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Article ; Online: A mathematical model of biofilm growth and spread within plant xylem: Case study of Xylella fastidiosa in olive trees.

Walker, N C / White, S M / Ruiz, S A / McKay Fletcher, D / Saponari, M / Roose, T

2024 Volume 581, Page(s) 111737

Abstract: Xylem-limited bacterial pathogens cause some of the most destructive plant diseases. Though imposed measures to control these pathogens are generally ineffective, even among susceptible taxa, some hosts can limit bacterial loads and symptom expression. ... ...

Abstract	Xylem-limited bacterial pathogens cause some of the most destructive plant diseases. Though imposed measures to control these pathogens are generally ineffective, even among susceptible taxa, some hosts can limit bacterial loads and symptom expression. Mechanisms by which this resistance is achieved are poorly understood. In particular, it is still unknown how differences in vascular structure may influence biofilm growth and spread within a host. To address this, we developed a novel theoretical framework to describe biofilm behaviour within xylem vessels, adopting a polymer-based modelling approach. We then parameterised the model to investigate the relevance of xylem vessel diameters on Xylella fastidiosa resistance among olive cultivars. The functionality of all vessels was severely reduced under infection, with hydraulic flow reductions of 2-3 orders of magnitude. However, results suggest wider vessels act as biofilm incubators; allowing biofilms to develop over a long time while still transporting them through the vasculature. By contrast, thinner vessels become blocked much earlier, limiting biofilm spread. Using experimental data on vessel diameter distributions, we were able to determine that a mechanism of resistance in the olive cultivar Leccino is a relatively low abundance of the widest vessels, limiting X. fastidiosa spread.
MeSH term(s)	Olea/metabolism ; Olea/microbiology ; Xylella ; Biofilms ; Xylem ; Plant Diseases/microbiology ; Models, Theoretical
Language	English
Publishing date	2024-01-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2972-5
ISSN	1095-8541 ; 0022-5193
ISSN (online)	1095-8541
ISSN	0022-5193
DOI	10.1016/j.jtbi.2024.111737
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Article ; Online: Integrated Feedforward and Feedback Mechanisms in Neurovascular Coupling.

Meng, Lingzhong / Rasmussen, Mads / Meng, Deyi M / White, Fletcher A / Wu, Long-Jun

Anesthesia and analgesia

2024

Abstract: Neurovascular coupling (NVC) is the mechanism that drives the neurovascular response to neural activation, and NVC dysfunction has been implicated in various neurologic diseases. NVC is driven by (1) nonmetabolic feedforward mechanisms that are mediated ... ...

Abstract	Neurovascular coupling (NVC) is the mechanism that drives the neurovascular response to neural activation, and NVC dysfunction has been implicated in various neurologic diseases. NVC is driven by (1) nonmetabolic feedforward mechanisms that are mediated by various signaling pathways and (2) metabolic feedback mechanisms that involve metabolic factors. However, the interplay between these feedback and feedforward mechanisms remains unresolved. We propose that feedforward mechanisms normally drive a swift, neural activation-induced regional cerebral blood flow (rCBF) overshoot, which floods the tissue beds, leading to local hypocapnia and hyperoxia. The feedback mechanisms are triggered by the resultant hypocapnia (not hyperoxia), which causes cerebral vasoconstriction in the neurovascular unit that counterbalances the rCBF overshoot and returns rCBF to a level that matches the metabolic activity. If feedforward mechanisms function improperly (eg, in a disease state), the rCBF overshoot, tissue-bed flooding, and local hypocapnia fail to occur or occur on a smaller scale. Consequently, the neural activation-related increase in metabolic activity results in local hypercapnia and hypoxia, both of which drive cerebral vasodilation and increase rCBF. Thus, feedback mechanisms ensure the brain milieu's stability when feedforward mechanisms are impaired. Our proposal integrates the feedforward and feedback mechanisms underlying NVC and suggests that these 2 mechanisms work like a fail-safe system, to a certain degree. We also discussed the difference between NVC and cerebral metabolic rate-CBF coupling and the clinical implications of our proposed framework.
Language	English
Publishing date	2024-02-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	80032-6
ISSN	1526-7598 ; 0003-2999
ISSN (online)	1526-7598
ISSN	0003-2999
DOI	10.1213/ANE.0000000000006891
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Article ; Online: No pain, no gain: Will migraine therapies increase bone loss and impair fracture healing?

