who matriculate to VET or HUM schools have similar academic records, including prerequisite coursework and grade point average. Median HUM class size was significantly larger, and the percentage of women enrolled in VET institutions was significantly higher. Training of anatomy educators was identical with one exception: VET educators are far more likely to hold a clinical degree. This study elucidates the substantial similarities between VET and HUM programs, particularly in anatomy education, underscoring the potential for collaboration between both types of programs in areas such as interprofessional education, bioethics, zoonotic disease management, and postgraduate training.
How signaling pathways link extracellular mechano‐environment to proline biosynthesis: A hypothesis
Authors: Chen Keng , Guo Ling , Wu Chuanyue 
Published: July 2021

AbstractWe propose a signaling pathway in which cell‐extracellular matrix (ECM) adhesion components PINCH‐1 and kindlin‐2 sense mechanical signals from ECM and link them to proline biosynthesis, a vital metabolic pathway for macromolecule synthesis, redox balance, and ECM remodeling. ECM stiffening promotes PINCH‐1 expression via integrin signaling, which suppresses dynamin‐related protein 1 (DRP1) expression and mitochondrial fission, resulting in increased kindlin‐2 translocation into mitochondria and interaction with Δ1‐pyrroline‐5‐carboxylate (P5C) reductase 1 (PYCR1). Kindlin‐2 interaction with PYCR1 protects the latter from proteolytic degradation, leading to elevated PYCR1 level. Additionally, PINCH‐1 promotes P5C synthase (P5CS) expression and P5C synthesis, which, together with increased PYCR1 level, support augmented proline biosynthesis. This signaling pathway is frequently activated in fibrosis and cancer, resulting in increased proline biosynthesis and excessive collagen matrix production, which in turn further promotes ECM stiffening. Targeting this signaling pathway, therefore, may provide an effective strategy for alleviating fibrosis and cancer progression.
Parallel and large‐scale antitumor investigation using stable chemical gradient and heterotypic three‐dimensional tumor coculture in a multi‐layered microfluidic device
Authors: Liu Wenming , Hu Rui , Han Kai , Sun Meilin , Liu Dan , Zhang Jinwei , Wang Jinyi 
Published: July 2021

AbstractBackgroundCancer has been responsible for a large number of human deaths in the 21st century. Establishing a controllable, biomimetic, and large‐scale analytical platform to investigate the tumor‐associated pathophysiological and preclinical events, such as oncogenesis and chemotherapy, is necessary.Methods and ResultsThis study presents antitumor investigation in a parallel, large‐scale, and tissue‐mimicking manner based on well‐constructed chemical gradients and heterotypic three‐dimensional (3D) tumor cocultures using a multifunction‐integrated device. The integrated microfluidic device was engineered to produce a controllable and steady chemical gradient by manipulative optimization. Array‐like and size‐homogeneous production of heterotypic 3D tumor cocultures with in vivo‐like features, including similar tumor‐stromal composition and functional phenotypic gradients of metabolic activity and viability, was successfully established. Furthermore, temporal, parallel, and high‐throughput analyses of tumor behaviors in different antitumor stimulations were performed in a device based on the integrated operations involving gradient generation and coculture.ConclusionThis achievement holds great potential for applications in the establishment of multifunctional tumor platforms to perform tissue‐biomimetic neoplastic research and therapy assessment in the fields of oncology, bioengineering, and drug discovery.
A cross‐linked anti‐TNF‐α aptamer for neutralization of TNF‐α‐induced cutaneous Shwartzman phenomenon: A simple and novel approach for improving aptamers' affinity and efficiency
Authors: Mashayekhi Kazem , Sankian Mojtaba , Haftcheshmeh Saeed Mohammadian , Taheri Ramezan Ali , Hassanpour Kazem , Farnoosh Gholamreza 
Published: July 2021

