24 research outputs found
ΠΠ½Π°Π»ΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠ°ΡΡΠ΅Ρ Π΄ΠΈΠ½Π°ΠΌΠΈΠΊΠΈ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ°
ΠΡΠΎΠ²Π΅Π΄Π΅Π½ΠΎ Π°Π½Π°Π»ΡΡΠΈΡΠ½ΠΈΠΉ ΡΠΎΠ·ΡΠ°Ρ
ΡΠ½ΠΎΠΊ ΡΡΡ
Ρ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ½ΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ° ΡΠ° Π²ΠΏΠ»ΠΈΠ² Π·ΠΎΠ²Π½ΡΡΠ½ΡΡ
Π΄Π΅ΡΡΠ°Π±ΡΠ»ΡΠ·ΡΡΡΠΈΡ
ΡΠ°ΠΊΡΠΎΡΡΠ², ΡΠ°ΠΊΠΈΡ
ΡΠΊ ΡΠ΄Π°ΡΠΈ Ρ Π²ΡΠ±ΡΠ°ΡΡΠΉΠ½Ρ Π½Π°Π²Π°Π½ΡΠ°ΠΆΠ΅Π½Π½Ρ.An analytical calculation of motion fiber optic accelerometer and impact of external destabilizing factors, such as impacts and vibration loads.ΠΡΠΎΠ²Π΅Π΄Π΅Π½ Π°Π½Π°Π»ΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠ°ΡΡΠ΅Ρ Π΄Π²ΠΈΠΆΠ΅Π½ΠΈΡ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ° ΠΈ Π²Π»ΠΈΡΠ½ΠΈΠ΅ Π²Π½Π΅ΡΠ½ΠΈΡ
Π΄Π΅ΡΡΠ°Π±ΠΈΠ»ΠΈΠ·ΠΈΡΡΡΡΠΈΡ
ΡΠ°ΠΊΡΠΎΡΠΎΠ², ΡΠ°ΠΊΠΈΡ
ΠΊΠ°ΠΊ ΡΠ΄Π°ΡΡ ΠΈ Π²ΠΈΠ±ΡΠ°ΡΠΈΠΎΠ½Π½ΡΠ΅ Π½Π°Π³ΡΡΠ·ΠΊΠΈ
ΠΠΏΡΠ°ΡΡΠ²Π°Π½Π½Ρ ΡΠΈΠ³Π½Π°Π»ΡΠ² Π² ΠΏΡΠ΅ΡΠΈΠ·ΡΠΉΠ½ΠΎΠΌΡ ΡΠΈΡΡΠΎΠ²ΠΎΠΌΡ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΡ Π· Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ½ΠΈΠΌ Π΄Π°Π²Π°ΡΠ΅ΠΌ
The algorithm of processing the signals in precision digital accelerometer with the fiberoptical sensor is brought. Advantages and features of use microcontroller device for processing signals from the fiber-optical sensor are considered.ΠΡΠΈΠ²Π΅Π΄Π΅Π½ Π°Π»Π³ΠΎΡΠΈΡΠΌ ΠΎΠ±ΡΠ°Π±ΠΎΡΠΊΠΈ ΡΠΈΠ³Π½Π°Π»ΠΎΠ² Π² ΠΏΡΠ΅ΡΠΈΠ·ΠΈΠΎΠ½Π½ΠΎΠΌ ΡΠΈΡΡΠΎΠ²ΠΎΠΌ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ΅ Ρ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΈΠΌ Π΄Π°ΡΡΠΈΠΊΠΎΠΌ. Π Π°ΡΡΠΌΠΎΡΡΠ΅Π½Ρ ΠΏΡΠ΅ΠΈΠΌΡΡΠ΅ΡΡΠ²Π° ΠΈ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΡ ΠΌΠΈΠΊΡΠΎΠΊΠΎΠ½ΡΡΠΎΠ»Π»Π΅ΡΠ½ΠΎΠ³ΠΎ ΡΡΡΡΠΎΠΉΡΡΠ²Π° Π΄Π»Ρ ΠΎΠ±ΡΠ°Π±ΠΎΡΠΊΠΈ ΡΠΈΠ³Π½Π°Π»ΠΎΠ² Π΄Π°ΡΡΠΈΠΊΠ°.ΠΠ°Π²Π΅Π΄Π΅Π½ΠΎ Π°Π»Π³ΠΎΡΠΈΡΠΌ ΠΎΠΏΡΠ°ΡΡΠ²Π°Π½Π½Ρ ΡΠΈΠ³Π½Π°Π»ΡΠ² Π² ΠΏΡΠ΅ΡΠΈΠ·ΡΠΉΠ½ΠΎΠΌΡ ΡΠΈΡΡΠΎΠ²ΠΎΠΌΡ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΡ Π· Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ½ΠΈΠΌ Π΄Π°Π²Π°ΡΠ΅ΠΌ. Π ΠΎΠ·Π³Π»ΡΠ½ΡΡΡ ΠΏΠ΅ΡΠ΅Π²Π°Π³ΠΈ ΡΠ° ΠΎΡΠΎΠ±Π»ΠΈΠ²ΠΎΡΡΡ Π²ΠΈΠΊΠΎΡΠΈΡΡΠ°Π½Π½Ρ ΠΌΡΠΊΡΠΎΠΊΠΎΠ½ΡΡΠΎΠ»Π΅ΡΠΎΠ³ΠΎ ΠΏΡΠΈΡΡΡΠΎΡ Π΄Π»Ρ ΠΎΠ±ΡΠΎΠ±ΠΊΠΈ ΡΠΈΠ³Π½Π°Π»ΡΠ² Π²ΡΠ΄ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ½ΠΎΠ³ΠΎ Π΄Π°Π²Π°ΡΠ°
Π£ΡΠ΅Ρ Π½Π΅ΠΊΠΎΡΠΎΡΡΡ ΠΎΠ³ΡΠ°Π½ΠΈΡΠ΅Π½ΠΈΠΉ ΠΏΠΎΡΠΎΠ³ΠΎΠ²ΠΎΠΉ ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ ΠΈ ΠΎΡΠΈΠ±ΠΊΠΈ ΠΈΠ·ΠΌΠ΅ΡΠ΅Π½ΠΈΠΉ Π² ΠΈΠΌΠΏΡΠ»ΡΡΠ½ΡΡ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΈΡ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ°Ρ