Kacena, Melissa A / White, Fletcher A

EBioMedicine

2020 Volume 60, Page(s) 103025

MeSH term(s)	Animals ; Bone Resorption/complications ; Bone Resorption/etiology ; Calcitonin Gene-Related Peptide Receptor Antagonists/adverse effects ; Calcitonin Gene-Related Peptide Receptor Antagonists/therapeutic use ; Fracture Healing/genetics ; Humans ; Migraine Disorders/complications ; Migraine Disorders/drug therapy ; Migraine Disorders/etiology ; Receptors, Calcitonin Gene-Related Peptide/genetics ; Receptors, Calcitonin Gene-Related Peptide/metabolism ; Risk Assessment
Chemical Substances	Calcitonin Gene-Related Peptide Receptor Antagonists ; Receptors, Calcitonin Gene-Related Peptide
Language	English
Publishing date	2020-09-22
Publishing country	Netherlands
Document type	Letter
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2020.103025
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Article: What Did We Learn About Fracture Pain from Animal Models?

Radulescu, Andreea / White, Fletcher A / Chenu, Chantal

Journal of pain research

2022 Volume 15, Page(s) 2845–2856

Abstract: Progress in bone fracture repair research has been made possible due to the development of reproducible models of fracture in rodents with more clinically relevant fracture fixation, where there is considerably better assessment of the factors that ... ...

Abstract	Progress in bone fracture repair research has been made possible due to the development of reproducible models of fracture in rodents with more clinically relevant fracture fixation, where there is considerably better assessment of the factors that affect fracture healing and/or novel therapeutics. However, chronic or persistent pain is one of the worst, longest-lasting and most difficult symptoms to manage after fracture repair, and an ongoing challenge remains for animal welfare as limited information exists regarding pain scoring and management in these rodent fracture models. This failure of adequate pre-clinical pain assessment following osteotomy in the rodent population may not only subject the animal to severe pain states but may also affect the outcome of the bone healing study. Animal models to study pain were also mainly developed in rodents, and there is increasing validation of fracture and pain models to quantitatively evaluate fracture pain and to study the factors that generate and maintain fracture pain and develop new therapies for treating fracture pain. This review aims to discuss the different animal models for fracture pain research and characterize what can be learned from using animal models of fracture regarding behavioral pain states and new molecular targets for future management of these behaviors.
Language	English
Publishing date	2022-09-13
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2495284-9
ISSN	1178-7090
ISSN	1178-7090
DOI	10.2147/JPR.S361826
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Article ; Online: Do Not Lose Your Nerve, Be Callus: Insights Into Neural Regulation of Fracture Healing.

Nazzal, Murad K / Morris, Ashlyn J / Parker, Reginald S / White, Fletcher A / Natoli, Roman M / Kacena, Melissa A / Fehrenbacher, Jill C

Current osteoporosis reports

2024 Volume 22, Issue 1, Page(s) 182–192

Abstract: Purpose of review: Fractures are a prominent form of traumatic injury and shall continue to be for the foreseeable future. While the inflammatory response and the cells of the bone marrow microenvironment play significant roles in fracture healing, the ... ...

Abstract	Purpose of review: Fractures are a prominent form of traumatic injury and shall continue to be for the foreseeable future. While the inflammatory response and the cells of the bone marrow microenvironment play significant roles in fracture healing, the nervous system is also an important player in regulating bone healing. Recent findings: Considerable evidence demonstrates a role for nervous system regulation of fracture healing in a setting of traumatic injury to the brain. Although many of the impacts of the nervous system on fracture healing are positive, pain mediated by the nervous system can have detrimental effects on mobilization and quality of life. Understanding the role the nervous system plays in fracture healing is vital to understanding fracture healing as a whole and improving quality of life post-injury. This review article is part of a series of multiple manuscripts designed to determine the utility of using artificial intelligence for writing scientific reviews.
MeSH term(s)	Humans ; Fracture Healing/physiology ; Artificial Intelligence ; Quality of Life ; Bony Callus ; Fractures, Bone
Language	English
Publishing date	2024-01-31
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-023-00850-2
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Article ; Online: Racial Differences in Head Pain and Other Pain-Related Outcomes After Mild Traumatic Brain Injury.

Naugle, Kelly M / Nguyen, Tyler / Smith, Jared A / Saxe, Jonathan / White, Fletcher A

Journal of neurotrauma

2023 Volume 40, Issue 15-16, Page(s) 1671–1683

Abstract: Recent research suggests that mild traumatic brain injury (TBI) may exert deleterious effects on endogenous pain modulatory function, potentially underlying the elevated risk for persistent headaches following injury. Accumulating research also shows ... ...

