Continuous energy supply, a necessary condition for life, excites a state far from thermodynamic equilibrium, in particular coherent electric polar vibrations depending on water ordering in the cell. Disturbances in oxidative metabolism and coherence are a central issue in cancer development. Oxidative metabolism may be impaired by decreased pyruvate transfer to the mitochondrial matrix, either by parasitic consumption and/or mitochondrial dysfunction. This can in turn lead to disturbance in water molecules' ordering, diminished power, and coherence of the electromagnetic field. In tumors with the Warburg (reverse Warburg) effect, mitochondrial dysfunction affects cancer cells (fibroblasts associated with cancer cells), and the electromagnetic field generated by microtubules in cancer cells has low power (high power due to transport of energy-rich metabolites from fibroblasts), disturbed coherence, and a shifted frequency spectrum according to changed power. Therapeutic strategies restoring mitochondrial function may trigger apoptosis in treated cells; yet, before this step is performed, induction (inhibition) of pyruvate dehydrogenase kinases (phosphatases) may restore the cancer state. In tumor tissues with the reverse Warburg effect, Caveolin-1 levels should be restored and the transport of energy-rich metabolites interrupted to cancer cells. In both cancer phenotypes, achieving permanently reversed mitochondrial dysfunction with metabolic-modulating drugs may be an effective, specific anti-cancer strategy.
- Publication type
- Journal Article MeSH
- Review MeSH
Human and animal diseases are brought about by pathological alterations of production, composition, and conformation of macromolecules and structures in cells. Additional contributing factors include changes in physiological states caused by disturbances of energy supply, energy transduction, energy dissipation in moving or oscillating parts, and parasitic energy consumption. Disturbances of energy states may endanger existence of the system. The cell-mediated immunity (CMI) response of T lymphocytes correlating with their adherence properties was examined using antigen prepared from the serum of inbred laboratory mice strain C3H H(2k) infected with lactate dehydrogenase elevating (LDH) virus. LDH virus is a parasite on the cellular energy system. Significant CMI response was elicited in T lymphocytes prepared from the blood of patients with cancer of different phenotypes, acute myocardial infarctions, schizophrenia, and recurrent spontaneous abortions in early pregnancy from unknown reasons. The CMI response is assumed to monitor transferred information about decreased levels of energy states and decoherence in the cells caused by mitochondrial malfunction, parasitic consumption, production of lactate, and possibly other disturbances. The LDH virus infection or similar pathological processes caused by different agents might be connected with the diseases and monitored by the examined CMI response. A large amount of mitoses with chromosome defects in aborted fetuses suggest increased mutability of genomes caused by defective energy states.
- MeSH
- Immunity, Cellular MeSH
- Energy Metabolism * MeSH
- Lactate dehydrogenase-elevating virus physiology MeSH
- Humans MeSH
- Mice MeSH
- Disease * MeSH
- T-Lymphocytes immunology MeSH
- Pregnancy MeSH
- Cell Survival MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
PURPOSE: To demonstrate the use of in vivo corneal confocal microscopy to reveal the reason for persistent disturbance of vision after a corneal abrasion. CASE REPORT: A 49-year-old man presented with a decrease in visual acuity and monocular diplopia after a traumatic corneal abrasion. Anterior segment optical coherence tomography was not beneficial. In vivo corneal confocal microscopy showed abnormal folding in the basal epithelial layer of the cornea. Based on these findings, a therapeutic abrasion of the affected epithelium was performed. Visual acuity returned to 1.0 after therapeutic abrasion, and overall findings on the eye were within physiological limits. Control corneal confocal microscopic examination confirmed reparation of the structure of epithelial cell layers. CONCLUSIONS: The in vivo corneal confocal microscopy can reveal corneal pathologic abnormality even in cases where other methods are not beneficial. Alongside other modern methods, it may become an important tool to help locate pathologic abnormality accurately and choose the proper therapeutic strategy.
