No abstract

In spite of recent significant advances in reduction of mortality and disability, coronary heart disease (CHD) remains widespread both in Russia and around the world. Coronary bypass graft surgery (CABG) has proved to be the most effective method of CHD treatment, providing that conservative therapy is not effective enough. The aim of the present study was to reveal and correct postoperative cognitive dysfunction (POCD), developed under the conditions of cardiopulmonary bypass (CB) in patients with CHD within 12 months after CABG. A total of 87 patients were examined, all the patients underwent a course of drug therapy, 50 patients underwent a course of rehabilitation using computer-based stimulation programmes (once per day for 20 minutes within 10 days) in addition to medical therapy. A reliable improvement in results of the conducted research suggests that the proposed method provides safety and high performance in cognitive rehabilitation of patients with impairments of the higher brain functions after CABG. A relatively short course of rehabilitation (10 days) corresponded to the length of hospital stay of patients in the cardiac unit. However, even in such a short course we could obtain significant advantage in terms of efficiency of higher cortical functions recovery. Therefore, a course of rehabilitation using computer-based stimulation programmes in patients with coronary heart disease after CABG was proved to be an effective way of correcting cognitive function.

The electronic and geometric structural changes of acetone upon protonation are studied by 3C NMR spectroscopy and by molecular orbital (MO) calculations using the LORG (local orbital/local origin) method to calculate chemical shieldings and the CLOPPA (contributions for localized orbitals within the polarised propagator approach) analysis of the J coupling constants. In protonated acetone the 13C NMR spectrum has been resolved and two different methyl resonances (1.2 ppm apart) have been assigned. The one-bond C-C coupling constants

Amyotrophic lateral sclerosis (ALS) is an incurable chronic progressive neurodegenerative disease with the progressive degeneration of motor neurons in the motor cortex and lower motor neurons in the spinal cord and the brain stem. The etiology and pathogenesis of ALS are being actively studied, but there is still no single concept. The study of ALS risk factors can help to understand the mechanism of this disease development and, possibly, slow down the rate of its progression in patients and also reduce the risk of its development in people with a predisposition toward familial ALS. The interest of researchers and clinicians in the protective role of nutrients in the development of ALS has been increasing in recent years. However, the role of some of them is not well-understood or disputed. The objective of this review is to analyze studies on the role of nutrients as environmental factors affecting the risk of developing ALS and the rate of motor neuron degeneration progression. Methods: We searched the PubMed, Springer, Clinical keys, Google Scholar, and E-Library databases for publications using keywords and their combinations. We analyzed all the available studies published in 2010–2020. Discussion: We analyzed 39 studies, including randomized clinical trials, clinical cases, and meta-analyses, involving ALS patients and studies on animal models of ALS. This review demonstrated that the following vitamins are the most significant protectors of ALS development: vitamin B12, vitamin E > vitamin C > vitamin B1, vitamin B9 > vitamin D > vitamin B2, vitamin B6 > vitamin A, and vitamin B7. In addition, this review indicates that the role of foods with a high content of cholesterol, polyunsaturated fatty acids, urates, and purines plays a big part in ALS development. Conclusion: The inclusion of vitamins and a ketogenic diet in disease-modifying ALS therapy can reduce the progression rate of motor neuron degeneration and slow the rate of disease progression, but the approach to nutrient selection must be personalized. The roles of vitamins C, D, and B7 as ALS protectors need further study.

In connection with the widespread use of anticonvulsants (antiepileptic drugs – AEDs) in psychiatric and neurological practice and the need for their long-term use to treat a wide range of mental disorders and neurological diseases, the question of their safety profile, including the assessment of the risk of developing life-threatening conditions and adverse reactions (ADRs), becomes relevant. In this regard, from the position of personalized medicine, it is critical to develop an interdisciplinary approach with the participation of doctors of various specialties and a new strategy of a personalized approach to predicting AED-induced prolongation of the QT interval as one of the most prognostically unfavorable cardiological ADRs (including sudden death syndrome – SDS). We searched for full-text publications for the period from 2011 to 2021 databases using the following keywords and its combination. We have found and systematized monogenic and multifactorial forms of long QT syndrome (LQTS) and candidate genes that slow down AEDs metabolism in the liver. Identification of risk alleles of single nucleotide variants (SNVs) of the candidate genes predisposing to the development of AED-induced LQTS and SDS will make it possible to adjust the choice and dosage of these drugs and prevent the development of ADRs, which will improve the quality of life of patients and prevent SDS in the patients with psychiatric and neurological disorders.