Abstract	Recent research suggests that mild traumatic brain injury (TBI) may exert deleterious effects on endogenous pain modulatory function, potentially underlying the elevated risk for persistent headaches following injury. Accumulating research also shows race differences in clinical and experimental pain, with African Americans (AA) generally reporting more severe pain, worse pain modulation, and greater pain sensitivity compared with Caucasians. However, race differences in pain-related outcomes following mild TBI have rarely been studied. The purpose of this study was to explore race differences in endogenous pain modulation, pain sensitivity, headache pain, and psychological factors among AA and Caucasian individuals with mild TBI in the first month following injury compared with healthy controls and across time. Patients with mild TBI were recruited from local emergency department trauma centers. Sixty-three participants with mild TBI (AAs:
MeSH term(s)	Humans ; Brain Concussion/complications ; Race Factors ; Headache ; Pain ; Brain Injuries, Traumatic/complications
Language	English
Publishing date	2023-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2022.0415
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Article ; Online: Using AI to Write a Review Article Examining the Role of the Nervous System on Skeletal Homeostasis and Fracture Healing.

Nazzal, Murad K / Morris, Ashlyn J / Parker, Reginald S / White, Fletcher A / Natoli, Roman M / Fehrenbacher, Jill C / Kacena, Melissa A

Current osteoporosis reports

2024 Volume 22, Issue 1, Page(s) 217–221

Abstract: Purpose of review: Three review articles have been written that discuss the roles of the central and peripheral nervous systems in fracture healing. While content among the articles is overlapping, there is a key difference between them: the use of ... ...

Abstract	Purpose of review: Three review articles have been written that discuss the roles of the central and peripheral nervous systems in fracture healing. While content among the articles is overlapping, there is a key difference between them: the use of artificial intelligence (AI). In one paper, the first draft was written solely by humans. In the second paper, the first draft was written solely by AI using ChatGPT 4.0 (AI-only or AIO). In the third paper, the first draft was written using ChatGPT 4.0 but the literature references were supplied from the human-written paper (AI-assisted or AIA). This project was done to evaluate the capacity of AI to conduct scientific writing. Importantly, all manuscripts were fact checked and extensively edited by all co-authors rendering the final manuscript drafts significantly different from the first drafts. Recent findings: Unsurprisingly, the use of AI decreased the time spent to write a review. The two AI-written reviews took less time to write than the human-written paper; however, the changes and editing required in all three manuscripts were extensive. The human-written paper was edited the most. On the other hand, the AI-only paper was the most inaccurate with inappropriate reference usage and the AI-assisted paper had the greatest incidence of plagiarism. These findings show that each style of writing presents its own unique set of challenges and advantages. While AI can theoretically write scientific reviews, from these findings, the extent of editing done subsequently, the inaccuracy of the claims it makes, and the plagiarism by AI are all factors to be considered and a primary reason why it may be several years into the future before AI can present itself as a viable alternative for traditional scientific writing.
MeSH term(s)	Humans ; Fracture Healing ; Artificial Intelligence ; Peripheral Nervous System ; Homeostasis ; Writing
Language	English
Publishing date	2024-01-13
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-023-00854-y
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Article ; Online: Role of the Neurologic System in Fracture Healing: An Extensive Review.

Parker, Reginald S / Nazzal, Murad K / Morris, Ashlyn J / Fehrenbacher, Jill C / White, Fletcher A / Kacena, Melissa A / Natoli, Roman M

Current osteoporosis reports

2024 Volume 22, Issue 1, Page(s) 205–216

Abstract: Purpose of review: Despite advances in orthopedics, there remains a need for therapeutics to hasten fracture healing. However, little focus is given to the role the nervous system plays in regulating fracture healing. This paucity of information has led ...

Abstract	Purpose of review: Despite advances in orthopedics, there remains a need for therapeutics to hasten fracture healing. However, little focus is given to the role the nervous system plays in regulating fracture healing. This paucity of information has led to an incomplete understanding of fracture healing and has limited the development of fracture therapies that integrate the importance of the nervous system. This review seeks to illuminate the integral roles that the nervous system plays in fracture healing. Recent findings: Preclinical studies explored several methodologies for ablating peripheral nerves to demonstrate ablation-induced deficits in fracture healing. Conversely, activation of peripheral nerves via the use of dorsal root ganglion electrical stimulation enhanced fracture healing via calcitonin gene related peptide (CGRP). Investigations into TLR-4, TrkB agonists, and nerve growth factor (NGF) expression provide valuable insights into molecular pathways influencing bone mesenchymal stem cells and fracture repair. Finally, there is continued research into the connections between pain and fracture healing with findings suggesting that anti-NGF may be able to block pain without affecting healing. This review underscores the critical roles of the central nervous system (CNS), peripheral nervous system (PNS), and autonomic nervous system (ANS) in fracture healing, emphasizing their influence on bone cells, neuropeptide release, and endochondral ossification. The use of TBI models contributes to understanding neural regulation, though the complex influence of TBI on fracture healing requires further exploration. The review concludes by addressing the neural connection to fracture pain. This review article is part of a series of multiple manuscripts designed to determine the utility of using artificial intelligence for writing scientific reviews.
MeSH term(s)	Humans ; Fracture Healing/physiology ; Artificial Intelligence ; Calcitonin Gene-Related Peptide ; Pain ; Nervous System/metabolism
Chemical Substances	Calcitonin Gene-Related Peptide (JHB2QIZ69Z)
Language	English
Publishing date	2024-01-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-023-00844-0
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Article ; Online: Cracking the Code: The Role of Peripheral Nervous System Signaling in Fracture Repair.

