Pub Date : 2024-09-25DOI: 10.1016/j.mehy.2024.111493
S. Akshatha
{"title":"Why is the inferior aspect of the shoulder joint unprotected and weakest? A theory on brachiation and bipedalism","authors":"S. Akshatha","doi":"10.1016/j.mehy.2024.111493","DOIUrl":"10.1016/j.mehy.2024.111493","url":null,"abstract":"","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"192 ","pages":"Article 111493"},"PeriodicalIF":2.1,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142358558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-25DOI: 10.1016/j.mehy.2024.111492
Nikola Todorovic , Dejan Javorac , Sergej M. Ostojic
{"title":"Comment on: “Can hydrogen prevent stress fractures in athletes?” Exploring the discussion of hydrogen use in sport medicine","authors":"Nikola Todorovic , Dejan Javorac , Sergej M. Ostojic","doi":"10.1016/j.mehy.2024.111492","DOIUrl":"10.1016/j.mehy.2024.111492","url":null,"abstract":"","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"192 ","pages":"Article 111492"},"PeriodicalIF":2.1,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142326682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-24DOI: 10.1016/j.mehy.2024.111487
Jordan N. Williamson , Beni Mulyana , Rita Huan-Ting Peng , Sanjiv Jain , Wael Hassaneen , Amrendra Miranpuri , Yuan Yang
Previous studies found that post-stroke motor impairments are associated with damage to the lesioned corticospinal tract and a maladaptive increase in indirect contralesional motor pathways. How the somatosensory system adapts to the change in the use of motor pathways and the role of adaptive sensory feedback to the abnormal movement control of the paretic arm remains largely unknown. We hypothesize that following a unilateral stroke, there is an adaptive hemispheric shift of somatosensory processing toward the contralesional sensorimotor areas to provide sensory feedback support to the contralesional indirect motor pathways. This research could provide new insights related to somatosensory reorganization after stroke, which could enrich future hypothesis-driven therapeutic rehabilitation strategies from a sensory or sensory-motor perspective. Understanding how somatosensory information shifts may provide a target for a novel method to therapeutically prevent and mitigate the emergence and expression of upper limb motor impairments, following a stroke.
{"title":"How the somatosensory system adapts to the motor change in Stroke: A hemispheric Shift?","authors":"Jordan N. Williamson , Beni Mulyana , Rita Huan-Ting Peng , Sanjiv Jain , Wael Hassaneen , Amrendra Miranpuri , Yuan Yang","doi":"10.1016/j.mehy.2024.111487","DOIUrl":"10.1016/j.mehy.2024.111487","url":null,"abstract":"<div><div>Previous studies found that post-stroke motor impairments are associated with damage to the lesioned corticospinal tract and a maladaptive increase in indirect contralesional motor pathways. How the somatosensory system adapts to the change in the use of motor pathways and the role of adaptive sensory feedback to the abnormal movement control of the paretic arm remains largely unknown. We hypothesize that following a unilateral stroke, there is an adaptive hemispheric shift of somatosensory processing toward the contralesional sensorimotor areas to provide sensory feedback support to the contralesional indirect motor pathways. This research could provide new insights related to somatosensory reorganization after stroke, which could enrich future hypothesis-driven therapeutic rehabilitation strategies from a sensory or sensory-motor perspective. Understanding how somatosensory information shifts may provide a target for a novel method to therapeutically prevent and mitigate the emergence and expression of upper limb motor impairments, following a stroke.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"192 ","pages":"Article 111487"},"PeriodicalIF":2.1,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-23DOI: 10.1016/j.mehy.2024.111488
Paula Fernanda Ribas Neves , Lisiê Valéria Paz , Andrea Wieck , Léder Leal Xavier
In this article we present a hypothesis based on the relationship between four physiological systems: the renin-angiotensin system (RAS), the kallikrein-kinin system (KKS), the arachidonic acid (AA) cascade, and platelet aggregation/coagulation − in the context of COVID-19. The central point of our proposition relies on ACE2 levels, which reduce following SARS-CoV-2 entry in the cell. The following cascade of events. Triggered by this reduction, involves the increase in Ang II levels and its consequent binding to AT1-R, initiating the release of pro-inflammatory cytokines such as TNF-α, IL-1, IL-10, and IL-12. These pro-inflammatory cytokines activate immune cells, including mast cells, which release heparin, thus activating Coagulation factor XII and increasing pre-kallikrein (PK) production. Consequently, there is an increase in bradykinin (BK) levels. BK, via its receptor BKB2-R, induces Ca2 + release increasing secreted phospholipase A2 (sPLA2) levels. Concomitantly, both the imbalance in Ang II/AT1-R and BK/BKB2-R signaling contribute to sPLA2 activation, inducing the release of arachidonic acid (AA) from cell membrane phospholipids, by cyclooxygenase-2 (COX-2) cleavage to produce prostaglandin G2 (PGG2), and later prostaglandin H2 (PGH2). At least, PGH2 is converted to thromboxane A2 (TXA2), which is involved in the platelet aggregation process. Platelet aggregation further increases TXA2 levels, initiating a positive feedback loop leading to further platelet activation and clot formation. Ultimately, this cascade of events may contribute to the development of a pre-thrombotic state and increase the risk of mortality, in COVID-19. We believe that this integrated approach could provide a deeper understanding of the underlying mechanisms of COVID-19 and guide future therapeutic strategies.