- MeSH
- Debridement MeSH
- Wound Healing physiology MeSH
- Microscopy, Confocal * MeSH
- Middle Aged MeSH
- Humans MeSH
- Tomography, Optical Coherence MeSH
- Eye Injuries diagnosis etiology physiopathology surgery MeSH
- Vision Disorders diagnosis etiology physiopathology MeSH
- Epithelium, Corneal injuries pathology MeSH
- Wounds, Nonpenetrating diagnosis etiology physiopathology surgery MeSH
- Visual Acuity physiology MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Publication type
- Journal Article MeSH
- Case Reports MeSH
- Research Support, Non-U.S. Gov't MeSH
- Keywords
- edém neuroretiny, hypertonická angiopatie,
- MeSH
- Optic Disk physiopathology MeSH
- Adult MeSH
- Fundus Oculi MeSH
- Hypertension * complications physiopathology MeSH
- Hypertensive Retinopathy * diagnosis etiology MeSH
- Middle Aged MeSH
- Humans MeSH
- Macular Edema diagnosis etiology MeSH
- Tomography, Optical Coherence MeSH
- Retinal Hemorrhage diagnosis etiology MeSH
- Vision, Low * diagnosis etiology MeSH
- Visual Acuity MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Publication type
- Case Reports MeSH
Arteriální hypertenze představuje závažný zdravotní problém. Dekompenzace krevního tlaku může být také zdrojem četných očních komplikací. Referujeme tři kasuistická sdělení případů mužů s dekompenzovaným krevním tlakem a změnami na očním pozadí. Při úspěšné kompenzaci krevného tlaku se objektivně zlepšil nález na očním pozadí i zrak.
Arterial hypertension is a serious health problem. Decompensation of blood pressure may cause many ocular complications. We present three case reports of men with decompensated blood pressure and associated ocular complications. Successful compensation of blood pressure leads to objective improvement of fundus changes and vision.
- Keywords
- edém neuroretiny, hypertonická angiopatie,
- MeSH
- Optic Disk physiopathology MeSH
- Adult MeSH
- Fundus Oculi MeSH
- Hypertension * complications physiopathology MeSH
- Hypertensive Retinopathy * diagnosis etiology MeSH
- Middle Aged MeSH
- Humans MeSH
- Macular Edema diagnosis etiology MeSH
- Tomography, Optical Coherence MeSH
- Retinal Hemorrhage diagnosis etiology MeSH
- Vision, Low * diagnosis etiology MeSH
- Visual Acuity MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Publication type
- Case Reports MeSH
Úvod: Diabetická retinopatie je významnou mikrovaskulární komplikací diabetu, protože ohrožuje zrak. Diabetická makulopatie je hlavní příčinou praktické slepoty obyvatel produktivního věku v západních zemích. Metodika vyšetření je založena na digitální fundusfotografii umožňující srovnání výskytu, počtu i velikosti a tvaru patologických ložisek na sítnici při jednotlivých návštěvách nemocného. Nezobrazuje jedinou významnou změnu - chronickou ischemii sítnice. Tu detekujeme pomocí kontrastního vyšetření - fluorescenční angiografie (FAG). Po vpichu kontrastní látky - fluoresceinu - do loketní žíly nám dokáže zobrazit i zóny neperfuze sítnice, které jsou indikací k laserovému ošetření v prevenci proliferativní diabetické retinopatie. V detekci diabetického makulárního edému je významným přínosem optická koherentní tomografie (OCT), která provede optický průřez všemi 10 vrstvami sítnice optickým paprskem. Zvláště její varianta spektrální OCT (S- OCT) je analogií histologického vyšetření sítnice, ovšem živé tkáně. Výsledky: S přibýváním nových vyšetřovacích a léčebných metod je diabetická retinopatie dnes plně diagnostikovatelná a stává se plně léčitelnou. Podmínkou je včasná diagnostika cévních a následně tkáňových změn v sítnici a hlavně v jejím centru. Při uzavřené vnitřní hematoretinální bariéře stačí přesná kontrola diabetu a rizikových faktorů k udržení dobré zrakové ostrosti. Při otevření vnitřní hematoretinální bariéry (poruše těsných spojů mezi endoteliemi retinálních cév) dnes zahajujeme léčbu fenofibráty ve spolupráci s diabetology. Výskyt fokálního makulárního edému redukujeme uzávěrem zdrojů prosakování tekutiny do centrální sítnice laserovým ošetřením mikroaneuryzmat. Difuzní makulární edém laserujeme vydatněji mřížkovou koagulací centrální krajiny i přilehlých oblastí neperfuze sítnice. Došli jsme k závěru, že výrazný makulární edém je často způsoben uzávěrem větve retinální či makulární venuly diabetika. Proto doporučujeme laserovou léčbu makulárního edému ve spolupráci s diabetology doplňovat trombolytiky. Cílem léčby diabetického makulárního edému je jeho včasná likvidace před vznikem nevratného poškození zevních segmentů a později buněk fotoreceptorů. Tyto změny jsou dnes dobře detekovatelné na S- OCT a jsou příčinou zmíněné praktické slepoty diabetika. Diskuze: Zlatým standardem léčby diabetického makulárního edému i diabetické retinopatie je laserová léčba. Bez přesné kompenzace diabetu a rizikových faktorů postrádá účinnost. Někteří autoři nahrazují laserový zákrok u diabetického makulárního edému nejen s makulární trakcí dražším a náročnějším operačním zákrokem (pars plana vitrektomií s peelingem lamina limitans interna) provedeným již v časných stadiích. Závěr: Základem úspěšnosti léčby diabetické retinopatie a makulopatie je prevence vzniku mikroangiopatie sítnicových cév přesnou kompenzací diabetu a rizikových faktorů. Vzniklou diabetickou retinopatii i makulopatii dnes umíme úspěšně léčit včetně stabilizace zrakových funkcí. Podmínkou je včasná diagnostika sítnicových změn.