Morris, Ashlyn J / Parker, Reginald S / Nazzal, Murad K / Natoli, Roman M / Fehrenbacher, Jill C / Kacena, Melissa A / White, Fletcher A

Current osteoporosis reports

2024 Volume 22, Issue 1, Page(s) 193–204

Abstract: Purpose of review: The traditionally understated role of neural regulation in fracture healing is gaining prominence, as recent findings underscore the peripheral nervous system's critical contribution to bone repair. Indeed, it is becoming more evident ...

Abstract	Purpose of review: The traditionally understated role of neural regulation in fracture healing is gaining prominence, as recent findings underscore the peripheral nervous system's critical contribution to bone repair. Indeed, it is becoming more evident that the nervous system modulates every stage of fracture healing, from the onset of inflammation to repair and eventual remodeling. Recent findings: Essential to this process are neurotrophins and neuropeptides, such as substance P, calcitonin gene-related peptide, and neuropeptide Y. These molecules fulfill key roles in promoting osteogenesis, influencing inflammation, and mediating pain. The sympathetic nervous system also plays an important role in the healing process: while local sympathectomies may improve fracture healing, systemic sympathetic denervation impairs fracture healing. Furthermore, chronic activation of the sympathetic nervous system, often triggered by stress, is a potential impediment to effective fracture healing, marking an important area for further investigation. The potential to manipulate aspects of the nervous system offers promising therapeutic possibilities for improving outcomes in fracture healing. This review article is part of a series of multiple manuscripts designed to determine the utility of using artificial intelligence for writing scientific reviews.
MeSH term(s)	Humans ; Artificial Intelligence ; Fractures, Bone ; Osteogenesis ; Fracture Healing/physiology ; Peripheral Nervous System ; Inflammation
Language	English
Publishing date	2024-01-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-023-00846-y
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Article ; Online: Effect of reactive oxygen, nitrogen, and sulfur species on signaling pathways in atherosclerosis.

Solanki, Kundan / Bezsonov, Evgeny / Orekhov, Alexander / Parihar, Suraj P / Vaja, Shivani / White, Fletcher A / Obukhov, Alexander G / Baig, Mirza S

Vascular pharmacology

2024 Volume 154, Page(s) 107282

Abstract: Atherosclerosis is a chronic inflammatory disease in which fats, lipids, cholesterol, calcium, proliferating smooth muscle cells, and immune cells accumulate in the intima of the large arteries, forming atherosclerotic plaques. A complex interplay of ... ...

Abstract	Atherosclerosis is a chronic inflammatory disease in which fats, lipids, cholesterol, calcium, proliferating smooth muscle cells, and immune cells accumulate in the intima of the large arteries, forming atherosclerotic plaques. A complex interplay of various vascular and immune cells takes place during the initiation and progression of atherosclerosis. Multiple reports indicate that tight control of reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive sulfur species (RSS) production is critical for maintaining vascular health. Unrestricted ROS and RNS generation may lead to activation of various inflammatory signaling pathways, facilitating atherosclerosis. Given these deleterious consequences, it is important to understand how ROS and RNS affect the signaling processes involved in atherogenesis. Conversely, RSS appears to exhibit an atheroprotective potential and can alleviate the deleterious effects of ROS and RNS. Herein, we review the literature describing the effects of ROS, RNS, and RSS on vascular smooth muscle cells, endothelial cells, and macrophages and focus on how changes in their production affect the initiation and progression of atherosclerosis. This review also discusses the contribution of ROS, RNS, and RSS in mediating various post-translational modifications, such as oxidation, nitrosylation, and sulfation, of the molecules involved in inflammatory signaling.
MeSH term(s)	Humans ; Reactive Oxygen Species/metabolism ; Oxygen ; Nitrogen ; Endothelial Cells/metabolism ; Signal Transduction ; Reactive Nitrogen Species/metabolism ; Sulfur ; Atherosclerosis
Chemical Substances	Reactive Oxygen Species ; Oxygen (S88TT14065) ; Nitrogen (N762921K75) ; Reactive Nitrogen Species ; Sulfur (70FD1KFU70)
Language	English
Publishing date	2024-02-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2082846-9
ISSN	1879-3649 ; 1537-1891 ; 1879-3649
ISSN (online)	1879-3649 ; 1537-1891
ISSN	1879-3649
DOI	10.1016/j.vph.2024.107282
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