Π ΠΎΠ·Π³Π»ΡΠ½ΡΡΠΎ Π²ΠΏΠ»ΠΈΠ² ΠΏΡΠΈΡΠΎΠ΄Π½ΠΈΡ
ΡΠ°ΠΊΡΠΎΡΡΠ², ΡΠΊΡ ΠΌΠΎΠΆΡΡΡ ΠΎΠ±ΠΌΠ΅ΠΆΡΠ²Π°ΡΠΈ ΠΌΠ΅ΡΡΠΎΠ»ΠΎΠ³ΡΡΠ½Ρ ΠΌΠΎΠΆΠ»ΠΈΠ²ΠΎΡΡΡ ΠΏΡΠ΅ΡΠΈΠ·ΡΠΉΠ½ΠΎΠ³ΠΎ ΡΠΈΡΡΠΎΠ²ΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ° Π½Π° ΠΎΡΠ½ΠΎΠ²Ρ ΡΠΌΠΏΡΠ»ΡΡΠ½ΠΎΠ³ΠΎ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ½ΠΎΠ³ΠΎ Π΄Π°Π²Π°ΡΠ°.Influence of natural factors, which can limit metrological possibilities of the precision digital accelerometer on the basis of pulse fiberoptical sensor unit, is considered.Π Π°ΡΡΠΌΠΎΡΡΠ΅Π½ΠΎ Π²Π»ΠΈΡΠ½ΠΈΠ΅ Π΅ΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΡΠ°ΠΊΡΠΎΡΠΎΠ², ΠΎΠ³ΡΠ°Π½ΠΈΡΠΈΠ²Π°ΡΡΠΈΡ
ΠΌΠ΅ΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΠΈ ΠΏΡΠ΅ΡΠΈΠ·ΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ ΡΠΈΡΡΠΎΠ²ΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ° Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΠΈΠΌΠΏΡΠ»ΡΡΠ½ΠΎΠ³ΠΎ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π°ΡΡΠΈΠΊΠ°
ΠΠ±Π»ΡΠΊ Π΄Π΅ΡΠΊΠΈΡ ΠΎΠ±ΠΌΠ΅ΠΆΠ΅Π½Ρ ΠΏΠΎΡΠΎΠ³ΠΎΠ²ΠΎΡ ΡΡΡΠ»ΠΈΠ²ΠΎΡΡΡ Ρ ΠΏΠΎΡ ΠΈΠ±ΠΊΠΈ Π²ΠΈΠΌΡΡΡΠ²Π°Π½Ρ Π² ΡΠΌΠΏΡΠ»ΡΡΠ½ΠΈΡ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ½ΠΈΡ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ°Ρ
Influence of natural factors, which can limit metrological possibilities of the precision digital accelerometer on the basis of pulse fiberoptical sensor unit, is considered.Π Π°ΡΡΠΌΠΎΡΡΠ΅Π½ΠΎ Π²Π»ΠΈΡΠ½ΠΈΠ΅ Π΅ΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΡΠ°ΠΊΡΠΎΡΠΎΠ², ΠΎΠ³ΡΠ°Π½ΠΈΡΠΈΠ²Π°ΡΡΠΈΡ
ΠΌΠ΅ΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΠΈ ΠΏΡΠ΅ΡΠΈΠ·ΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ ΡΠΈΡΡΠΎΠ²ΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ° Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΠΈΠΌΠΏΡΠ»ΡΡΠ½ΠΎΠ³ΠΎ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π°ΡΡΠΈΠΊΠ°.Π ΠΎΠ·Π³Π»ΡΠ½ΡΡΠΎ Π²ΠΏΠ»ΠΈΠ² ΠΏΡΠΈΡΠΎΠ΄Π½ΠΈΡ
ΡΠ°ΠΊΡΠΎΡΡΠ², ΡΠΊΡ ΠΌΠΎΠΆΡΡΡ ΠΎΠ±ΠΌΠ΅ΠΆΡΠ²Π°ΡΠΈ ΠΌΠ΅ΡΡΠΎΠ»ΠΎΠ³ΡΡΠ½Ρ ΠΌΠΎΠΆΠ»ΠΈΠ²ΠΎΡΡΡ ΠΏΡΠ΅ΡΠΈΠ·ΡΠΉΠ½ΠΎΠ³ΠΎ ΡΠΈΡΡΠΎΠ²ΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ° Π½Π° ΠΎΡΠ½ΠΎΠ²Ρ ΡΠΌΠΏΡΠ»ΡΡΠ½ΠΎΠ³ΠΎ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ½ΠΎΠ³ΠΎ Π΄Π°Π²Π°ΡΠ°
ΠΠ½Π°Π»ΡΡΠΈΡΠ½Ρ ΡΠΎΠ·ΡΠ°Ρ ΡΠ½ΠΊΠΈ Π΄ΠΈΠ½Π°ΠΌΡΠΊΠΈ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ½ΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ°
