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Medical hypotheses
Churchill Livingstone
Medical hypotheses

Churchill Livingstone

0306-9877

Medical hypotheses/Journal Medical hypothesesAHCISCIISTP
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    COVID-19 patients could be at high risk for dry socket

    Domah, TrivinaRaj, A. ThirumalShetty, LakshmiNahar, Shruti...
    1页

    Acute kidney injury due to COVID-19 and the circadian rhythm

    Mercan, MerveSehirli, Ahmet OzerChukwunyere, UgochukwuAbacioglu, Nurettin...
    1页
    查看更多>>摘要:The COVID-19 pandemic caused by the novel coronavirus (SARS-CoV-2) affects several organs including the kidneys。 When examining patients with acute kidney injury (AKI) due to COVID-19, it is important to consider the circadian rhythm because in addition to its biological clock function, disruption of the circadian rhythm has been reported to be associated with the pathogenesis of several disorders, including AKI。 Angiotensin-converting enzyme 2 (ACE2), an important component of the renin-angiotensin-aldosterone system (RAAS), displays circadian rhythmicity。 Studies have shown that over-expression of human ACE2 increases the replication of SARS-CoV-2, which may lead to disruptions and tissue damage due to the suppression of the brain and muscle ARNT-like protein-1(Bmal1) gene and high pro-inflammatory cytokines expressions in the tissues。 Therefore, understanding and regulating the circadian rhythm and expression pattern of the key components of RAAS can prevent or reduce the severity of acute kidney injury that may occur with COVID-19 infection。

    Closing the portal to SARS-CoV-2 cellular entry: May open newer avenues ...

    Sharma, RidhimaMagoon, RohanKaushal, Brajesh
    1页

    Reduction in the incidence of infectious diseases during the COVID-19 pandemic: A hypothesis

    MohammadSadeghi, Ashkan
    1页

    Peptidyl arginine deiminase 4 and its potential role in Alzheimer's disease

    Wang, Li-lingSong, Ye-pingMi, Jian-huaDing, Meng-lei...
    1页
    查看更多>>摘要:Alzheimer's disease (AD) is the main cause of dementia, and its pathogenesis is still not clear。 Peptidyl arginine deiminases 4(PAD4) as one of the important members of PAD family, is the only protein with nuclear transfer function, it can regulate the expression of many proteins through citrullinating histone。 PAD4 can also interact with many transcription factors, involved in regulating gene expression。 PAD4 expression is closely related to the inflammatory factors secreted, cell autophagy, tumorigenesis and other neurodegenerative diseases。 More importantly, PAD4 and its citrullinated protein were found in cortical and hippocampal neurons of AD patients。 To study the expression and regulatory pathway of PAD4 in vivo and in vitro experiments on AD may be of helpful to elucidate the pathogenesis of AD。 Meanwhile, detection of anti-citrullinated antibody will have potential value as novel biomarkers of AD。

    Folinic acid over rescue of high dose methotrexate: How problematic citations conserve discredited concepts

    Cohen, Ian J.
    1页
    查看更多>>摘要:Background: The outdated axiom that the dose of Folinic acid (FA) rescue used after high dose Methotrexate (HDMTX) should be kept to a minimum in order to prevent a reduction of prognosis ("over rescue") continues to be expressed even though the concept has been seriously challenged。

