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[The effects of vitamin D in bone health have been known since the 1920s. Recently, it has been proven that its role in the body is much more complex. Activated vitamin D is a steroid hormone that regulates transcription of more than 200 human genes through its receptor that is detectable in almost all types of cells. In contrast to the former conceptions, it can be activated not only in the kidneys; moreover, local 1-α-hydroxylation plays a greater role in its extraskeletal effects. Vitamin D deficiency, currently defined as serum levels of <30 ng/ml, is caused by the lack of ‘effective’ sunlight exposition. Thus, vitamin D deficiency is one of the most frequent deficiencies in the developed world that plays a role not only in the development of skeletal conditions but many other diseases, as well. A low vitamin D level causes a reduced calcium absorption, a higher bone remodelling rate and increased bone loss. It also reduces muscle strength and increases the risk of falling. Normal vitamin D status is required for the effectiveness of drugs for osteoporosis treatment; however vitamin D treatment in itself is not effective in osteoporosis. An increasing number of studies show the benefits of vitamin D supplementation and treatment in extraskeletal conditions. Vitamin D plays an important role in the prevention of several auto-immune diseases, infections, cardiovascular diseases, and cancers. Therefore, all UV-B radiation-deprived adults require an intake of vitamin D to maintain a level of >30 ng/ml. Vitamin D3 treatment is safe. The necessary dose can be reliably approximated by the calculation that an incremental consumption of 100 IU/day raises serum vitamin levels by 1,0 ng/ml. Clinical trials suggest that for the vast majority of individuals, a prolonged intake of 10,000 IU/day does not pose any risk.]
[Sudden cardiac death of athletes is very rare (1/50 000 to 1/100 000 annually) but it is still 2 to 4 times more frequent than that of the agematched normal population. In addition, it attracts peculiar media attention. Sudden cardiac death in athletes is supposed to not primarily have an ischemic origin but most likely relates to repolarization abnormalities. These may be caused by several independent and/or dependent factors such as benign cardiac hypertrophy developing normally in athletes (athlete’s heart), hypertrophic cardiomyopathy, increased sympathetic activity, genetic defects, seemingly harmless drugs, doping agents, food, and dietary supplements. These factors together can increase inhomogeneities in myocardial repolarization (“substrate”). In this case, an otherwise harmless extrasystole (“trigger”) occurring with unlucky timing may - although very seldomly - elicit fatal arrhythmias. Thus, effective prevention of sudden cardiac death may include new types of cost-effective cardiac electrophysiological screening methods (ECG or echocardiography) and, in case of a high level of suspicion, more costly genetic tests can be considered.]
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Clinical Neuroscience
[Headache registry in Szeged: Experiences regarding to migraine patients]2.
Clinical Neuroscience
[The new target population of stroke awareness campaign: Kindergarten students ]3.
Clinical Neuroscience
Is there any difference in mortality rates of atrial fibrillation detected before or after ischemic stroke?4.
Clinical Neuroscience
Factors influencing the level of stigma in Parkinson’s disease in western Turkey5.
Clinical Neuroscience
[The effects of demographic and clinical factors on the severity of poststroke aphasia]1.
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Clinical Oncology
[Pancreatic cancer: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up]3.
Clinical Oncology
[Pharmacovigilance landscape – Lessons from the past and opportunities for future]4.
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