An analytical calculation of motion fiber optic accelerometer and impact of external destabilizing factors, such as impacts and vibration loads.ΠΡΠΎΠ²Π΅Π΄Π΅Π½ Π°Π½Π°Π»ΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠ°ΡΡΠ΅Ρ Π΄Π²ΠΈΠΆΠ΅Π½ΠΈΡ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ° ΠΈ Π²Π»ΠΈΡΠ½ΠΈΠ΅ Π²Π½Π΅ΡΠ½ΠΈΡ
Π΄Π΅ΡΡΠ°Π±ΠΈΠ»ΠΈΠ·ΠΈΡΡΡΡΠΈΡ
ΡΠ°ΠΊΡΠΎΡΠΎΠ², ΡΠ°ΠΊΠΈΡ
ΠΊΠ°ΠΊ ΡΠ΄Π°ΡΡ ΠΈ Π²ΠΈΠ±ΡΠ°ΡΠΈΠΎΠ½Π½ΡΠ΅ Π½Π°Π³ΡΡΠ·ΠΊΠΈ.ΠΡΠΎΠ²Π΅Π΄Π΅Π½ΠΎ Π°Π½Π°Π»ΡΡΠΈΡΠ½ΠΈΠΉ ΡΠΎΠ·ΡΠ°Ρ
ΡΠ½ΠΎΠΊ ΡΡΡ
Ρ Π²ΠΎΠ»ΠΎΠΊΠΎΠ½Π½ΠΎ-ΠΎΠΏΡΠΈΡΠ½ΠΎΠ³ΠΎ Π°ΠΊΡΠ΅Π»Π΅ΡΠΎΠΌΠ΅ΡΡΠ° ΡΠ° Π²ΠΏΠ»ΠΈΠ² Π·ΠΎΠ²Π½ΡΡΠ½ΡΡ
Π΄Π΅ΡΡΠ°Π±ΡΠ»ΡΠ·ΡΡΡΠΈΡ
ΡΠ°ΠΊΡΠΎΡΡΠ², ΡΠ°ΠΊΠΈΡ
ΡΠΊ ΡΠ΄Π°ΡΠΈ Ρ Π²ΡΠ±ΡΠ°ΡΡΠΉΠ½Ρ Π½Π°Π²Π°Π½ΡΠ°ΠΆΠ΅Π½Π½Ρ
Treatment of ADHD : Drugs, psychological therapies, devices, complementary and alternative methods as well as the trends in clinical trials
Attention-deficit/hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders having a high influence on social interactions. The number of approved treatments and clinical trials for ADHD have increased markedly during the recent decade. This analytical review provides a quantitative overview of the existing pharmacological and non-pharmacological methods of ADHD treatments investigated in clinical trials during 1999-2021. A total of 695 interventional trials were manually assessed from clinicaltrial.gov with the search term "ADHD", and trial data has been used for analysis. A clear majority of the studies investigated non-pharmacological therapies (similar to 80%), including many behavioral options, such as social skills training, sleep and physical activity interventions, meditation and hypnotherapy. Devices, complementary and other alternative methods of ADHD treatment are also gaining attention. The pharmacological group accounts for similar to 20% of all the studies. The most common drug classes include central nervous system stimulants (e.g., methylphenidate hydrochloride, lisdexamfetamine dimesylate, amphetamine sulfate, mixed amphetamine salts, a combination of dexmethylphenidate hydrochloride and serdexmethylphenidate chloride), selective noradrenaline reuptake inhibitors (atomoxetine, viloxazine), and alpha2 adrenergic receptor agonists (guanfacine hydrochloride, clonidine hydrochloride). Several studies investigated antidepressants (e.g., bupropion hydrochloride, vortioxetine), and atypical antipsychotics (e.g., quetiapine, aripiprazole) but these are yet not approved by the FDA for ADHD treatment. We discuss the quantitative trends in clinical trials and provide an overview of the new drug agents and non-pharmacological therapies, drug targets, and novel treatment options
