Pub Date : 2024-12-01DOI: 10.1016/j.mehy.2024.111541
Elise H. Mallon BS, Arnold Brown MD, FIDSA
Primary Amebic Meningoencephalitis (PAM) caused by Naegleria fowleri is a rare, usually fatal disease. It is thought that PAM occurs most often in southern US states because of the warmer surface waters in these states. To better understand the epidemiology of this disease we converted the raw number of cases reported in each state from 1962 to 2022, to an estimate of cases per individual at potential risk. Our relative risk estimates paint a slightly different picture, suggesting that in addition to the temperature of surface waters other epidemiologic factors are also at play, and that there may be an association between waterfowl nesting areas and risk of disease acquisition. We hypothesize that waterfowl serve as reservoirs that maintain the environmental sources of human infection. If this can be shown, control measures can be implemented to reduce the risk of disease acquisition.
{"title":"Hypothesis: Waterfowl may be important intermediary reservoirs of Naegleria fowleri","authors":"Elise H. Mallon BS, Arnold Brown MD, FIDSA","doi":"10.1016/j.mehy.2024.111541","DOIUrl":"10.1016/j.mehy.2024.111541","url":null,"abstract":"<div><div>Primary Amebic Meningoencephalitis (PAM) caused by <em>Naegleria fowleri</em> is a rare, usually fatal disease. It is thought that PAM occurs most often in southern US states because of the warmer surface waters in these states. To better understand the epidemiology of this disease we converted the raw number of cases reported in each state from 1962 to 2022, to an estimate of cases per individual at potential risk. Our relative risk estimates paint a slightly different picture, suggesting that in addition to the temperature of surface waters other epidemiologic factors are also at play, and that there may be an association between waterfowl nesting areas and risk of disease acquisition. We hypothesize that waterfowl serve as reservoirs that maintain the environmental sources of human infection. If this can be shown, control measures can be implemented to reduce the risk of disease acquisition.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111541"},"PeriodicalIF":2.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142758842","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 : 2024-11-30DOI: 10.1016/j.mehy.2024.111540
Lana Frankle
{"title":"Miller Fisher’s telephone effect is a consequence of generative rationality","authors":"Lana Frankle","doi":"10.1016/j.mehy.2024.111540","DOIUrl":"10.1016/j.mehy.2024.111540","url":null,"abstract":"","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111540"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142758841","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}
Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions resulting from aberrant sensory integration, enhanced cortical plasticity, and lack of intracortical inhibition. Deep brain stimulation of the globus pallidus internus (GPi-DBS) effectively treats dystonia, reducing abnormal neural oscillations and improving motor function. However, systemic infections can significantly impact brain function, altering brain wave dynamics and cortical excitability. We hypothesize that dystonia patients treated with DBS exhibit altered cortical excitability and changes in brain wave dynamics during early recovery from systemic infections, necessitating DBS parameters adjustment to prevent symptoms exacerbation. We propose a two-year clinical study involving 15 dystonia patients with DBS capable of local field potential (LFP) recording to evaluate this hypothesis. The study will analyze brain activity patterns, symptom severity and infection impact on neural activity. Continuous and infection-triggered LFP recording will provide data for advanced analysis to identify LFP patterns associated with dystonia symptoms and the effects of infections. This paper underscored the importance of individualized and dynamic DBS management, especially post-infection. Systemic infections can induce neuroinflammation, disrupting neural circuits and increasing brain sensitivity to DBS. Timely DBS adjustments are crucial to mitigate overstimulation and optimize outcomes. Enhanced post-infection care, including thorough evaluations and parameter adjustments, is essential for managing dystonia patients with DBS. Future research into the neuroinflammatory mechanism and their effect on neural circuits will improve our understanding and treatment of dystonia in the context of systemic infections.