{"title":"A hypothesis linking the renin-angiotensin, kallikrein-kinin systems, and disseminated coagulation in COVID-19","authors":"Paula Fernanda Ribas Neves , Lisiê Valéria Paz , Andrea Wieck , Léder Leal Xavier","doi":"10.1016/j.mehy.2024.111488","DOIUrl":"10.1016/j.mehy.2024.111488","url":null,"abstract":"<div><div>In this article we present a hypothesis based on the relationship between four physiological systems: the renin-angiotensin system (RAS), the kallikrein-kinin system (KKS), the arachidonic acid (AA) cascade, and platelet aggregation/coagulation − in the context of COVID-19. The central point of our proposition relies on ACE<sub>2</sub> levels, which reduce following SARS-CoV-2 entry in the cell. The following cascade of events. Triggered by this reduction, involves the increase in Ang II levels and its consequent binding to AT1-R, initiating the release of pro-inflammatory cytokines such as TNF-α, IL-1, IL-10, and IL-12. These pro-inflammatory cytokines activate immune cells, including mast cells, which release heparin, thus activating Coagulation factor XII and increasing pre-kallikrein (PK) production. Consequently, there is an increase in bradykinin (BK) levels. BK, via its receptor BKB2-R, induces Ca<sup>2</sup> + release increasing secreted phospholipase A<sub>2</sub> (sPLA<sub>2</sub>) levels. Concomitantly, both the imbalance in Ang II/AT1-R and BK/BKB2-R signaling contribute to sPLA<sub>2</sub> activation, inducing the release of arachidonic acid (AA) from cell membrane phospholipids, by cyclooxygenase-2 (COX-2) cleavage to produce prostaglandin G<sub>2</sub> (PGG<sub>2</sub>), and later prostaglandin H<sub>2</sub> (PGH<sub>2</sub>). At least, PGH<sub>2</sub> is converted to thromboxane A<sub>2</sub> (TXA<sub>2</sub>), which is involved in the platelet aggregation process. Platelet aggregation further increases TXA<sub>2</sub> levels, initiating a positive feedback loop leading to further platelet activation and clot formation. Ultimately, this cascade of events may contribute to the development of a pre-thrombotic state and increase the risk of mortality, in COVID-19. We believe that this integrated approach could provide a deeper understanding of the underlying mechanisms of COVID-19 and guide future therapeutic strategies.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"192 ","pages":"Article 111488"},"PeriodicalIF":2.1,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-19DOI: 10.1016/j.mehy.2024.111491
Sadia Ahmad , Amna Rehman , Ali Afzal , Muhammad Babar Khawar
Age-related disorders are exacerbated by senescent cells (SnCs) due to their secretion of proinflammatory molecules, yet current therapeutic strategies have limited success in preclinical settings and clinical trials. A novel approach is needed to enhance SnCs clearance by targeting immune checkpoints, particularly the PD-1/PD-L1 axis, combined with tissue-specific delivery of therapeutic agents. This strategy is critical in reducing the chronic inflammation and improving tissue health in aging populations. However, challenges such as immune evasion by SnCs and potential autoimmune responses must be addressed. The aim of this manuscript is to propose a combined approach to improve the efficacy of senolytic therapy.
