bluuebunny/crossref_metadata_2025_split huggingface dataset:
Telemedicine for Potential Application in Austere Military Environments: Neurosurgical Support for a Decompressive Craniectomy
Authors: Stark Pieter W , van Waes O J F , Soria van Hoeve John S , Borger van der Burg Boudewijn L S , Hoencamp Rigo 
Published: March 2024

ABSTRACT

Introduction
The main goal of this study was to assess the feasibility of a head-mounted display (HMD) providing telemedicine neurosurgical support during a decompressive craniectomy by a military surgeon who is isolated from readily available neurosurgical care. The secondary aim was to assess the usability perceived by the military surgeon and to evaluate technical aspects of the head-mounted display.

Materials and Methods
After a standard concise lecture, 10 military surgeons performed a decompressive craniectomy on a AnubiFiX-embalmed post-mortem human head. Seven military surgeons used a HMD to receive telemedicine neurosurgical support. In the control group, three military surgeons performed a decompressive craniectomy without guidance. The performance of the decompressive craniectomy was evaluated qualitatively by the supervising neurosurgeon and quantified with the surgeons’ operative performance tool. The military surgeons rated the usability of the HMD with the telehealth usability questionnaire.

Results
All military surgeons performed a decompressive craniectomy adequately directly after a standard concise lecture. The HMD was used to discuss potential errors and reconfirmed essential steps. The military surgeons were very satisfied with the HMD providing telemedicine neurosurgical support. Military surgeons in the control group were faster. The HMD showed no hard technical errors.

Conclusions
It is feasible to provide telemedicine neurosurgical support with a HMD during a decompressive craniectomy performed by a non-neurosurgically trained military surgeon. All military surgeons showed competence in performing a decompressive craniectomy after receiving a standardized concise lecture. The use of a HMD clearly demonstrated the potential to improve the quality of these neurosurgical procedures performed by military surgeons.
Transcription factor FveMYB117a inhibits axillary bud outgrowth by regulating cytokinin homeostasis in woodland strawberry
Authors: Han Yafan , Qu Minghao , Liu Zhongchi , Kang Chunying 
Published: March 2024

Abstract
Shoot branching affects plant architecture. In strawberry (Fragaria L.), short branches (crowns) develop from dormant axillary buds to form inflorescences and flowers. While this developmental transition contributes greatly to perenniality and yield in strawberry, its regulatory mechanism remains unclear and understudied. In the woodland strawberry (Fragaria vesca), we identified and characterized 2 independent mutants showing more crowns. Both mutant alleles reside in FveMYB117a, a R2R3-MYB transcription factor gene highly expressed in shoot apical meristems, axillary buds, and young leaves. Transcriptome analysis revealed that the expression of several cytokinin pathway genes was altered in the fvemyb117a mutant. Consistently, active cytokinins were significantly increased in the axillary buds of the fvemyb117a mutant. Exogenous application of cytokinin enhanced crown outgrowth in the wild type, whereas the cytokinin inhibitors suppressed crown outgrowth in the fvemyb117a mutant. FveMYB117a binds directly to the promoters of the cytokinin homeostasis genes FveIPT2 encoding an isopentenyltransferase and FveCKX1 encoding a cytokinin oxidase to regulate their expression. Conversely, the type-B Arabidopsis response regulators FveARR1 and FveARR2b can directly inhibit the expression of FveMYB117a, indicative of a negative feedback regulation. In conclusion, we identified FveMYB117a as a key repressor of crown outgrowth by inhibiting cytokinin accumulation and provide a mechanistic basis for bud fate transition in an herbaceous perennial plant.
Methyltransferase TaSAMT1 mediates wheat freezing tolerance by integrating brassinosteroid and salicylic acid signaling
Authors: Chu Wei , Chang Shumin , Lin Jingchen , Zhang Chenji , Li Jinpeng , Liu Xingbei , Liu Zehui , Liu Debiao , Yang Qun , Zhao Danyang , Liu Xiaoyu , Guo Weilong , Xin Mingming , Yao Yingyin , Peng Huiru , Xie Chaojie , Ni Zhongfu , Sun Qixin , Hu Zhaorong 
Published: March 2024