{"title":"Could systemic infections influence the effectiveness of deep brain stimulation therapy in patients with dystonia?","authors":"Valentino Rački , Mario Hero , Eliša Papić , Gloria Rožmarić , Marina Raguž , Darko Chudy , Olivio Perković , Vladimira Vuletić","doi":"10.1016/j.mehy.2024.111527","DOIUrl":"10.1016/j.mehy.2024.111527","url":null,"abstract":"<div><div>Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions resulting from aberrant sensory integration, enhanced cortical plasticity, and lack of intracortical inhibition. Deep brain stimulation of the globus pallidus internus (GPi-DBS) effectively treats dystonia, reducing abnormal neural oscillations and improving motor function. However, systemic infections can significantly impact brain function, altering brain wave dynamics and cortical excitability. We hypothesize that dystonia patients treated with DBS exhibit altered cortical excitability and changes in brain wave dynamics during early recovery from systemic infections, necessitating DBS parameters adjustment to prevent symptoms exacerbation. We propose a two-year clinical study involving 15 dystonia patients with DBS capable of local field potential (LFP) recording to evaluate this hypothesis. The study will analyze brain activity patterns, symptom severity and infection impact on neural activity. Continuous and infection-triggered LFP recording will provide data for advanced analysis to identify LFP patterns associated with dystonia symptoms and the effects of infections. This paper underscored the importance of individualized and dynamic DBS management, especially post-infection. Systemic infections can induce neuroinflammation, disrupting neural circuits and increasing brain sensitivity to DBS. Timely DBS adjustments are crucial to mitigate overstimulation and optimize outcomes. Enhanced post-infection care, including thorough evaluations and parameter adjustments, is essential for managing dystonia patients with DBS. Future research into the neuroinflammatory mechanism and their effect on neural circuits will improve our understanding and treatment of dystonia in the context of systemic infections.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111527"},"PeriodicalIF":2.1,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142722108","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 : 2024-11-22DOI: 10.1016/j.mehy.2024.111528
Erdoğan Bulut , Murat Arslan , Cem Uzun
Peripheral dysfunction and hearing loss are known risk factors for tinnitus; however, a portion of tinnitus patients exhibit no apparent peripheral auditory deficits. This article proposes that tinnitus may originate in the cochlea due to, undetectable damage to outer hair cells (OHCs) in individuals with normal hearing. The study further suggests that peripheral auditory deficits can be identified through the outer hair cell motor protein Prestin, which has potential as a biomarker for early detection. Minor OHC losses, which do not result in clinically detectable hearing loss, may lead to insufficient depolarization of inner hair cells (IHCs), thereby reducing sensory input along the cochlea-cortex pathway in the central auditory system. From a homeostatic gain control perspective, decreased amplification by OHCs, including abnormal electromotile responses, may lead to inadequate encoding by IHCs, contributing to the cochlear origin of tinnitus. Damage to OHCs that does not affect hearing thresholds, or abnormal electromotile contractions influenced by Prestin, may contribute to peripheral auditory dysfunction underlying tinnitus. As a result, pre-neural mismatched synchronization between OHCs and IHCs, driven by abnormal OHC electromotility, could cause sound processing disorders within the central auditory system. This pathophysiological mechanism at the cochlear level may lead to pathological alterations at multiple levels of the central auditory system. Prestin may serve as a potential biomarker for tinnitus, offering valuable insights into its cochlear origin and guiding future therapeutic developments.