AbstractTo increase the efficiency of aptamers to their targets, a simple and novel method has been developed based on aptamer oligomerization. To this purpose, previously anti‐human TNF‐α aptamer named T1–T4 was trimerized through a trimethyl aconitate core for neutralization of in vitro and in vivo of TNF‐α. At first, 54 mer T1–T4 aptamers with 5′‐NH2 groups were covalently coupled to three ester residues in the trimethyl aconitate. In vitro activity of novel anti‐TNF‐α aptamer and its dissociation constant (Kd) was done using the L929 cell cytotoxicity assay. In vivo anti‐TNF‐α activity of new oligomerized aptamer was assessed in a mouse model of cutaneous Shwartzman. Anchoring of three T1–T4 aptamers to trimethyl aconitate substituent results in formation of the 162 mer fragment, which was well revealed by gel electrophoresis. In vitro study indicated that the trimerization of T1–T4 aptamer significantly improved its anti‐TNF‐α activity compared to non‐modified aptamers (P < 0.0001) from 40% to 60%. The determination of Kd showed that trimerization could effectively enhance Kd of aptamer from 67 nM to 36 nM. In vivo study showed that trimer aptamer markedly reduced mean scar size from 15.2 ± 1.2 mm to 1.6 ± 0.1 mm (P < 0.0001), which prevent the formation of skin lesions. In vitro and in vivo studies indicate that trimerization of anti‐TNF‐α aptamer with a novel approach could improve the anti‐TNF‐α activity and therapeutic efficacy. According to our findings, a new anti‐TNF‐α aptamer described here could be considered an appropriate therapeutic agent in treating several inflammatory diseases.
Difference in the airway luminal area between the standing and supine positions using upright and conventional computed tomography
Authors: Matsumoto Shunsuke , Yamada Yoshitake , Yamada Minoru , Chubachi Shotaro , Yokoyama Yoichi , Matsuoka Shiho , Tanabe Akiko , Niijima Yuki , Murata Mitsuru , Fukunaga Koichi , Jinzaki Masahiro 
Published: July 2021

AbstractNo clinical studies to date have compared the airway luminal area between supine and standing positions. Our aim was therefore to compare the airway luminal area between these two positions on computed tomography (CT) and to determine its correlation with forced expiratory volume in 1 s (FEV1). Thirty‐two asymptomatic volunteers underwent both conventional (supine position) and upright (standing position) CT during deep inspiration breath‐holding. Pulmonary function tests were conducted on the same day. We measured the airway luminal area on CT in each position. Paired t‐tests and Pearson's correlation coefficients were used for statistical analysis. The average luminal areas of the trachea, right and left main bronchi, and average third‐generation airway were greater in the standing than the supine position by 3.4%, 6.1%, 5.5%, and 5.2%, respectively. The correlation coefficients between airway luminal areas and FEV1 tended to be higher in the standing than the supine position; this correlation was highest for the average third‐generation airway (r = 0.70, P < 0.0001). The airway luminal areas of the trachea, bilateral main bronchi, and average third‐generation airway were greater in the standing than the supine position. The average third‐generation airway area in the standing position had the highest correlation with FEV1.
What's your name again? A review of the superior longitudinal and arcuate fasciculus evolving nomenclature
Authors: Porto de Oliveira João Vítor Miranda , Raquelo‐Menegassio Antônio Felipe , Maldonado Igor Lima 
Published: July 2021

AbstractStudies of the superior longitudinal fasciculus (SLF) have multiplied in recent decades owing to methodological advances, but the absence of a convention for nomenclature remains a source of confusion. Here, we have reviewed existing nomenclatures in the context of the research studies that generated them and we have identified their agreements and disagreements. A literature search was conducted using PubMed/MEDLINE, Web‐of‐Science, Embase, and a review of seminal publications, without restrictions regarding publication date. Our search revealed that diffusion imaging, autoradiography, and fiber dissection have been the main methods contributing to tract designation. The first two have been particularly influential in systematizing the horizontal elements distant from the lateral sulcus. Twelve approaches to naming were identified, eight of them differing considerably from each other. The terms SLF and arcuate fasciculus (AF) were often used as synonyms until the second half of the 20th century. During the last 15 years, this has ceased to be the case in a growing number of publications. The term AF has been used to refer to the assembly of three different segments, or exclusively to long frontotemporal fibers. Similarly, the term SLF has been employed to denote the whole superior longitudinal associative system, or only the horizontal frontoparietal parts. As only partial correspondence can be identified among the available nomenclatures, and in the absence of an official designation of all anatomical structures that can be encountered in clinical practice, a high level of vigilance regarding the effectiveness of every oral or written act of communication is mandatory.
Performance of glucoamylase self‐producing eBOOST™ GT yeast on ethanol production
Authors: Viswanathan Mothi Bharath , Bhatia Gitanshu , Jansen Mickel , Basu Rahul , Singh Vijay 
Published: July 2021

