Levodopa as Treatment for Adults with Amblyopia

2017 ◽  
Vol 68 (7) ◽  
pp. 1595-1597
Author(s):  
Camelia Bogdanici ◽  
Tudor Bogdanici ◽  
Andreea Moraru ◽  
Danut Costin ◽  
Crenguta Feraru

Levodopa is a medication used in treatment for Parkinson�s disease, which is associated with low levels of a chemical called dopamine in the brain. Levodopa is turned into dopamine in the body and therefore increases levels of this chemical. Levodopa was used as a treatment of amblyopia alone or in combination with classical treatment of occlusion. Visual acuity is improved after treatment with oral Levodopa. When is used as an adjunct to the occlusion therapy, Levodopa can be associated with long-term improvement in the vision, and may have also better compliance for patching. Levodopa stimulates the brain plasticity in adult age and can be used in treatment for amblyopia. Patients have also an increase of the visual acuity after orthoptic treatment for amblyopia and when Levodopa is administered, the vision increases much more. Contrary to the classical conception, according to which amblyopia cannot be treated after 10-12 years of age and it is untreatable in adults, studies about treatment with Levodopa in amblyopic eyes, may allow the improvement of the visual acuity in adults, as well.

Author(s):  
Angela Duckworth ◽  

For more than a century, scientists have known that acute stress activates the fight-or-flight response. When your life is on the line, your body reacts instantly: your heart races, your breath quickens, and a cascade of hormones sets off physiological changes that collectively improve your odds of survival. More recently, scientists have come to understand that the fight-or-flight response takes a toll on the brain and the body—particularly when stress is chronic rather than acute. Systems designed to handle transient threats also react to stress that occurs again and again, for weeks, months, or years. It turns out that poverty, abuse, and other forms of adversity repeatedly activate the fight-or-flight response, leading to long-term effects on the immune system and brain, which in turn increase the risk for an array of illnesses, including asthma, diabetes, arthritis, depression, and cardiovascular disease. Pioneering neuroscientist Bruce McEwen called this burden of chronic stress “allostatic load.”


1988 ◽  
Vol 65 (1) ◽  
pp. 482-486 ◽  
Author(s):  
K. Shiraki ◽  
S. Sagawa ◽  
F. Tajima ◽  
A. Yokota ◽  
M. Hashimoto ◽  
...  

Temperature within the brain and the esophagus and at the tympanum were obtained in a 12-yr-old male in a series of experiments that began 8 days after surgery for implantation of a drainage catheter. Fanning the face did reduce tympanic temperature but not temperature in the brain; brain temperatures followed esophageal temperatures. In long-term monitoring, temperature in the lateral ventricle was 0.5 degree C above esophageal temperature and 0.2 degree C below that in white matter 1 cm above, with the offsets fixed throughout the overnight cycle. All temperatures went through similar excursions when the face was excluded from fanning applied to the body. These observations highlight the fact that in humans the defense against hyperthermia takes advantage of cooling distributed over the entire skin surface.


1986 ◽  
Vol 112 (1) ◽  
pp. 93-99 ◽  
Author(s):  
B.J. Potter ◽  
G. H. McIntosh ◽  
M. T. Mano ◽  
P. A. Baghurst ◽  
J. Chavadej ◽  
...  

Abstract. Merino ewes were surgically thyroidectomized, and mated 6 weeks later when their plasma thyroxine (T4) levels were negligible. Their foetuses were delivered by hysterotomy at 52, 71, 84, 98, 125, 140 days gestation or at term (150 days). Despite the very low levels of T4 in maternal plasma, the concentrations of T4 in foetal plasma were not significantly different after 71 days gestation from those of foetuses of sham-operated (control) ewes. Foetal brain and body weights, however, were reduced from 71 days compared to those of foetuses of sham-operated ewes. The foetal brain weights but not the body weights were restored to normal from 125 days to term. In additon to the weights, cell number (DNA) and cell size (protein:DNA ratio) appeared to be normal in the neonatal brain at parturition and this was confirmed by histological examination of the brains. Thus lack of maternal thyroid hormones in early pregnancy may cause a reduction in brain and body growth in the foetus which, in the case of the brain, appears to be restored to normal after the onset of foetal thyroid function.


2007 ◽  
Vol 293 (4) ◽  
pp. E965-E969 ◽  
Author(s):  
Markus Neumeier ◽  
Johanna Weigert ◽  
Roland Buettner ◽  
Josef Wanninger ◽  
Andreas Schäffler ◽  
...  

Adiponectin circulates in the body in high concentrations, and 100-fold lower amounts were described in the cerebrospinal fluid (CSF) of mice, whereas in humans, contradictory results have been published. To clarify whether adiponectin is present in human CSF and is derived from the circulation, it was determined in human CSF and plasma of 52 nonselected patients. Adiponectin was detected by immunoblot in CSF and was quantified in CSF and serum by ELISA. CSF adiponectin was positively correlated to systemic levels, and the CSF/serum adiponectin ratio was correlated to the CSF/serum albumin ratio. Furthermore, disturbed function of the blood-brain barrier (BBB) was associated with an elevated CSF/serum adiponectin ratio. Adiponectin mRNA was not found in the brain, indicating that adiponectin crosses the BBB and/or the blood-cerebrospinal fluid barrier (BCB). Rat adiponectin with a COOH-terminal tag was injected into the tail vein of rats and was detected 3 h later in CSF. However, CSF adiponectin in humans and rats was ∼0.1% of the serum concentration and therefore was below the 0.5% expected in the CSF because of the residual leakage of an undisturbed BBB/BCB. Taken together, data from the present study show that adiponectin in human CSF is far below the level expected by the baseline BBB/BCB permeability, indicating that adiponectin enters the brain much less efficiently than albumin, thus supporting recent data that exclude adiponectin transport to the CSF. Additional studies are needed to reveal whether these low levels of adiponectin in CSF have a physiological function.


Ciencia Unemi ◽  
2018 ◽  
Vol 10 (25) ◽  
pp. 123
Author(s):  
Maria Alejandra Vallejo-Johnson ◽  
Patricia Marcial-Velastegui

Existen diversos estudios que proponen las causas de la Enfermedad de Alzheimer (EA), las cuales pueden ser: biológicas, genéticas, cronológicas y ambientales, dentro de ésta última se encuentra el estrés como una influencia para el inicio de dicha patología. Según las distintas teorías del estrés, el sujeto, al encontrarse frente a una situación estresante, sufre diversos cambios en su cuerpo para sobrellevar dicho acontecimiento. El cerebro es el encargado de poner al cuerpo en alerta y en marcha para actuar frente a dicho cambio. El estrés prolongado conlleva a alteraciones en las vías cerebrales, específicamente un daño neuronal del hipocampo, el cual es el encargado de los recuerdos y memoria. Éste al verse afectado, repercute en la memoria del sujeto y por lo tanto empieza a fallar; el sujeto se ve en la incapacidad para recordar y realizar distintas actividades rutinarias. Mediante la investigación documental y encuestas a profesionales de la salud, se obtuvo información tanto del estrés como de la Enfermedad de Alzheimer para luego concluir en la influencia del mismo en el origen de la enfermedad. Se concluye que el estrés perenne repercute en la muerte de neuronas del hipocampo lo que conlleva a la EA. AbstractThere are different studies that propose that the causes of Alzheimer might be biological, genetic, chronological and environmental. Within the environmental aspects, the stress influences the beginning of this pathology. There are several studies that propose the causes of Alzheimer's disease (AD), which can be: biological, genetic, chronological and environmental, within the latter is the stress that influences the beginning of this pathology. According to different theories of stress, the individual, while facing a stressful situation, experiences many changes in the body in order to deal with this situation. The brain is in charge of alerting the body to protect itself against that change. The long-term stress alters the brain pathways, producing specifically a neuronal damage in the hippocampus that is responsible for memories and memory. This affects memory and therefore individual begins to fail, and then, the person cannot remember how to do the daily routine. Through bibliographical research and surveys applied to healthcare professionals, information was obtained on both stress and Alzheimer's disease to establish the influence of that condition on the disease. The study concludes that long-term stress affects the death of neurons in the hippocampus, which leads to AD.


Author(s):  
A. Aleksandrov ◽  
V. Konopelniuk ◽  
I. Kompanets ◽  
L. Ostapchenko

Obesity is one of the most common complex health problem. The pathway of serotonin synthesis takes part in neuroendocrine regulation, as well as in the regulation of a number of behavioral functions of the body and fat deposition. Serotonin is a mediator of the amine nature, which functions as a neurotransmitter and tissue hormone. The greatest amount of serotonin is synthesized in the brain and 12 duodenum. As a neurotransmitter, serotonin affects both directly and indirectly on the function of most brain cells. Female hormone progesterone influence on serotonin functions. One of the effect of progesterone is increasing of amount of fat tissue during the pregnancy. Long-term using of progesterone in hormone substitution therapy or as part of contraception also lead to fat accumulation effect. The levels of activity of serotonergic system enzymes, tryptophan hydroxylase, tryptophan decarboxylase and monoamine oxidase (MAO), and tryptophan, 5-hydroxytryptophan, serotonin and 5-hydroxyindoleacetic acid concentrations in the rat brain under obesity conditions caused by prolonged administration of progesterone were determined in this study. Studies have shown that the content of tryptophan, 5-hydroxytryptophan, serotonin and 5-hydroxyindoleacetic acid in the brain of rats under obesity caused by prolonged administration of progesterone increased in comparison with the rats of the control group. The levels of tryptophan hydroxylase and MAO activity decreased, and tryptophan decarboxylase activity levels increased in the rat brain under obesity conditions caused by prolonged administration of progesterone. Thus, as a result of our studies, we found an imbalance in the system of serotonin metabolism in the brain of rats with the development of hormonal obesity induced by prolonged administration of progesterone, which may indicate the involvement of the serotonergic neurotransmitter system in the mechanisms of the development of obesity and concomitant diseases.


2021 ◽  
Vol 17 (2) ◽  
pp. 6-15
Author(s):  
L.A. Dziak ◽  
O.S. Tsurkalenko ◽  
K.V. Chekha ◽  
V.M. Suk

Coronavirus infection is a systemic pathology resulting in impairment of the nervous system. The involvement of the central nervous system in COVID-19 is diverse by clinical manifestations and main mechanisms. The mechanisms of interrelations between SARS-CoV-2 and the nervous system include a direct virus-induced lesion of the central nervous system, inflammatory-mediated impairment, thrombus burden, and impairment caused by hypoxia and homeostasis. Due to the multi-factor mechanisms (viral, immune, hypoxic, hypercoagulation), the SARS-CoV-2 infection can cause a wide range of neurological disorders involving both the central and peripheral nervous system and end organs. Dizziness, headache, altered level of consciousness, acute cerebrovascular diseases, hypogeusia, hyposmia, peripheral neuropathies, sleep disorders, delirium, neuralgia, myalgia are the most common signs. The structural and functional changes in various organs and systems and many neurological symptoms are determined to persist after COVID-19. Regardless of the numerous clinical reports about the neurological and psychiatric symptoms of COVID-19 as before it is difficult to determine if they are associated with the direct or indirect impact of viral infection or they are secondary to hypoxia, sepsis, cytokine reaction, and multiple organ failure. Penetrated the brain, COVID-19 can impact the other organs and systems and the body in general. Given the mechanisms of impairment, the survivors after COVID-19 with the infection penetrated the brain are more susceptible to more serious diseases such as Parkinson’s disease, cognitive decline, multiple sclerosis, and other autoimmune diseases. Given the multi-factor pathogenesis of COVID-19 resulting in long-term persistence of the clinical symptoms due to impaired neuroplasticity and neurogenesis followed by cholinergic deficiency, the usage of Neuroxon® 1000 mg a day with twice-day dosing for 30 days. Also, a long-term follow-up and control over the COVID-19 patients are recommended for the prophylaxis, timely determination, and correction of long-term complications.


Genetika ◽  
2020 ◽  
Vol 52 (1) ◽  
pp. 379-392
Author(s):  
Jakub Kubiś ◽  
Marek Kmiec ◽  
Jan Bińkowski ◽  
Marta Sróżyńska

Arsenic is a metallic element commonly found in soil, water and plants, and thereby can easily enter the food chain. When arsenic enters the body through food consumption, it subsequently passes into the cells through water channels (AQP) and glucose transporters (GLUT), where it may exert a various metabolic alterations including genotoxicity, which may finally promote carcinogenesis. However, there are human populations showing a reduced adverse effects of arsenic. This is mainly due to a natural selection caused by a long-term environmental exposure to a large doses of arsenic. Aquaporins AQP3, AQP7, AQP9, AQP10 and glucose transporters SLC2A1 (GLUT1), SLC2A4 (GLUT4) are considered as the candidate genes associated with resistance to arsenic in the carcinogenesis process as they are closely related to the occurrence of a various types of cancers, while their products are associated with arsenic transport.


Author(s):  
Töres Theorell

This chapter is devoted to the biology of singing. Immediate effects have been extensively scientifically studied. Breathing and its synchronization with heart rate variability has been an important theme. Endocrine (endorphins, oxytocin, cortisol, testosterone) and immunological (TNF alpha, fibrinogen, immunoglobulines) reactions have also been studied during singing. In collective singing, cohesiveness is a major factor. Singing in a group during a choir rehearsal has stronger stimulation effects on oxytocin secretion than chatting in the same group. High levels of oxtytocin coincide with strong feelings of cohesiveness. In addition, oxytocin dampens anxiety and pain. Long-term effects of singing training and regular practice have been less extensively studied but there is evidence that singing training may influence such things as the brain´s development, the ability to synchronize heart and lung function, and the level of regenerative activity in the body.


2021 ◽  
Vol 171 (2) ◽  
pp. 228-231
Author(s):  
M. S. Bugaeva ◽  
◽  
O. I. Bondarev ◽  
N. N. Mikhailova ◽  
A. G. Zhukova ◽  
...  
Keyword(s):  
The Body ◽  

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