{"title":"Cochlear origin of tinnitus and outer hair cell motor protein Prestin as a biomarker for tinnitus","authors":"Erdoğan Bulut , Murat Arslan , Cem Uzun","doi":"10.1016/j.mehy.2024.111528","DOIUrl":"10.1016/j.mehy.2024.111528","url":null,"abstract":"<div><div>Peripheral dysfunction and hearing loss are known risk factors for tinnitus; however, a portion of tinnitus patients exhibit no apparent peripheral auditory deficits. This article proposes that tinnitus may originate in the cochlea due to, undetectable damage to outer hair cells (OHCs) in individuals with normal hearing. The study further suggests that peripheral auditory deficits can be identified through the outer hair cell motor protein Prestin, which has potential as a biomarker for early detection. Minor OHC losses, which do not result in clinically detectable hearing loss, may lead to insufficient depolarization of inner hair cells (IHCs), thereby reducing sensory input along the cochlea-cortex pathway in the central auditory system. From a homeostatic gain control perspective, decreased amplification by OHCs, including abnormal electromotile responses, may lead to inadequate encoding by IHCs, contributing to the cochlear origin of tinnitus. Damage to OHCs that does not affect hearing thresholds, or abnormal electromotile contractions influenced by Prestin, may contribute to peripheral auditory dysfunction underlying tinnitus. As a result, pre-neural mismatched synchronization between OHCs and IHCs, driven by abnormal OHC electromotility, could cause sound processing disorders within the central auditory system. This pathophysiological mechanism at the cochlear level may lead to pathological alterations at multiple levels of the central auditory system. Prestin may serve as a potential biomarker for tinnitus, offering valuable insights into its cochlear origin and guiding future therapeutic developments.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111528"},"PeriodicalIF":2.1,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142706508","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 : 2024-11-19DOI: 10.1016/j.mehy.2024.111526
Zixiang Zhao , Yu Liu , Yuhao Zou , Yi Liu , Man Yu
Keratoconus (KC) is a corneal ectasia with a complex etiology, and its pathogenesis remains incompletely understood. Research indicates that the development of KC is closely linked to inflammation and local oxidative stress (OS) triggered by alterations in the microenvironment of the ocular surface. Intense pulsed light (IPL) has been shown to enhance the ocular surface microenvironment, decrease inflammatory cytokines, and mitigate oxidative stress associated with KC progression. We hypothesize that IPL may impede the advancement of KC through several mechanisms. IPL treatment could lead to a decrease in inflammatory mediators (such as IL-1, IL-17, IL-6, etc.) in the eyelid margin and ocular surface, as well as a reduction in matrix metalloproteinases (MMPs) levels in tears, while elevating tissue inhibitor of metalloproteinases (TIMPs) levels, thereby slowing down extracellular matrix (ECM) degradation. Moreover, IPL stimulates fibroblasts to upregulate the expression of type I and type III procollagen mRNA and enhance ECM synthesis. Additionally, IPL regulates tear reactive oxygen species (ROS) levels, elevating tissue superoxide dismutase (SOD) levels through light modulation, maintaining the balance between oxidation and antioxidation, and lessening OS-induced damage. Lastly, IPL diminishes the urge of patients to rub their eyes by alleviating the itching sensation. In conclusion, IPL holds promise as a potential therapeutic approach for managing KC.
{"title":"Intense pulsed light alleviates keratoconus by improving the local corneal microenvironment","authors":"Zixiang Zhao , Yu Liu , Yuhao Zou , Yi Liu , Man Yu","doi":"10.1016/j.mehy.2024.111526","DOIUrl":"10.1016/j.mehy.2024.111526","url":null,"abstract":"<div><div>Keratoconus (KC) is a corneal ectasia with a complex etiology, and its pathogenesis remains incompletely understood. Research indicates that the development of KC is closely linked to inflammation and local oxidative stress (OS) triggered by alterations in the microenvironment of the ocular surface. Intense pulsed light (IPL) has been shown to enhance the ocular surface microenvironment, decrease inflammatory cytokines, and mitigate oxidative stress associated with KC progression. We hypothesize that IPL may impede the advancement of KC through several mechanisms. IPL treatment could lead to a decrease in inflammatory mediators (such as IL-1, IL-17, IL-6, etc.) in the eyelid margin and ocular surface, as well as a reduction in matrix metalloproteinases (MMPs) levels in tears, while elevating tissue inhibitor of metalloproteinases (TIMPs) levels, thereby slowing down extracellular matrix (ECM) degradation. Moreover, IPL stimulates fibroblasts to upregulate the expression of type I and type III procollagen mRNA and enhance ECM synthesis. Additionally, IPL regulates tear reactive oxygen species (ROS) levels, elevating tissue superoxide dismutase (SOD) levels through light modulation, maintaining the balance between oxidation and antioxidation, and lessening OS-induced damage. Lastly, IPL diminishes the urge of patients to rub their eyes by alleviating the itching sensation. In conclusion, IPL holds promise as a potential therapeutic approach for managing KC.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111526"},"PeriodicalIF":2.1,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142706509","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}
Parvovirus B19 (B19V) is the causative agent of erythema infectiosum and other diseases, including aplastic anemia in individuals with underlying hemolytic disorders such as sickle cell disease, spherocytosis or thalassemia. It has been well-established that B19V affects the development of red blood cells (RBC) by infecting erythroid progenitor cells (EPC) in the bone marrow. The first step in B19V infection is the binding of the virion to the glycosphingolipid (GSL) globoside (Gb4) on the EPC surface and temporarily stopping erythropoiesis. Although this infection is tolerated well by healthy patients, it can lead to severe aplastic crises in anemia patients. Gb4 is also the most abundant neutral glycolipid in the erythrocyte membrane. It has been documented that B19V and its virus-like particles (VLP) produce hemagglutination of RBCs. We hypothesized that B19V binding to the RBC membrane must induce changes impairing its function and reducing the cell’s half-life, being an aggravating cause of anemias produced by B19V. Here, we present optic and electronic microscopy evidence of morphological changes on the surface of the RBC produced by the presence of B19V VLP, supporting this hypothesis.