Abstract
Cold injury is a major environmental stress affecting the growth and yield of crops. Brassinosteroids (BRs) and salicylic acid (SA) play important roles in plant cold tolerance. However, whether or how BR signaling interacts with the SA signaling pathway in response to cold stress is still unknown. Here, we identified an SA methyltransferase, TaSAMT1 that converts SA to methyl SA (MeSA) and confers freezing tolerance in wheat (Triticum aestivum). TaSAMT1 overexpression greatly enhanced wheat freezing tolerance, with plants accumulating more MeSA and less SA, whereas Tasamt1 knockout lines were sensitive to freezing stress and accumulated less MeSA and more SA. Spraying plants with MeSA conferred freezing tolerance to Tasamt1 mutants, but SA did not. We revealed that BRASSINAZOLE-RESISTANT 1 (TaBZR1) directly binds to the TaSAMT1 promoter and induces its transcription. Moreover, TaBZR1 interacts with the histone acetyltransferase TaHAG1, which potentiates TaSAMT1 expression via increased histone acetylation and modulates the SA pathway during freezing stress. Additionally, overexpression of TaBZR1 or TaHAG1 altered TaSAMT1 expression and improved freezing tolerance. Our results demonstrate a key regulatory node that connects the BR and SA pathways in the plant cold stress response. The regulatory factors or genes identified could be effective targets for the genetic improvement of freezing tolerance in crops.
Auxin resistant 2 and short hypocotyl 2 regulate cotton fiber initiation and elongation
Authors: Jin Fei , Zhu Liping , Hou Liyong , Li Hongbin , Li Ling , Xiao Guanghui 
Published: March 2024

Abstract
Auxin, a pivotal regulator of diverse plant growth processes, remains central to development. The auxin-responsive genes auxin/indole-3-acetic acids (AUX/IAAs) are indispensable for auxin signal transduction, which is achieved through intricate interactions with auxin response factors (ARFs). Despite this, the potential of AUX/IAAs to govern the development of the most fundamental biological unit, the single cell, remains unclear. In this study, we harnessed cotton (Gossypium hirsutum) fiber, a classic model for plant single-cell investigation, to determine the complexities of AUX/IAAs. Our research identified 2 pivotal AUX/IAAs, auxin resistant 2 (GhAXR2) and short hypocotyl 2 (GhSHY2), which exhibit opposite control over fiber development. Notably, suppressing GhAXR2 reduced fiber elongation, while silencing GhSHY2 fostered enhanced fiber elongation. Investigating the mechanistic intricacies, we identified specific interactions between GhAXR2 and GhSHY2 with distinct ARFs. GhAXR2's interaction with GhARF6-1 and GhARF23-2 promoted fiber cell development through direct binding to the AuxRE cis-element in the constitutive triple response 1 promoter, resulting in transcriptional inhibition. In contrast, the interaction of GhSHY2 with GhARF7-1 and GhARF19-1 exerted a negative regulatory effect, inhibiting fiber cell growth by activating the transcription of xyloglucan endotransglucosylase/hydrolase 9 and cinnamate-4-hydroxylase. Thus, our study reveals the intricate regulatory networks surrounding GhAXR2 and GhSHY2, elucidating the complex interplay of multiple ARFs in AUX/IAA-mediated fiber cell growth. This work enhances our understanding of single-cell development and has potential implications for advancing plant growth strategies and agricultural enhancements.
Macrophages suppress cardiac reprogramming of fibroblasts in vivo via IFN-mediated intercellular self-stimulating circuit
Authors: Wang Hao , Yang Junbo , Cai Yihong , Zhao Yang 
Published: March 2024

