Medical Hypothesis, Discovery & Innovation (MEHDI) Journals
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    182 research outputs found

    A Ketogenic Diet May Offer Neuroprotection in Glaucoma and Mitochondrial Diseases of the Optic Nerve

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    Glaucoma is a chronic optic nerve disease in which the primary damage occurs to the retinal ganglion cell axons. Therapies that prevent the death of retinal ganglion cells should be theoretically beneficial. Despite promising preclinical studies, however, almost all clinical studies with pharmacological approaches for neuroprotection in neurologic and eye diseases, including glaucoma, have so far failed to show efficacy. As the evidence supporting the neuroprotective efficacy of a ketogenic diet (KD) in a number of neurodegenerative diseases continues to grow, it is conceivable that this metabolic approach might be useful in chronic glaucoma. Putative cellular mechanisms underlying the neuroprotective activity of the KD have been identified in neurological studies, including effects on energy metabolism, the GABA system, glutamate-mediated toxicity, antioxidant mechanisms, programmed cell death, anti-inflammatory mechanisms, and the production of kynurenic acid. Of note, the same mechanisms are thought to be involved in glaucoma. Given these mechanistic similarities, testing the KD for its efficacy in neurodegenerative diseases of the eye is proposed

    Potential Negative Impacts of Social Inequality on Visual Health: the Possible Pathophysiology Mechanisms

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    Letter/ No abstrac

    Ideas to Assist the Underprivileged Dispossessed Individuals

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    Editorial/ No abstrac

    Therapeutic Possibilities of Ceftazidime Nanoparticles in Devastating Pseudomonas Ophthalmic Infections; Keratitis and Endophthalmitis

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    As the number of contact‐lens wearers rises worldwide, Pseudomonas aeruginosa (PA) keratitis is attracting more attention as a major public health issue. Corneal lesions of PA, being the most intimidating complication of contact‐lens wearer, can progress rapidly in spite of local antibiotic treatment, and may result in perforation and the permanent loss of vision. One of the explanations proposed for the evasion of the pathogen from immune responses of the host as well as antibacterial treatment is the fact that invasive clinical isolates of PA have the unusual ability to invade and replicate within surface corneal epithelial cells. In this manner, PA is left with an intracellular sanctuary. Endophthalmitis, albeit rare, is another ophthalmic infection faced by the challenge of drug delivery that can be potentially catastrophic. The present hypothesis is that nanoparticles can carry anti‐pseudomonas antibiotics (e.g. ceftazidime) through the membranes, into the “hidden zone” of the pathogen, hence being an effective and potent therapeutic approach against pseudomonas keratitis and endophthalmitis

    Melatonin and Abeta, Macular Degeneration and Alzheimers Disease: Same Disease, Different Outcomes?

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    Aging is the common denominator and the highest risk factor for macular degeneration and Alzheimers Disease (AD). Important pathological hallmarks common to both diseases are the presence of amyloid β (Aβ) in the senile plaques of the AD brain and in the drusen of age-related macular degeneration (AMD) patients, oxidative stress, and apoptotic cell death. Data suggest that a common pathogenic mechanism might exist between AMD and AD. Brain and eye depend on redox electrons from pyridinic and flavinic nucleotides to produce ATP, and reactive oxygen intermediates (ROI). Disorganization of mitochondrial structure and decline in mitochondrial oxidative phosphorylation (OXPHOS) functioning, as well as hypometabolism and alterations in mitochondrial DNA are aging features. Because ROI damage and mitochondrial dysregulation are prominent in AMD and AD and their relationship to the redox state is unclear we addressed a new hypothesis according to which the interaction of melatonin vs Aβ are intertwined to balance of the intra- and extra-mitochondrial energy production. This balance would be impaired by the ageing process and environmental/genetic factors, ultimately leading to AD and /or AMD

    Does Apoptosis Regulate the Function of Retinal Photoreceptors?

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    Apoptosis, or programmed cell death, is an integral component of developmental biology, embryology, and anatomy. All eukaryotic cells possess the molecular machinery necessary to execute apoptosis. However, dysregulated apoptosis in the form of too much or too little cell death results in diseases such as Alzheimer’s disease, autoimmune disorders, and cancer. It is postulated that apoptosis of the photoreceptors in the retina plays a vital role in mediating vision, and evidence is presented here to support this hypothesis. However, the precise mechanisms that regulate this cell death in photoreceptors have yet to be fully elucidated

    Toxoplasmosis Infection and Cognitive Deficit after Electroconvulsive Treatment (ECT), Is There a Connection?

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    Electroconvulsive treatment (ECT) has developed over 70 years to a modern, effective way of lifting depressive moods. Memory loss and visual acuity after electroconvulsive treatment is the only remaining relevant criticism of the treatment modality when considering the overall rate of remission from this treatment compared to all other treatment modalities. A depressive state impedes memory, and memory improves on several qualities of cognition after treatment. However, the comparison of a person’s memory ability from the months before depression started to the level after a course of ECT is never performed, for obvious reasons. Some infectious diseases are known to influence memory negatively through effects on the dopamine receptors. More specifically, former toxoplasmosis infection may be a factor. Preliminary data on titres of toxoplasma IgG may indicate a connection to the development of long-standing memory problems after ECT

    Intravitreal Bevacizumab as Anti-Vascular Endothelial Growth Factor in the Management of Complications of Proliferative Diabetic Retinopathy

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    Vascular endothelial growth factor (VEGF) has been shown to be an endothelial cell-specific mitogen and an angiogenic inducer in a variety of in vitro and in vivo models. Furthermore, it has been demonstrated to increase retinal vessel permeability by increasing the phosphorylation of tight junction proteins. Recent work has found elevated levels of VEGF in ocular fluids of patients with proliferative diabetic retinopathy (PDR). Thus, it makes sense to consider anti-VEGF treatments in the management of PDR. The purpose of the current research is to determine if intravitreal bevacizumab as anti-VEGF is helpful in the management of complications of PDR

    Is Reticular Macular Disease a Choriocapillaris Perfusion Problem?

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    The etiology of reticular macular disease (RMD), a sub-phenotype of age-related macular degeneration (AMD), is controversial and has not been clarified. RMD is suspected to be a multifactorial, complex disease with genetic, environmental, and systemic factors playing an important role in its origin. Findings from combinations of different imaging modalities suggest that the pattern that characterizes this condition is associated with an alteration of the choriocapillaris blood flow. If the choroid is indeed affected in RMD, the possible linkage with inflammatory or other systemic diseases could be better supported

    Malarial Retinopathy: the Summary on Contemporaneous Hypothesis

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    Malaria is a life-threatening disease caused by parasites that are transmitted to people through the bites of infected mosquitoes. Malaria retinopathy is misdiagnosed in the clinical setting, leading to a failure to treat other life-threatening illnesses. Indeed, the problem can be severe and should be the focus in tropical ophthalmology. In this brief article, the author summarises and comments on the present hypothesis for malarial retinopathy. This hypothesis could be justified by further basic and clinical studies

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