{"title":"Membrane damage produced by parvovirus B19 tags erythrocytes as senescent and is an aggravating cause of virus-triggered anemias","authors":"Josefina Valadez-García , Iris Ashanty Soto-Valerio , Maximiliano Cueva-Berea , Guadalupe Trinidad Zavala-Padilla , Ismael Bustos-Jaimes","doi":"10.1016/j.mehy.2024.111524","DOIUrl":"10.1016/j.mehy.2024.111524","url":null,"abstract":"<div><div>Parvovirus B19 (B19V) is the causative agent of <em>erythema infectiosum</em> and other diseases, including aplastic anemia in individuals with underlying hemolytic disorders such as sickle cell disease, spherocytosis or thalassemia. It has been well-established that B19V affects the development of red blood cells (RBC) by infecting erythroid progenitor cells (EPC) in the bone marrow. The first step in B19V infection is the binding of the virion to the glycosphingolipid (GSL) globoside (Gb4) on the EPC surface and temporarily stopping erythropoiesis. Although this infection is tolerated well by healthy patients, it can lead to severe aplastic crises in anemia patients. Gb4 is also the most abundant neutral glycolipid in the erythrocyte membrane. It has been documented that B19V and its virus-like particles (VLP) produce hemagglutination of RBCs. We hypothesized that B19V binding to the RBC membrane must induce changes impairing its function and reducing the cell’s half-life, being an aggravating cause of anemias produced by B19V. Here, we present optic and electronic microscopy evidence of morphological changes on the surface of the RBC produced by the presence of B19V VLP, supporting this hypothesis.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111524"},"PeriodicalIF":2.1,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142705694","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 : 2024-11-19DOI: 10.1016/j.mehy.2024.111525
Ryo Kataoka, Yujiro Yamada, William B. Hammert, Anna Kang, Jeremy P. Loenneke
Within the resistance training literature, a within-subject training model is often used to compare two separate training interventions within the same individual. While this model has some advantages related to statistical power, potential concerns have been raised when investigating changes in muscle strength. Conversely, it is currently believed that muscle growth is driven by local mechanisms. Thus, a within-subject design could potentially still be used if the sole outcome variable is changes in muscle size. What remains less clear, however, is whether the magnitude of skeletal muscle growth with resistance training is negatively influenced by the amount of muscle recruited within a given training period (e.g., upper body exercise only vs. same upper body exercise plus lower body resistance exercises). We hypothesize that there might be a competition for resources on skeletal muscle growth when more muscles are activated within a given training session and/or period, which might be moderated by energy availability. Determining the extent to which muscle exercised during resistance training influences skeletal muscle growth may provide important methodological considerations for researchers and practitioners alike. From a practical sense, if the competition of resources exists, one may benefit from specializing a certain muscle group to train within a given training period while deemphasizing other muscle groups.