AbstractBackground and objectivesThis study demonstrates ethanol production using a new yeast strain called eBOOST™ GT, that can self‐produce glucoamylase and reduce glycerol production. The advanced yeast’s potential with added glucoamylase expression was investigated by observing and comparing its final ethanol and glycerol concentration against granular starch hydrolyzing enzyme (GSHE) catalyzed Ethanol Red fermentation.FindingsThe ethanol concentration in advanced yeast fermentation with self‐produced glucoamylase was measured at 10.03% v/v, which is 40% less than GSHE catalyzed Ethanol Red fermentation. However, upon externally providing additional glucoamylase (at 50% of the recommended dosage), eBOOST™ GT was able to produce similar ethanol concentration, compared to Ethanol Red fermentation catalyzed with GSHE enzyme. Furthermore, in this scenario, the glycerol concentration at the end of fermentation was 31% less than observed concentrations in operating with only self‐produced glucoamylase and 72% less than conventional GSHE fermentation.ConclusionsThe newly engineered yeast strain proves its capability to meet GSHE catalyzed ethanol yield at reduced enzyme consumption, and therefore, reduction in enzyme costs. The rate of substrate consumption and process economics are areas of future research for eBOOST™ GT ethanol fermentation.Significance and noveltyThis study provides important information on enzyme reduction and ethanol production, while using a self‐enzyme producing yeast.
FFNet: A simple image dedusting network with feature fusion
Authors: Huang Jiayan , Li Zuoyong , Wang Chuansheng , Yu Zhaochai , Cao Xinrong 
Published: July 2021

SummaryDust is a common air pollution source. The color of images captured under dusty weather is usually yellow even brown, which reduces scene visibility and causes the loss of image details. To remove the dust and make image scene clear, this article presents a simple and effective image dedusting network called FFNet. In the process of image feature extraction, the FFNet uses several residual blocks with smoothed dilated convolution, that is, common dilated convolution followed by separable and shared (SS) blockwise fully connected operation to extend the receptive field and reduce gridding artifacts caused by common dilated convolution. Furthermore, the FFNet fuses image features from different layers via an adaptive weighting scheme. Due to the difficulty of collecting real dusty images, we used our proposed dusty image synthesis scheme to achieve data augmentation for better network training. Experiments on a series of synthetic and real dusty images demonstrate that the FFNet obtains better image dedusting performance than several state‐of‐the‐art image restoration methods.
A computational model for investigating the evolution of colonic crypts during Lynch syndrome carcinogenesis
Authors: Haupt Saskia , Gleim Nils , Ahadova Aysel , Bläker Hendrik , von Knebel Doeberitz Magnus , Kloor Matthias , Heuveline Vincent 
Published: July 2021