Introduction: Diabetic retinopathy is an important microvascular complication of diabetes as it threatens the vision. Diabetic maculopathy is the main cause of legal blindness in the adult population in western countries. The examination method involves digital fundus photography that enables comparison of the incidence, number as well as the size and the shape of pathological foci on the retina during patient visits. It, however, does not depict one important change – chronic retinal ischemia. This is identified using contrast imaging – fluorescein angiography (FAG). Administration of a contrast medium – fluorescein – into cubital vein enables depiction of non‑perfused regions of the retina that form the basis for laser therapy indication as part of the prevention of proliferative diabetic retinopathy. Optical coherence tomography (OCT), during which an optical beam makes a cross‑ section through all 10 layers of the retina, is an important advance in the diagnostics of diabetic macular oedema. The spectral OCT (S‑ OCT) in particular is an analogy of a histological examination of retina but on a living tissue. Results: Owing to the advances in examination techniques and treatment methods, diabetic neuropathy can now be diagnosed and treated. Early diagnosis of vascular and, consequently, tissue changes in the retina, and in its midsection in particular, is a prerequisite. Tight control of diabetes and the risk factors is sufficient to maintain good visual acuity in patients with intact inner blood‑ retinal barrier. In collaboration with a diabetologist, fenofibrates are used as the first line treatment when the inner blood‑ retinal barrier is disturbed (damaged tight junctions between endothelial cells of retinal vessels). To reduce focal macular oedema, the sources of fluid leakage into central retina are occluded using laser interventions on microaneurysms. In diffuse macular oedema, a more intensive laser technique using grid laser coagulation is applied to the central region as well as the surrounding areas of non‑perfused retina. It is our view that major macular oedemas often result from an occlusion of a branch of retinal or macular venule. This is why we recommend complementing, in collaboration with a diabetologist, laser treatment of macular oedema with trombolytics. The aim of diabetic macular oedema treatment is its early elimination to avoid irreversible damage to the outer segments and later to photoreceptor cells. These changes are the main cause of the previously mentioned legal blindness in diabetic patients and are well identifiable on S‑ OCT. Discussion: Laser therapy is the gold standard in the treatment of diabetic macular oedema as well as diabetic retinopathy. However, efficacy is lacking if diabetes and the risk factors are not tightly controlled. Instead of laser therapy to treat diabetic macular oedema with or without macular traction, some authors use a more expensive and more complicated surgery technique (pars plana vitrectomy with internal limiting membrane peeling) performed at early stages of the disease. Conclusion: Prevention of microangiopathy of retinal vessels through tight compensation of diabetes and the risk factors form the basis of successful treatment of diabetic retinopathy and maculopathy. At present, we are able to successfully treat developed diabetic retinopathy as well as maculaopathy, including stabilisation of visual function, subject to early diagnosis of retinal changes.