{"title":"Do skeletal muscles compete with each other for growth?","authors":"Ryo Kataoka, Yujiro Yamada, William B. Hammert, Anna Kang, Jeremy P. Loenneke","doi":"10.1016/j.mehy.2024.111525","DOIUrl":"10.1016/j.mehy.2024.111525","url":null,"abstract":"<div><div>Within the resistance training literature, a within-subject training model is often used to compare two separate training interventions within the same individual. While this model has some advantages related to statistical power, potential concerns have been raised when investigating changes in muscle strength. Conversely, it is currently believed that muscle growth is driven by local mechanisms. Thus, a within-subject design could potentially still be used if the sole outcome variable is changes in muscle size. What remains less clear, however, is whether the magnitude of skeletal muscle growth with resistance training is negatively influenced by the amount of muscle recruited within a given training period (e.g., upper body exercise only vs. same upper body exercise plus lower body resistance exercises). We hypothesize that there might be a competition for resources on skeletal muscle growth when more muscles are activated within a given training session and/or period, which might be moderated by energy availability. Determining the extent to which muscle exercised during resistance training influences skeletal muscle growth may provide important methodological considerations for researchers and practitioners alike. From a practical sense, if the competition of resources exists, one may benefit from specializing a certain muscle group to train within a given training period while deemphasizing other muscle groups.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111525"},"PeriodicalIF":2.1,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142705693","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}
Retinopathy of Prematurity (ROP) is a disorder affecting the developing retinal vasculature in preterm infants and is one of the major preventable causes of childhood blindness worldwide. The pathogenesis of ROP is characterized by two distinct phases: Phase 1 occurs when preterm infants are exposed to relative hyperoxia compared to in-utero conditions, either from atmospheric oxygen or supplemental therapy. This exposure causes vaso-obliteration and disrupts peripheral retinal vascularization. In Phase 2, the resulting peripheral avascular retina becomes hypoxic, triggering the release of pro-angiogenic factors like VEGF. This leads to proliferative retinopathy, potentially causing complications such as retinal detachment and permanent blindness in affected neonates. Current management strategies in ROP include intravitreal anti-VEGF injections and laser photocoagulation.
Lactate is a well-known pro-angiogenic molecule. We hypothesize that topical administration of lactate in the form of Ringer’s lactate solution in the eye in Phase 1 of ROP would allow normal retinal vascularisation, potentially preventing the progression of ROP to Phase 2. This approach warrants investigation as a potential therapy to reduce the incidence of phase 2 ROP and its complications.
{"title":"Topical application of Ringer’s lactate for Stage 1 Retinopathy of Prematurity: A potential treatment hypothesis","authors":"Vignesh Elamurugan , Siddharth Narendran , Toshit Varshney , K.Naresh Babu , Renu P Rajan , Pragathi Shankaralingappa , Gopinathan Mathiyazhagan","doi":"10.1016/j.mehy.2024.111523","DOIUrl":"10.1016/j.mehy.2024.111523","url":null,"abstract":"<div><div>Retinopathy of Prematurity (ROP) is a disorder affecting the developing retinal vasculature in preterm infants and is one of the major preventable causes of childhood blindness worldwide. The pathogenesis of ROP is characterized by two distinct phases: Phase 1 occurs when preterm infants are exposed to relative hyperoxia compared to in-utero conditions, either from atmospheric oxygen or supplemental therapy. This exposure causes vaso-obliteration and disrupts peripheral retinal vascularization. In Phase 2, the resulting peripheral avascular retina becomes hypoxic, triggering the release of pro-angiogenic factors like VEGF. This leads to proliferative retinopathy, potentially causing complications such as retinal detachment and permanent blindness in affected neonates. Current management strategies in ROP include intravitreal anti-VEGF injections and laser photocoagulation.</div><div>Lactate is a well-known pro-angiogenic molecule. We hypothesize that topical administration of lactate in the form of Ringer’s lactate solution in the eye in Phase 1 of ROP would allow normal retinal vascularisation, potentially preventing the progression of ROP to Phase 2. This approach warrants investigation as a potential therapy to reduce the<!--> <!-->incidence of phase 2 ROP and its complications.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111523"},"PeriodicalIF":2.1,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142658544","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}
This paper introduces a novel diagnostic approach for disease discrimination through the development of transgenic animals with highly sensitive olfactory receptor cells. Traditional diagnostic methods, such as enzyme-linked immunosorbent assay (ELISA) and nucleic acid-based amplification assay, face challenges related to false positives/negatives, limited sensitivity, or complex and costly procedures. Building on the advances in olfaction understanding and the documented ability of individuals and animals to detect diseases through scent, we propose a paradigm shift in disease diagnosis. The paper highlights the remarkable case of Joy Milne, who identified a distinct odor associated with Parkinson’s disease, leading to subsequent scientific validation. Building upon such research, we hypothesize that transgenic animals, engineered for heightened olfactory capabilities, could revolutionize disease diagnosis. The molecular recognition process and specificity of olfactory receptor cells are explored to elucidate the potential of transgenic animals in reducing the detection limit in diagnostics. Creating genetically modified animals with overexpressed olfactory receptors holds promise for early disease detection, improving prognosis and treatment outcomes. This innovative approach may significantly impact the core principles of illness diagnosis, opening up new perspectives for research and application in the field of disease diagnosis and treatment strategies.