{"title":"Can tissue-specific PD-1/PD-L1 targeting combined with other immune checkpoint blockades enhance immune clearance?","authors":"Sadia Ahmad , Amna Rehman , Ali Afzal , Muhammad Babar Khawar","doi":"10.1016/j.mehy.2024.111491","DOIUrl":"10.1016/j.mehy.2024.111491","url":null,"abstract":"<div><p>Age-related disorders are exacerbated by senescent cells (SnCs) due to their secretion of proinflammatory molecules, yet current therapeutic strategies have limited success in preclinical settings and clinical trials. A novel approach is needed to enhance SnCs clearance by targeting immune checkpoints, particularly the PD-1/PD-L1 axis, combined with tissue-specific delivery of therapeutic agents. This strategy is critical in reducing the chronic inflammation and improving tissue health in aging populations. However, challenges such as immune evasion by SnCs and potential autoimmune responses must be addressed. The aim of this manuscript is to propose a combined approach to improve the efficacy of senolytic therapy.</p></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"192 ","pages":"Article 111491"},"PeriodicalIF":2.1,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-19DOI: 10.1016/j.mehy.2024.111490
Yingsuo Zhao , Xiang Ren , Pratiksha Paudel , Meili Ge , Qianwei Liu
Immune thrombocytopenia (ITP) is an autoimmune disease due to increased peripheral platelets destruction and inappropriate bone marrow production of platelets by megakaryocytes (MKs). The pathophysiology of ITP is complex and multifactorial, which remains not fully understood. However, the production of antiplatelet autoantibodies and the destruction of antibody-coated platelets through antibody-dependent cellular phagocytosis by macrophages (Mθ) expressing Fc gamma receptor (FcγR) are regarded as the key mechanisms. Glycoprotein (GP) Ⅱb/Ⅲa is the main target of antiplatelet antibodies leading to platelet phagocytosis by splenic Mθ, through interactions with FcγR. As GPⅡb/Ⅲa is normally expressed both on platelets and the MKs from which they are derived, we inferred that partial phagocytosis (definitely trogocytosis) of MKs by bone marrow Mθ might exist, leading to the increased amount of granular MKs (or non-platelets-producing MKs) in ITP. And we further hypothesized that the “bitten” MKs cannot sustain their normal function of maturation. Such trogocytosis mechanism may shed new light on the understanding of morphology alterations, maturation defects and decreased platelets production of MKs in ITP, and provide appealing implications in therapeutic modifications targeting the interplay of MKs and Mθ in bone marrow.
{"title":"Trogocytosis: A potential pathogenic mechanism in immune thrombocytopenia leading to impaired megakaryocyte maturation and reduced platelet production","authors":"Yingsuo Zhao , Xiang Ren , Pratiksha Paudel , Meili Ge , Qianwei Liu","doi":"10.1016/j.mehy.2024.111490","DOIUrl":"10.1016/j.mehy.2024.111490","url":null,"abstract":"<div><div>Immune thrombocytopenia (ITP) is an autoimmune disease due to increased peripheral platelets destruction and inappropriate bone marrow production of platelets by megakaryocytes (MKs). The pathophysiology of ITP is complex and multifactorial, which remains not fully understood. However, the production of antiplatelet autoantibodies and the destruction of antibody-coated platelets through antibody-dependent cellular phagocytosis by macrophages (Mθ) expressing Fc gamma receptor (FcγR) are regarded as the key mechanisms. Glycoprotein (GP) Ⅱb/Ⅲa is the main target of antiplatelet antibodies leading to platelet phagocytosis by splenic Mθ, through interactions with FcγR. As GPⅡb/Ⅲa is normally expressed both on platelets and the MKs from which they are derived, we inferred that partial phagocytosis (definitely trogocytosis) of MKs by bone marrow Mθ might exist, leading to the increased amount of granular MKs (or non-platelets-producing MKs) in ITP. And we further hypothesized that the “bitten” MKs cannot sustain their normal function of maturation. Such trogocytosis mechanism may shed new light on the understanding of morphology alterations, maturation defects and decreased platelets production of MKs in ITP, and provide appealing implications in therapeutic modifications targeting the interplay of MKs and Mθ in bone marrow.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"193 ","pages":"Article 111490"},"PeriodicalIF":2.1,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142441382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oxygen delivery systems are crucial in critical care medicine, particularly for managing acute respiratory distress. This study presents a novel approach, exploring the potential of Metal-Organic Frameworks (MOFs) as oxygen delivery systems. We highlight their unique properties and potential for enhancing oxygenation in medical settings. Understanding their biocompatibility, oxygen-carrying capacity, and controlled release mechanisms is pivotal for successful implementation in clinical practice. Thanks to their exceptional porosity, structural diversity, lower crystal density, and tunability, MOFs offer a fresh perspective on developing innovative oxygen carriers. We propose that MOFs will demonstrate biocompatibility, stability, and the ability to deliver oxygen in a controlled and sustained manner when administered intravenously in living organisms. Gas adsorption and molecular simulation techniques will demonstrate reversible oxygen binding within MOFs and predict controlled release kinetics. The findings of the simulations and experiments should indicate the feasibility of utilising MOFs as intravenous oxygen carriers with controlled and reversible oxygen release behaviour.