AbstractLynch syndrome (LS), the most common inherited colorectal cancer (CRC) syndrome, increases the cancer risk in affected individuals. LS is caused by pathogenic germline variants in one of the DNA mismatch repair (MMR) genes, complete inactivation of which causes numerous mutations in affected cells. As CRC is believed to originate in colonic crypts, understanding the intra‐crypt dynamics caused by mutational processes is essential for a complete picture of LS CRC and may have significant implications for cancer prevention.We propose a computational model describing the evolution of colonic crypts during LS carcinogenesis. Extending existing modeling approaches for the non‐Lynch scenario, we incorporated MMR deficiency and implemented recent experimental data demonstrating that somaticCTNNB1mutations are common drivers of LS‐associated CRCs, if affecting both alleles of the gene. Further, we simulated the effect of different mutations on the entire crypt, distinguishing non‐transforming and transforming mutations.As an example, we analyzed the spread of mutations in the genesAPCandCTNNB1, which are frequently mutated in LS tumors, as well as of MMR deficiency itself. We quantified each mutation's potential for monoclonal conversion and investigated the influence of the cell location and of stem cell dynamics on mutation spread.Thein silicoexperiments underline the importance of stem cell dynamics for the overall crypt evolution. Further, simulating different mutational processes is essential in LS since mutations without survival advantages (the MMR deficiency‐inducing second hit) play a key role. The effect of other mutations can be simulated with the proposed model. Our results provide first mathematical clues towards more effective surveillance protocols for LS carriers.
Rebalancing TGF‐β/Smad7 signaling via Compound kushen injection in hepatic stellate cells protects against liver fibrosis and hepatocarcinogenesis
Authors: Yang Yang , Sun Mayu , Li Weida , Liu Chaobao , Jiang Zheshun , Gu Pengfei , Li Jingquan , Wang Wei , You Rongli , Ba Qian , Li Xiaoguang , Wang Hui 
Published: July 2021

AbstractBackgroundLiver fibrosis and fibrosis‐related hepatocarcinogenesis are a rising cause for morbidity and death worldwide. Although transforming growth factor‐β (TGF‐β) is a critical mediator of chronic liver fibrosis, targeting TGF‐β isoforms and receptors lead to unacceptable side effect. This study was designed to explore the antifibrotic effect of Compound kushen injection (CKI), an approved traditional Chinese medicine formula, via a therapeutic strategy of rebalancing TGF‐β/Smad7 signaling.MethodsA meta‐analysis was performed to evaluate CKI intervention on viral hepatitis‐induced fibrosis or cirrhosis in clinical randomized controlled trials (RCTs). Mice were given carbon tetrachloride (CCl4) injection or methionine‐choline deficient (MCD) diet to induce liver fibrosis, followed by CKI treatment. We examined the expression of TGF‐β/Smad signaling and typical fibrosis‐related genes in hepatic stellate cells (HSCs) and fibrotic liver tissues by qRT‐PCR, Western blotting, RNA‐seq, immunofluorescence, and immunohistochemistry.ResultsBased on meta‐analysis results, CKI improved the liver function and relieved liver fibrosis among patients. In our preclinical studies by using two mouse models, CKI treatment demonstrated promising antifibrotic effects and postponed hepatocarcinogenesis with improved liver function and histopathologic features. Mechanistically, we found that CKI inhibited HSCs activation by stabilizing the interaction of Smad7/TGF‐βR1 to rebalance Smad2/Smad3 signaling, and subsequently decreased the extracellular matrix formation. Importantly, Smad7 depletion abolished the antifibrotic effect of CKI in vivo and in vitro. Moreover, matrine, oxymatrine, sophocarpine, and oxysophocarpine were identified as material basis responsible for the antifibrosis effect of CKI.ConclusionsOur results unveil the approach of CKI in rebalancing TGF‐β/Smad7 signaling in HSCs to protect against hepatic fibrosis and hepatocarcinogenesis in both preclinical and clinical studies. Our study suggests that CKI can be a candidate for treatment of hepatic fibrosis and related oncogenesis.
Fcγ receptor activation mediates vascular inflammation and abdominal aortic aneurysm development
Authors: Lopez‐Sanz Laura , Bernal Susana , Jimenez‐Castilla Luna , Prieto Ignacio , La Manna Sara , Gomez‐Lopez Sergio , Blanco‐Colio Luis Miguel , Egido Jesus , Martin‐Ventura Jose Luis , Gomez‐Guerrero Carmen 
Published: July 2021