- MeSH
- Diabetic Retinopathy diagnosis surgery prevention & control MeSH
- Fluorescein Angiography MeSH
- Laser Coagulation MeSH
- Humans MeSH
- Macular Edema diagnosis surgery MeSH
- Tomography, Optical Coherence MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
Autoři uvádí kazuistiku tříleté dívky s bilaterálními idiopatickými mnohočetnými cystami v předních partiích sklivce. V průběhu vyšetření pro intermitentní esotropii pravého oka byly diagnostikovány kromě hypermetropie, astigmatismu a anisometropie pigmentované změny v periferních retrolentárních prostorech obou očí. Klinické vyšetření v celkové anestezii odhalilo oboustranné mnohočetné pigmentované a nepohyblivé vitreální cysty. Bylo nalezeno pět téměř kulových, různě velkých, průhledných, avšak na povrchu jemně pigmentovaných cyst v předním sklivci pravého oka a čtyři obdobné na oku levém, viditelné pouze při dilatovaných zornicích. Navození mydriázy bylo pomalejší a vyžadovalo více mydriatik než u dětí stejného věku. Dívku sledujeme deset let. Okluzní léčba amblyopie byla prováděna do devíti let věku. Léčba refrakční odchylky a esotropie korekcí hypermetropie, astigmatismu a anisometropie trvá. Nejlepší korigovaná zraková ostrost nyní třináctileté dívky, celkově zdravě a bez mentálního deficitu, je 1,0 na obou očích, bez jakékoli poruchy vidění, kterou by sama pozorovala (VOP: 1,0 s +3,5 = -3,5/175, VOL: 1,0 s +7,5 = -3,0/35). Pozice všech cyst zůstala stejná v průběhu celého sledování, s úvodním doporučením vyvarovat se celoživotně úderů do hlavy (hlavně při sportu). Zaznamenali jsme vytvoření a v čase i mírnou progresi lokalizované kortikální katarakty v místě kontaktu jedné z cyst se zadní plochou čočky v inferonazálním kvadrantu na pravém oku, stav sledujeme. OCT zobrazení odhalilo drobný retinální lamelární extrafoveální defekt v zadním pólu pravého oka, který rovněž sledujeme.
The authors present a case report of a three-year-old female patient with bilateral multiple anterior vitreous cysts. During examination for intermittent esotropia of the right eye was diagnosed not only hypermetropia, astigmatism and anisometropia, but also pigmented changes in peripheral retrolental space of both eyes. Clinical examination under general anaesthesia revealed bilateral multiple pigmented immobile vitreous cysts. There were five almost spherical, translucent, but slightly pigmented cysts on its cover on the right eye and four similar on the left, but visible only with dilated pupils. A dilating of pupils was slow and required more mydriatics than in similar aged children. Follow up period is ten years now. Occlusion therapy of amblyopia was performed to nine years of age. Treatment of refractive error and esotropia with correction for hypermetropia, astigmatism and anisometropia continues. Best corrected visual acuity in thirteen-year-old girl is 1,0 in both eyes without any visual disturbances described by patient. Corrected visual acuity in each eye is 1,0, right eye with +3,5 D sph., -3,5D cyl., axis 175°, left eye with +7,5 D sph., -3,0 D cyl., axis 35°. Patient is otherwise healthy and without any mental deficit. Position of all cysts remains unchanged and stabile during the follow up period (with recommendation to avoid hits to the head for all time, mainly in sports). Formation and slow progression of partial cortical cataract in the area of contact of the lens and one cyst in inferonasal quadrant of the lens on the right eye is monitored. A lamellar retinal extrafoveal defect of posterior pole of the right eye was found by OCT imaging.