{"title":"Oxygen Gas-Filled Metal-Organic Frameworks (MOFs) Delivery System: A Hypothetical Design for Injectable Oxygen","authors":"Chitrangda Singh , Chandan Bhogendra Jha , Sreedevi Upadhyayula , Rashi Mathur","doi":"10.1016/j.mehy.2024.111489","DOIUrl":"10.1016/j.mehy.2024.111489","url":null,"abstract":"<div><div>Oxygen delivery systems are crucial in critical care medicine, particularly for managing acute respiratory distress. This study presents a novel approach, exploring the potential of Metal-Organic Frameworks (MOFs) as oxygen delivery systems. We highlight their unique properties and potential for enhancing oxygenation in medical settings. Understanding their biocompatibility, oxygen-carrying capacity, and controlled release mechanisms is pivotal for successful implementation in clinical practice. Thanks to their exceptional porosity, structural diversity, lower crystal density, and tunability, MOFs offer a fresh perspective on developing innovative oxygen carriers. We propose that MOFs will demonstrate biocompatibility, stability, and the ability to deliver oxygen in a controlled and sustained manner when administered intravenously in living organisms. Gas adsorption and molecular simulation techniques will demonstrate reversible oxygen binding within MOFs and predict controlled release kinetics. The findings of the simulations and experiments should indicate the feasibility of utilising MOFs as intravenous oxygen carriers with controlled and reversible oxygen release behaviour.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"192 ","pages":"Article 111489"},"PeriodicalIF":2.1,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142312572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-17DOI: 10.1016/j.mehy.2024.111486
Pooya Moghimzadeh-Mohebbi, Mohammad Mahdi Sohrabi, Roham Mazloom
Impairment in social interactions is a prominent feature of autism spectrum disorder (ASD). The present hypothesis explains the possible role of vagal afferent stimulation in the modification of prefrontal-amygdala connectivity in the amelioration of social impairments in ASD. Currently, there is no definitive treatment for ASD. However, there is documented evidence showing that interventions that increase vagal tone lead to the improvement of autism-related social symptoms. However, the exact mechanism that explains the correlation between the elevation of vagal tone and the amelioration of autism-related symptoms has not been elucidated. In the present hypothesis, it is proposed that the increase in vagal tone affects the nucleus tractus solitarius (NTS) in the brainstem. The NTS has strong connections with other brainstem nuclei, such as the locus coeruleus and dorsal raphe nucleus. The aforementioned nuclei are the main sources of norepinephrine and serotonin, with extensive projections to various brain areas, especially the prefrontal cortex (PFC) and amygdala. PFC-amygdala functional connectivity plays an important role in social behavior and emotion regulation. Therefore, visceral stimulation, which subsequently increases the vagal tone, possibly leads to the improvement of autistic social deficits through the enhancement of PFC-amygdala functional connectivity. Further investigations are needed to evaluate the function of the mentioned neural pathways during visceral stimulation in individuals with ASD.
{"title":"Amelioration of social impairments in autism: Possible role of vagal afferent stimulation in modification of the prefrontal-amygdala connectivity","authors":"Pooya Moghimzadeh-Mohebbi, Mohammad Mahdi Sohrabi, Roham Mazloom","doi":"10.1016/j.mehy.2024.111486","DOIUrl":"10.1016/j.mehy.2024.111486","url":null,"abstract":"<div><p>Impairment in social interactions is a prominent feature of autism spectrum disorder (ASD). The present hypothesis explains the possible role of vagal afferent stimulation in the modification of prefrontal-amygdala connectivity in the amelioration of social impairments in ASD. Currently, there is no definitive treatment for ASD. However, there is documented evidence showing that interventions that increase vagal tone lead to the improvement of autism-related social symptoms. However, the exact mechanism that explains the correlation between the elevation of vagal tone and the amelioration of autism-related symptoms has not been elucidated. In the present hypothesis, it is proposed that the increase in vagal tone affects the nucleus tractus solitarius (NTS) in the brainstem. The NTS has strong connections with other brainstem nuclei, such as the locus coeruleus and dorsal raphe nucleus. The aforementioned nuclei are the main sources of norepinephrine and serotonin, with extensive projections to various brain areas, especially the prefrontal cortex (PFC) and amygdala. PFC-amygdala functional connectivity plays an important role in social behavior and emotion regulation. Therefore, visceral stimulation, which subsequently increases the vagal tone, possibly leads to the improvement of autistic social deficits through the enhancement of PFC-amygdala functional connectivity. Further investigations are needed to evaluate the function of the mentioned neural pathways during visceral stimulation in individuals with ASD.</p></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"192 ","pages":"Article 111486"},"PeriodicalIF":2.1,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lumbar disc herniation frequently causes low back pain and sciatica, significantly impacting patients’ quality of life. The pathogenesis of sciatica is complex, involving both mechanical compression and inflammatory processes. Recent studies have suggested a potential role of inflammatory mechanisms in the development of sciatica. We hypothesize that these inflammatory mediators contribute to the neuropathic pain experienced by patients with lumbar disc herniation. Understanding these inflammatory mechanisms may lead to novel therapeutic targets for managing sciatica in lumbar disc herniation, ultimately improving patient outcomes. Future research should focus on testing this hypothesis through scientific investigation to validate these potential new therapies.