AbstractBackgroundAbdominal aortic aneurysm (AAA), a degenerative vascular pathology characterized by permanent dilation of the aorta, is considered a chronic inflammatory disease involving innate/adaptive immunity. However, the functional role of antibody‐dependent immune response against antigens present in the damaged vessel remains unresolved. We hypothesized that engagement of immunoglobulin G (IgG) Fc receptors (FcγR) by immune complexes (IC) in the aortic wall contributes to AAA development. We therefore evaluated FcγR expression in AAA lesions and analysed whether inhibition of FcγR signaling molecules (γ‐chain and Syk kinase) influences AAA formation in mice.MethodsFcγR gene/protein expression was assessed in human and mouse AAA tissues. Experimental AAA was induced by aortic elastase perfusion in wild‐type (WT) mice and γ‐chain knockout (γKO) mice (devoid of activating FcγR) in combination with macrophage adoptive transfer or Syk inhibitor treatment. To verify the mechanisms of FcγR in vitro, vascular smooth muscle cells (VSMC) and macrophages were stimulated with IgG IC.ResultsFcγR overexpression was detected in adventitia and media layers of human and mouse AAA. Elastase‐perfused γKO mice exhibited a decrease in AAA incidence, aortic dilation, elastin degradation, and VSMC loss. This was associated with (1) reduced infiltrating leukocytes and immune deposits in AAA lesions, (2) inflammatory genes and metalloproteinases downregulation, (3) redox balance restoration, and (4) converse phenotype of anti‐inflammatory macrophage M2 and contractile VSMC. Adoptive transfer of FcγR‐expressing macrophages aggravated aneurysm in γKO mice. In vitro, FcγR deficiency attenuated inflammatory gene expression, oxidative stress, and phenotypic switch triggered by IC. Additionally, Syk inhibition prevented IC‐mediated cell responses, reduced inflammation, and mitigated AAA formation.ConclusionOur findings provide insight into the role and mechanisms mediating IgG‐FcγR‐associated inflammation and aortic wall injury in AAA, which might represent therapeutic targets against AAA disease.
CB1R and iNOS are distinct players promoting pulmonary fibrosis in Hermansky–Pudlak syndrome
Authors: Cinar Resat , Park Joshua K. , Zawatsky Charles N. , Coffey Nathan J. , Bodine Steven P. , Abdalla Jasmina , Yokoyama Tadafumi , Jourdan Tony , Jay Lindsey , Zuo Mei Xing G. , O'Brien Kevin J. , Huang Junfeng , Mackie Ken , Alimardanov Asaf , Iyer Malliga R. , Gahl William A. , Kunos George , Gochuico Bernadette R. , Malicdan May Christine V. 
Published: July 2021

AbstractHermansky–Pudlak syndrome (HPS) is a rare genetic disorder which, in its most common and severe form, HPS‐1, leads to fatal adult‐onset pulmonary fibrosis (PF) with no effective treatment. We evaluated the role of the endocannabinoid/CB1R system and inducible nitric oxide synthase (iNOS) for dual‐target therapeutic strategy using human bronchoalveolar lavage fluid (BALF), lung samples from patients with HPS and controls, HPS‐PF patient‐derived lung fibroblasts, and bleomycin‐induced PF in pale ear mice (HPS1ep/ep). We found overexpression of CB1R and iNOS in fibrotic lungs of HPSPF patients and bleomycin‐infused pale ear mice. The endocannabinoid anandamide was elevated in BALF and negatively correlated with pulmonary function parameters in HPSPF patients and pale ear mice with bleomycin‐induced PF. Simultaneous targeting of CB1R and iNOS by MRI‐1867 yielded greater antifibrotic efficacy than inhibiting either target alone by attenuating critical pathologic pathways. Moreover, MRI‐1867 treatment abrogated bleomycin‐induced increases in lung levels of the profibrotic interleukin‐11 via iNOS inhibition and reversed mitochondrial dysfunction via CB1R inhibition. Dual inhibition of CB1R and iNOS is an effective antifibrotic strategy for HPSPF.