Abstract
Direct conversion of cardiac fibroblasts (CFs) to cardiomyocytes (CMs) in vivo to regenerate heart tissue is an attractive approach. After myocardial infarction (MI), heart repair proceeds with an inflammation stage initiated by monocytes infiltration of the infarct zone establishing an immune microenvironment. However, whether and how the MI microenvironment influences the reprogramming of CFs remains unclear. Here, we found that in comparison with cardiac fibroblasts (CFs) cultured in vitro, CFs that transplanted into infarct region of MI mouse models resisted to cardiac reprogramming. RNA-seq analysis revealed upregulation of interferon (IFN) response genes in transplanted CFs, and subsequent inhibition of the IFN receptors increased reprogramming efficiency in vivo. Macrophage-secreted IFN-β was identified as the dominant upstream signaling factor after MI. CFs treated with macrophage-conditioned medium containing IFN-β displayed reduced reprogramming efficiency, while macrophage depletion or blocking the IFN signaling pathway after MI increased reprogramming efficiency in vivo. Co-IP, BiFC and Cut-tag assays showed that phosphorylated STAT1 downstream of IFN signaling in CFs could interact with the reprogramming factor GATA4 and inhibit the GATA4 chromatin occupancy in cardiac genes. Furthermore, upregulation of IFN-IFNAR-p-STAT1 signaling could stimulate CFs secretion of CCL2/7/12 chemokines, subsequently recruiting IFN-β-secreting macrophages. Together, these immune cells further activate STAT1 phosphorylation, enhancing CCL2/7/12 secretion and immune cell recruitment, ultimately forming a self-reinforcing positive feedback loop between CFs and macrophages via IFN-IFNAR-p-STAT1 that inhibits cardiac reprogramming in vivo. Cumulatively, our findings uncover an intercellular self-stimulating inflammatory circuit as a microenvironmental molecular barrier of in situ cardiac reprogramming that needs to be overcome for regenerative medicine applications.
A whale of a tale: whale cells evade the driving mechanism for hexavalent chromium-induced chromosome instability
Authors: Lu Haiyan , Toyoda Jennifer H , Wise Sandra S , Browning Cynthia L , Speer Rachel M , Croom-Pérez Tayler J , Bolt Alicia , Meaza Idoia , Wise John Pierce 
Published: March 2024

Abstract
Chromosome instability, a hallmark of lung cancer, is a driving mechanism for hexavalent chromium [Cr(VI)] carcinogenesis in humans. Cr(VI) induces structural and numerical chromosome instability in human lung cells by inducing DNA double-strand breaks and inhibiting homologous recombination repair and causing spindle assembly checkpoint (SAC) bypass and centrosome amplification. Great whales are long-lived species with long-term exposures to Cr(VI) and accumulate Cr in their tissue, but exhibit a low incidence of cancer. Data show Cr(VI) induces fewer chromosome aberrations in whale cells after acute Cr(VI) exposure suggesting whale cells can evade Cr(VI)-induced chromosome instability. However, it is unknown if whales can evade Cr(VI)-induced chromosome instability. Thus, we tested the hypothesis that whale cells resist Cr(VI)-induced loss of homologous recombination repair activity and increased SAC bypass and centrosome amplification. We found Cr(VI) induces similar amounts of DNA double-strand breaks after acute (24 h) and prolonged (120 h) exposures in whale lung cells, but does not inhibit homologous recombination repair, SAC bypass, or centrosome amplification, and does not induce chromosome instability. These data indicate whale lung cells resist Cr(VI)-induced chromosome instability, the major driver for Cr(VI) carcinogenesis at a cellular level, consistent with observations that whales are resistant to cancer.
Emissions from plastic incineration induce inflammation, oxidative stress, and impaired bioenergetics in primary human respiratory epithelial cells
Authors: Rogers Keith , WaMaina Elisa , Barber Andrew , Masood Syed , Love Charlotte , Kim Yong Ho , Gilmour M Ian , Jaspers Ilona 
Published: March 2024

AbstractInhalation exposure to plastic incineration emissions (PIEs) is a problem of increasing human relevance, as plastic production and waste creation have drastically increased since mainstream integration during the 20th century. We investigated the effects of PIEs on human nasal epithelial cells (HNECs) to understand if such exposures cause damage and dysfunction to respiratory epithelia. Primary HNECs from male and female donors were cultured at air–liquid interface (ALI), and 16HBE cells were cultured on coverslips. Smoke condensates were generated from incineration of plastic at flaming (640°C) and smoldering (500°C) temperatures, and cells were subsequently exposed to these materials at 5–50 μg/cm2 concentrations. HNECs were assessed for mitochondrial dysfunction and 16HBE cells for glutathione oxidation in real-time analyses. HNEC culture supernatants and total RNA were collected at 4-h postexposure for cytokine and gene expression analysis, and results show that PIEs can acutely induce inflammation, oxidative stress, and mitochondrial dysfunction in HNECs, and that incineration temperature modifies biological responses. Specifically, condensates from flaming and smoldering PIEs significantly increased HNEC secretion of cytokines IL-8, IL-1β, and IL-13, as well as expression of xenobiotic metabolism pathways and genes such as CYP1A1 and CYP1B1 at 5 and 20 μg/cm2 concentrations. Only 50 μg/cm2 flaming PIEs significantly increased glutathione oxidation in 16HBEs, and decreased respiration and ATP production in HNEC mitochondria. Impact Statement: Our data reveal the impact of incineration temperatures on biological outcomes associated with PIE exposures, emphasizing the importance of temperature as a factor when evaluating respiratory disease associated with PIEs exposure.
Repeated exposure to eucalyptus wood smoke alters pulmonary gene and metabolic profiles in male Long-Evans rats
Authors: Cochran Samuel J , Dunigan-Russell Katelyn , Hutton Grace M , Nguyen Helen , Schladweiler Mette C , Jones Dean P , Williams Wanda C , Fisher Anna A , Gilmour M Ian , Dye Janice A , Smith M Ryan , Miller Colette N , Gowdy Kymberly M 
Published: March 2024