- Keywords
- pigmentovaná vitreální cysta,
- MeSH
- Astigmatism MeSH
- Cysts * diagnosis etiology therapy congenital MeSH
- Fovea Centralis pathology MeSH
- Hyperopia MeSH
- Cataract MeSH
- Humans MeSH
- Longitudinal Studies MeSH
- Tomography, Optical Coherence MeSH
- Child, Preschool MeSH
- Vitreous Body * MeSH
- Check Tag
- Humans MeSH
- Child, Preschool MeSH
- Female MeSH
- Publication type
- Case Reports MeSH
BACKGROUND: Central serous chorioretinopathy (CSC) is characterised by a serous detachment of the neurosensory retina in the macula. Chronic CSC tends to affect older individuals with a less favourable visual outcome. Photodynamic therapy (PDT) with verteporfin is a possible therapeutic approach in cases of CSC with no tendency for spontaneous resorption. PDT has shown good anatomic and functional results in treating chronic CSC. For the purpose of diminishing side effects, modifications of the standard protocol were used. MATERIALS AND METHODS: This is a retrospective study of 32 eyes with CSC of 32 patients treated by half-fluence PDT. The patients underwent complete ophthalmology examination. On optical coherence tomography (OCT) we measured central retinal thickness (CRT), the outer nuclear layer (ONL), presence of subfoveolar detachment of retinal pigment epithelium (PED), disturbance of external limiting membrane (ELM), morphological changes in the inner segment/outer segment (IS/OS) line and retinal pigment epithelium (RPE) atrophy. We evaluated at baseline, 3 and 12 months after PDT. RESULTS: The mean BCVA at baseline was 0.41 ± 0.23 log MAR, the mean BCVA at 3 months was 0.24 ± 0.20 and at the end of the follow-up it was 0.23 ± 0.200. We observed statistically significant improvements of visual acuity after 3 and 12 months (p < 0.001, Wilcoxon test). The mean central retinal thickness at baseline was 373 ± 87 µm, the mean CRT after 3 months was 234 ± 42 µm and after 12 months 223 ± 39 µm. A significant reduction from baseline was seen after 3 months and 12 months (p < 0.001, Wilcoxon test). Baseline ONL reached 80 ± 27 µm, after 3 months it was 78 ± 20 and after 12 months it was 74 ± 20 µm. We observed a statistically significant change in diminishing the amount of PED after PDT after 3 months and after 12 months (p = 0.021, McNemar's test). We observed that in patients with RPE ablation, there is lower chance for the restitution of the IS/OS layer (p = 0.045, Mann-Whitney test). We observed a negative association between the improvement of visual acuity after 12 months and the presence of RPE ablation (p = 0.031, Mann-Whitney test). Restitution of ELM was significantly more often in patients with shorter duration of symptoms, (p = 0.027 after 3 months, p = 0.033 after 12 months after PDT, Spearman correlation). Neither ocular nor systemic adverse effects were observed during the follow-up period. CONCLUSIONS: Half-fluence PDT treatment has shown to be a usually safe and often effective therapy in patients with chronic CSC. This study suggests that the most important predictive factor is baseline visual acuity. The important anatomical change detected using OCT is a thinning of the outer nuclear layer. Nonetheless, other studies with a larger number of patients and a longer follow-up are required.
- MeSH
- Central Serous Chorioretinopathy diagnosis drug therapy physiopathology MeSH
- Chronic Disease MeSH
- Adult MeSH
- Fluorescein Angiography MeSH
- Photochemotherapy methods MeSH
- Photosensitizing Agents therapeutic use MeSH
- Fundus Oculi MeSH
- Middle Aged MeSH
- Humans MeSH
- Follow-Up Studies MeSH
- Tomography, Optical Coherence MeSH
- Porphyrins therapeutic use MeSH
- Retinal Pigment Epithelium pathology MeSH
- Retrospective Studies MeSH
- Aged MeSH
- Treatment Outcome MeSH
- Visual Acuity * MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
Mitochondrial dysfunction is a central defect in cells creating the Warburg and reverse Warburg effect cancers. However, the link between mitochondrial dysfunction and cancer has not yet been clearly explained. Decrease of mitochondrial oxidative energy production to about 50 % in comparison with healthy cells may be caused by inhibition of pyruvate transfer into mitochondrial matrix and/or disturbed H+ ion transfer across inner mitochondrial membrane into cytosol. Lowering of the inner membrane potential and shifting of the working point of mitochondria to high values of pH above an intermediate point causes reorganization of the ordered water layer at the mitochondrial membrane. The reorganized ordered water layers at high pH values release electrons which are transferred to the cytosol rim of the layer. The electrons damp electromagnetic activity of Warburg effect cancer cells or fibroblasts associated with reverse Warburg effect cancer cells leading to lowered electromagnetic activity, disturbed coherence, increased frequency of oscillations and decreased level of biological functions. In reverse Warburg effect cancers, associated fibroblasts supply energy-rich metabolites to the cancer cell resulting in increased power of electromagnetic field, fluctuations due to shift of oscillations to an unstable nonlinear region, decreased frequency and loss of coherence.
- MeSH
- Electromagnetic Fields * MeSH
- Fibroblasts pathology MeSH
- Hydrogen-Ion Concentration MeSH
- Cells, Cultured MeSH
- Humans MeSH
- Mitochondria pathology MeSH
- Neoplasms pathology MeSH
- Oscillometry MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH