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måndag 23 mars 2015

Lyhyt altistus 900 MHz elektromagneettisellle säteilylle (radioaaltofrekvenssille).

Bratisl Lek Listy. 2015;116(2):101-3. Effect of Short-term 900 MHz low level electromagnetic radiation exposure on blood serotonin and glutamate levels.
 
TAUSTA:  Tiedetään että pitkäaikainen altistus matalataajuiselle elektromagneettiselle säteilylle (LLER) ,jota kännykästä tulee, voi aiheuttaa haittoja

BACKGROUND:
Long term exposure to low level electromagnetic radiation (LLER) by using cellular phones causes serious health problems.

Koejärjestelyssä käytettiin Wistar rottia.  ja ne altistettiin 45 minuutin LLER:lle  900 MHz etäisyydeltä, joka vastasi kännykän käyttäjien  etäisyyttä altistukseen.  Siten otettiin verinäyte ja katsottiin  serotoniinit ja  glutamiinihapot. Veren serotoniinit olivat   kaiketi nousseet merkitsevästi  mutta glutamiinihapoissa ei ollut muutosta. Jos  5-HT pitoisuudet siten nousevat altistuksesta, se  voinee johtaa  viivästyneeseen  oppimiskykyyn spatiaalisen muistin vajeeseen.

METHODS:  Ten male Wistar Albino rats were anesthetized 30 min before the LLER exposure, 0.5 ml blood was taken from the tail vein of rats in order to determine control values. Rats were grouped by three and placed on a plexi-glass flat. A fixed equivalent frequency emitter device was used. A sign to be an electromagnetic field 15.14 V/m (608 mW/m2) in strength in the head region with 100 kHz FM modulation at 900 MHz was applied to the animals. After calculating the ideal position for the device, electromagnetic LLER energy was applied for 45 minutes from a distance to be equal with energy transmitted by a mobile phone from a 0.5-1 cm distance to their head regions. After 1.5 hours and before the rats awoke, 0.5 ml of blood was taken from the tail veins in order to determine the treatment values.

RESULTS:

Plasma 5-HT and glutamate levels were measured by enzyme immunoassay (EIA) using commercial kits. It was found that a single 45 min of LLER exposure increased the blood 5-HT level significantly, but did not change the glutamate level of rats.

                                                                                                                                                                                                                                                                           

CONCLUSION: It was concluded that even a single 45 min of LLER exposure may produce an increase in 5-HT level without changing the blood glutamate level. Increased 5-HT level may lead to a retarded learning and a deficit in spatial memory (Tab. 2, Fig. 2, Ref. 24).

5HT, tryptofaani, serotonerginen neuroni ja dieetti

LÄHDE:  Neurochem Int. 2013 Feb;62(3):324-9. doi: 10.1016/j.neuint.2012.12.014. Epub 2013 Jan 7.

Effect of diet on serotonergic neurotransmission in depression.  Shabbir F1, Patel A, Mattison C, Bose S, Krishnamohan R, Sweeney E, Sandhu S, Nel W, Rais A, Sandhu R, Ngu N, Sharma S.

Abstract

Depression is characterized by sadness, purposelessness, irritability, and impaired body functions. Depression causes severe symptoms for several weeks, and dysthymia, which may cause chronic, low-grade symptoms. Treatment of depression involves psychotherapy, medications, or phototherapy. Clinical and experimental evidence indicates that an appropriate diet can reduce symptoms of depression. The neurotransmitter, serotonin (5-HT), synthesized in the brain, plays an important role in mood alleviation, satiety, and sleep regulation. Although certain fruits and vegetables are rich in 5-HT, it is not easily accessible to the CNS due to blood brain barrier. However the serotonin precursor, tryptophan, can readily pass through the blood brain barrier. Tryptophan is converted to 5-HT by tryptophan hydroxylase and 5-HTP decarboxylase, respectively, in the presence of pyridoxal phosphate, derived from vitamin B(6). Hence diets poor in tryptophan may induce depression as this essential amino acid is not naturally abundant even in protein-rich foods. Tryptophan-rich diet is important in patients susceptible to depression such as certain females during pre and postmenstrual phase, post-traumatic stress disorder, chronic pain, cancer, epilepsy, Parkinson's disease, Alzheimer's disease, schizophrenia, and drug addiction. Carbohydrate-rich diet triggers insulin response to enhance the bioavailability of tryptophan in the CNS which is responsible for increased craving of carbohydrate diets. Although serotonin reuptake inhibitors (SSRIs) are prescribed to obese patients with depressive symptoms, these agents are incapable of precisely regulating the CNS serotonin and may cause life-threatening adverse effects in the presence of monoamine oxidase inhibitors. However, CNS serotonin synthesis can be controlled by proper intake of tryptophan-rich diet. This report highlights the clinical significance of tryptophan-rich diet and vitamin B(6) to boost serotonergic neurotransmission in depression observed in various neurodegenerative diseases. However pharmacological interventions to modulate serotonergic neurotransmission in depression, remains clinically significant. Depression may involve several other molecular mechanisms as discussed briefly in this report.

onsdag 4 mars 2015

AIVO ja AGMATIINI

https://www.bioscience.org/2014/v6e/af/710/fulltext.htm
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Muistiin 4.3. 2015