{"title":"Transgenic animal models for diagnosis of Disease: A hypothesis","authors":"Vala Kafil , Benjamin Sreenan , Farzaneh Naghdi Eshratabad , Xiaoshan Zhu","doi":"10.1016/j.mehy.2024.111521","DOIUrl":"10.1016/j.mehy.2024.111521","url":null,"abstract":"<div><div>This paper introduces a novel diagnostic approach for disease discrimination through the development of transgenic animals with highly sensitive olfactory receptor cells. Traditional diagnostic methods, such as enzyme-linked immunosorbent assay (ELISA) and nucleic acid-based amplification assay, face challenges related to false positives/negatives, limited sensitivity, or complex and costly procedures. Building on the advances in olfaction understanding and the documented ability of individuals and animals to detect diseases through scent, we propose a paradigm shift in disease diagnosis. The paper highlights the remarkable case of Joy Milne, who identified a distinct odor associated with Parkinson’s disease, leading to subsequent scientific validation. Building upon such research, we hypothesize that transgenic animals, engineered for heightened olfactory capabilities, could revolutionize disease diagnosis. The molecular recognition process and specificity of olfactory receptor cells are explored to elucidate the potential of transgenic animals in reducing the detection limit in diagnostics. Creating genetically modified animals with overexpressed olfactory receptors holds promise for early disease detection, improving prognosis and treatment outcomes. This innovative approach may significantly impact the core principles of illness diagnosis, opening up new perspectives for research and application in the field of disease diagnosis and treatment strategies.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111521"},"PeriodicalIF":2.1,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142658543","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}
The chronic form of Lyme’s disease is gaining general recognition by the CDC in Atlanta.
The factors contributing to the chronicity of this disease are well-documented in the current literature. Biofilms are known being key-factors for the persistence of many infections and thus may explain the passage to further disease’s chronicity. Other mechanisms of bacteria’s persistence into the human host may involve the ecosystem and the Borrelia’s ability to interact with the surrounding microorganisms, like Candida. Moreover, candidiasis could be at the origin of clinical syndromes resembling Lyme’s disease, via the production of mycotoxins. In addition to antibiotic therapy, we hypothesize that the treatment of chronic Lyme’s disease could include the administration of antifungal drugs. It also seems important to evaluate the drugs that could destroy biofilms. An unconventional and original approach could be to add to the conventional therapy mechanical tools to destroying these biofilms by using low-frequency ultrasound.
{"title":"The importance of combined Candida & Borrelia biofilms in Lyme’s disease and the value of ultrasound treatment: A medical hypothesis","authors":"Jean-Pierre Tournier , Pierre-Yves Marcy , Christian Perronne , Alexis Lacout","doi":"10.1016/j.mehy.2024.111522","DOIUrl":"10.1016/j.mehy.2024.111522","url":null,"abstract":"<div><div>The chronic form of Lyme’s disease is gaining<!--> <!-->general recognition by the CDC in Atlanta.</div><div>The factors contributing to the chronicity of this disease are well-documented in the current literature. Biofilms are known being key-factors for the persistence of many infections and thus may explain the passage to further disease’s chronicity. Other mechanisms of bacteria’s persistence into the human host may involve the ecosystem and the <em>Borrelia</em>’s ability to interact with the surrounding microorganisms, like <em>Candida.</em> Moreover, candidiasis could be at the origin of clinical syndromes resembling Lyme’s disease, via the production of mycotoxins. In addition to antibiotic therapy, we hypothesize that the treatment of chronic Lyme’s disease could include the administration of antifungal drugs. It also seems important to evaluate the drugs that could destroy biofilms. An unconventional and original approach could be to add to the conventional therapy mechanical tools to destroying these biofilms by using low-frequency ultrasound.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111522"},"PeriodicalIF":2.1,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142658542","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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