    The plausible mechanisms of tramadol for treatment of COVID-19

    El-Ashmawy, Nahla E.Lashin, Abdel-Halim A.Okasha, Kamal M.Kamer, Amal M. Abo...
    1页
    查看更多>>摘要:Currently, no single medication has been approved for the management of coronavirus disease-2019 (COVID-19) caused by the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)。 Therefore, drug repositioning by investigating the use of existing drugs for management of COVID-19 patients is considered a desperate need。 Tramadol is a commonly prescribed analgesic drug for treatment of moderate to severe pain with less potential for dependence and respiratory depression。 Multiple evidence support that tramadol is a promising drug for treatment of COVID-19 patients。 Herein, we discuss the possible beneficial effects of using tramadol against SARS-CoV-2 infection and their underlying mechanism of action。 The anti-inflammatory effect of tramadol may help to suppress the COVID-19 related cytokine storm through decreasing interleukin (IL)-6, tumor necrosis factor-alpha (TNF-alpha), and C-reactive protein (CRP)。 Besides, tramadol activates natural killer (NK) and T-cells and enhances IL-2 secretion, which produce immune-enhancing effect against SARS-CoV-2。 Recent studies confirmed that COVID-19 patients with acute respiratory failure showed increased fibrin formation and polymerization that may lead to thrombosis。 Tramadol owing to its hypocoagulable effect may protect against venous thromboembolism in these patients。 Moreover, tramadol can exert a cardioprotective effect via decreasing lactate dehydrogenase (LDH) level which is elevated in most of patients with COVID-19。 Furthermore, the severity and mortality of COVID-19 have been correlated with old age patients, which may be due to the lack of antioxidant mechanisms and increased oxidative damage。 Tramadol could protect COVID-19 patient from disease complications by increases the antioxidant enzymes superoxide dismutase and glutathione peroxidase while diminished malondialdehyde。 More interestingly, tramadol as an effective analgesic and antitussive may have a beneficial effect on COVID-19 patients suffering from cough, headache, ache, and pain。 The tramadol anti-psychotic effect may also protect against psychiatric disorders associated with SARS-CoV-2 infection。 Moreover, tramadol has bactericidal activity against a wide range of pathogens including Pseudomonas aeruginosa which is common in severe COVID-19 patients leading to pneumonia with worse clinical outcomes。 Therefore, we hypothesize that tramadol might be a promising adjuvant therapeutic option against SARS-CoV-2 infection。 Based on that, tramadol should be considered as adjuvant therapy for COVID-19 clinical trials。

    COVID-19 and chronic fatigue syndrome: Is the worst yet to come?

    Wostyn, Peter
    1页
    查看更多>>摘要:There has been concern about possible long-term sequelae resembling myalgic encephalomyelitis/chronic fatigue syndrome in COVID-19 patients。 Clarifying the mechanisms underlying such a "post-COVID-19 fatigue syndrome" is essential for the development of preventive and early treatment methods for this syndrome。 In the present paper, by integrating insights pertaining to the glymphatic system and the nasal cerebrospinal fluid outflow pathway with findings in patients with chronic fatigue syndrome, idiopathic intracranial hypertension, and COVID-19, I provide a coherent conceptual framework for understanding the pathophysiology of post-COVID-19 fatigue syndrome。 According to this hypothesis, this syndrome may result from damage to olfactory sensory neurons, causing reduced outflow of cerebrospinal fluid through the cribriform plate, and further leading to congestion of the glymphatic system with subsequent toxic build-up within the central nervous system。 I further postulate that patients with post-COVID-19 fatigue syndrome may benefit from cerebrospinal fluid drainage by restoring glymphatic transport and waste removal from the brain。 Obviously, further research is required to provide further evidence for the presence of this post-viral syndrome, and to provide additional insight regarding the relative contribution of the glymphatic-lymphatic system to it。 Other mechanisms may also be involved。 If confirmed, the glymphatic-lymphatic system could represent a target in combating post-COVID-19 fatigue syndrome。 Moreover, further research in this area could also provide new insights into the understanding of chronic fatigue syndrome。

    Polycations and polyanions in SARS-CoV-2 infection

    Ginsburg, IFibach, E.
    1页
    查看更多>>摘要:We hypothesize that polycations, such as nuclear histones, released by neutrophils COVID-19 aggravate COVID-19 by multiple mechanisms: (A) Neutralization of the electrostatic repulsion between the virus particles and the cell membrane, thereby enhancing receptor-mediated entry。 (B) Binding to the virus particles, thereby inducing opsonin-mediated endocytosis。 (C) Adding to the cytotoxicity, in conjunction with oxidants, cytokines and other pro-inflammatory substances secreted by cells of the innate immunity system。 These effects may be alleviated by the administration of negatively charged polyanions such as heparins and heparinoids。

    COVID-19/takotsubo/spontaneous coronary artery dissection: Lost in the Bermuda triangle

    Madias, John E.
    1页