{"title":"Inflammatory mechanisms as a potential cause of sciatica in lumbar disc herniation: A hypothesis","authors":"Lei Zhou, Yong Tang, Jihong Jiang, Yangsheng Wang, Changwei Chen, Feng Zhu","doi":"10.1016/j.mehy.2024.111485","DOIUrl":"10.1016/j.mehy.2024.111485","url":null,"abstract":"<div><p>Lumbar disc herniation frequently causes low back pain and sciatica, significantly impacting patients’ quality of life. The pathogenesis of sciatica is complex, involving both mechanical compression and inflammatory processes. Recent studies have suggested a potential role of inflammatory mechanisms in the development of sciatica. We hypothesize that these inflammatory mediators contribute to the neuropathic pain experienced by patients with lumbar disc herniation. Understanding these inflammatory mechanisms may lead to novel therapeutic targets for managing sciatica in lumbar disc herniation, ultimately improving patient outcomes. Future research should focus on testing this hypothesis through scientific investigation to validate these potential new therapies.</p></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"192 ","pages":"Article 111485"},"PeriodicalIF":2.1,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0306987724002287/pdfft?md5=2a5b1e970a34f61fe6e655e9a0259a27&pid=1-s2.0-S0306987724002287-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142239858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-15DOI: 10.1016/j.mehy.2024.111484
Xiangyu Cao , Hongkuan Deng
The increasing rate of Carbapenem-resistant Enterobacteriaceaer (CRE) infections poses a significant threat to global public health. Patients infected with CRE often experience frequent recurrences after antibiotic treatment, making it difficult to cure. The design of better antimicrobials that can not only kill CRE but also disrupt biofilms and eliminate persister cells will play a crucial role in improving antibacterial efficacy and preventing recurrent infections. In this hypothesis, we employ an innovative “water pipe” theory to elucidate the potential underlying causes of CRE infection recurrence. We propose a potential therapeutic approach utilizing engineered phages to combat CRE infections, demonstrating the mechanism of action of phages carrying lytic enzymes or antimicrobial peptides against biofilms and persister cells. Furthermore, we evaluate its efficacy and feasibility, which may effectively address the recurrence of CRE infections and reduce antibiotic usage.
{"title":"Engineered phage therapy for the effective treatment of recurrent Carbapenem-resistant Enterobacteriaceae infections: A hypothesis","authors":"Xiangyu Cao , Hongkuan Deng","doi":"10.1016/j.mehy.2024.111484","DOIUrl":"10.1016/j.mehy.2024.111484","url":null,"abstract":"<div><p>The increasing rate of Carbapenem-resistant Enterobacteriaceaer (CRE) infections poses a significant threat to global public health. Patients infected with CRE often experience frequent recurrences after antibiotic treatment, making it difficult to cure. The design of better antimicrobials that can not only kill CRE but also disrupt biofilms and eliminate persister cells will play a crucial role in improving antibacterial efficacy and preventing recurrent infections. In this hypothesis, we employ an innovative “water pipe” theory to elucidate the potential underlying causes of CRE infection recurrence. We propose a potential therapeutic approach utilizing engineered phages to combat CRE infections, demonstrating the mechanism of action of phages carrying lytic enzymes or antimicrobial peptides against biofilms and persister cells. Furthermore, we evaluate its efficacy and feasibility, which may effectively address the recurrence of CRE infections and reduce antibiotic usage.</p></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"192 ","pages":"Article 111484"},"PeriodicalIF":2.1,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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