AbstractExposure to wildfire smoke is associated with both acute and chronic cardiopulmonary illnesses, which are of special concern for wildland firefighters who experience repeated exposure to wood smoke. It is necessary to better understand the underlying pathophysiology by which wood smoke exposure increases pulmonary disease burdens in this population. We hypothesize that wood smoke exposure produces pulmonary dysfunction, lung inflammation, and gene expression profiles associated with future pulmonary complications. Male Long-Evans rats were intermittently exposed to smoldering eucalyptus wood smoke at 2 concentrations, low (11.0 ± 1.89 mg/m3) and high (23.7 ± 0.077 mg/m3), over a 2-week period. Whole-body plethysmography was measured intermittently throughout. Lung tissue and lavage fluid were collected 24 h after the final exposure for transcriptomics and metabolomics. Increasing smoke exposure upregulated neutrophils and select cytokines in the bronchoalveolar lavage fluid. In total, 3446 genes were differentially expressed in the lungs of rats in the high smoke exposure and only 1 gene in the low smoke exposure (Cd151). Genes altered in the high smoke group reflected changes to the Eukaryotic Initiation Factor 2 stress and oxidative stress responses, which mirrored metabolomics analyses. xMWAS-integrated analysis revealed that smoke exposure significantly altered pathways associated with oxidative stress, lung morphogenesis, and tumor proliferation pathways. These results indicate that intermittent, 2-week exposure to eucalyptus wood smoke leads to transcriptomic and metabolic changes in the lung that may predict future lung disease development. Collectively, these findings provide insight into cellular signaling pathways that may contribute to the chronic pulmonary conditions observed in wildland firefighters.
Towards enhanced control of mycetoma: a roadmap to achieve the UN's sustainable development goals by 2030
Authors: Fahal Ahmed , Smith Dallas J , Nyaoke Borna , Asiedu Kingsley , Falves Fabiana , Warusavithanas Supriya , Argaw Daniel , Hay Roderick 
Published: March 2024

Abstract
Mycetoma is a neglected tropical disease (NTD) with devastating morbidity and stigma. Despite increased awareness and international collaboration, the burden of mycetoma is largely unknown and diagnosis and treatment are difficult. Addressing mycetoma globally aligns with several United Nation's Sustainable Development Goals (SDGs). Little progress has been made since the WHO’s NTD roadmap publication in 2020. The Global Mycetoma Working Group proposes an enhanced mycetoma-control roadmap to meet the SDGs, stimulate progress and improve the lives of patients experiencing mycetoma. By aligning mycetoma management with the goals and targets of this enhanced roadmap, it becomes possible to leverage existing resources, infrastructure and partnerships to improve the lives of affected individuals and communities. This updated assessment is designed for the benefit of health workers and providers in mycetoma-endemic areas, NTD government officials, civil society and funding and implementing agencies.
A New ToxA Haplotype in the Wheat Fungal Pathogen Bipolaris sorokiniana
Authors: See Pao Theen , Iagallo Elyce M. , Marathamuthu Kalai A. , Wood Blake , Aboukhaddour Reem , Moffat Caroline S. 
Published: March 2024

The necrotrophic effector ToxA is a well-studied virulence factor produced by several fungal necrotrophs. Initially cloned from the wheat tan spot pathogen Pyrenophora tritici-repentis in 1996, ToxA was found almost a decade later in another fungal pathogen, Parastagonospora nodorum, and its sister species, Parastagonospora pseudonodorum. In 2018, ToxA was detected in a third wheat fungal pathogenic species, Bipolaris sorokiniana, which causes spot blotch disease. However, unlike the case with P. tritici-repentis and P. nodorum, the ToxA in B. sorokiniana has only been investigated in recent years. In this report, five Australian B. sorokiniana isolates were assessed for the presence of ToxA. Four isolates were found to contain ToxA. While one isolate harbored the previously reported ToxA haplotype sequence ( ToxA19), three isolates contain a different haplotype, designated herein as ToxA25, which has a nonsynonymous mutation resulting in an amino acid change of glycine to arginine at position 168. Both B. sorokiniana ToxA isoforms, when heterologously expressed in Escherichia coli, exhibited the classic ToxA necrosis-inducing activity on ToxA-sensitive Tsn1 cultivars. Preliminary analysis of the B. sorokiniana isolates in Australian wheat cultivars showed that isolates with ToxA19, ToxA25, or ToxA-deficient displayed various degrees of virulence, with the most aggressive isolates observed for those producing ToxA. Differences in spot blotch disease severity between Tsn1 and tsn1 cultivars were observed; however, this was not limited to the ToxA-producing isolates. The overall results suggest that the virulence of the Australian B. sorokiniana isolates is diverse, with the significance of ToxA− Tsn1 interactions depending on individual isolates. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .
Robotic Assistance in Percutaneous Liver Ablation Therapies: A Systematic Review and Meta-Analysis
Authors: Uribe Rivera Ana K. , Seeliger Barbara , Goffin Laurent , García-Vázquez Alain , Mutter Didier , Giménez Mariano E. 
Published: March 2024

Objective:
The aim of this systematic review and meta-analysis is to identify current robotic assistance systems for percutaneous liver ablations, compare approaches, and determine how to achieve standardization of procedural concepts for optimized ablation outcomes.

Background:
Image-guided surgical approaches are increasingly common. Assistance by navigation and robotic systems allows to optimize procedural accuracy, with the aim to consistently obtain adequate ablation volumes.

Methods:
Several databases (PubMed/MEDLINE, ProQuest, Science Direct, Research Rabbit, and IEEE Xplore) were systematically searched for robotic preclinical and clinical percutaneous liver ablation studies, and relevant original manuscripts were included according to the Preferred Reporting items for Systematic Reviews and Meta-Analyses guidelines. The endpoints were the type of device, insertion technique (freehand or robotic), planning, execution, and confirmation of the procedure. A meta-analysis was performed, including comparative studies of freehand and robotic techniques in terms of radiation dose, accuracy, and Euclidean error.

Results:
The inclusion criteria were met by 33/755 studies. There were 24 robotic devices reported for percutaneous liver surgery. The most used were the MAXIO robot (8/33; 24.2%), Zerobot, and AcuBot (each 2/33, 6.1%). The most common tracking system was optical (25/33, 75.8%). In the meta-analysis, the robotic approach was superior to the freehand technique in terms of individual radiation (0.5582, 95% confidence interval [CI] = 0.0167–1.0996, dose-length product range 79–2216 mGy.cm), accuracy (0.6260, 95% CI = 0.1423–1.1097), and Euclidean error (0.8189, 95% CI = –0.1020 to 1.7399).

Conclusions:
Robotic assistance in percutaneous ablation for liver tumors achieves superior results and reduces errors compared with manual applicator insertion. Standardization of concepts and reporting is necessary and suggested to facilitate the comparison of the different parameters used to measure liver ablation results. The increasing use of image-guided surgery has encouraged robotic assistance for percutaneous liver ablations. This systematic review analyzed 33 studies and identified 24 robotic devices, with optical tracking prevailing. The meta-analysis favored robotic assessment, showing increased accuracy and reduced errors compared with freehand technique, emphasizing the need for conceptual standardization.
Borderline Case in Reconstructive Plastic Surgery of the Lower Limb Treated with Bone Drilling and Use of Dermal Regeneration Template
Authors: Verdura Vincenzo , Cagiano Luigi , Molle Marcello , Bisceglia Pasquale , Fini Nicola , Annacontini Luigi , Mazzarella Vincenzo , Parisi Domenico , Portincasa Aurelio 
Published: March 2024

Summary:
The traumatic pathology of the lower limb represents a very complex branch of medicine, which, despite the wide presence of guidelines, aimed at regulating the various therapeutic procedures, and is still greatly influenced by random variables and by the multiple responses to treatments. In this report, we present our experience with a borderline case, where the timing of the trauma and the patient’s characteristics made it difficult to use the most recommended procedures in trauma management.