Pharmacogenetics and Pain Treatment with a Focus on Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) and Antidepressants : A Systematic Review
Background: This systematic review summarizes the impact of pharmacogenetics on the effect and safety of non-steroidal anti-inflammatory drugs (NSAIDs) and antidepressants when used for pain treatment. Methods: A systematic literature search was performed according to the preferred reporting items for systematic reviews and meta-analysis (PRISMA) guidelines regarding the human in vivo efficacy and safety of NSAIDs and antidepressants in pain treatment that take pharmacogenetic parameters into consideration. Studies were collected from PubMed, Scopus, and Web of Science up to the cutoff date 18 October 2021. Results: Twenty-five articles out of the 6547 initially detected publications were identified. Relevant medication-gene interactions were noted for drug safety. Interactions important for pain management were detected for (1) ibuprofen/CYP2C9; (2) celecoxib/CYP2C9; (3) piroxicam/CYP2C8, CYP2C9; (4) diclofenac/CYP2C9, UGT2B7, CYP2C8, ABCC2; (5) meloxicam/CYP2C9; (6) aspirin/CYP2C9, SLCO1B1, and CHST2; (7) amitriptyline/CYP2D6 and CYP2C19; (8) imipramine/CYP2C19; (9) nortriptyline/CYP2C19, CYP2D6, ABCB1; and (10) escitalopram/HTR2C, CYP2C19, and CYP1A2. Conclusions: Overall, a lack of well powered human in vivo studies assessing the pharmacogenetics in pain patients treated with NSAIDs or antidepressants is noted. Studies indicate a higher risk for partly severe side effects for the CYP2C9 poor metabolizers and NSAIDs. Further in vivo studies are needed to consolidate the relevant polymorphisms in NSAID safety as well as in the efficacy of NSAIDs and antidepressants in pain management
The Epigenetics of Migraine
Migraine is a complex neurological disorder and a major cause of disability. A wide range of different drug classes such as triptans, antidepressants, anticonvulsants, analgesics, and beta-blockers are used in acute and preventive migraine therapy. Despite a considerable progress in the development of novel and targeted therapeutic interventions during recent years, e.g., drugs that inhibit the calcitonin gene-related peptide (CGRP) pathway, therapy success rates are still unsatisfactory. The diversity of drug classes used in migraine therapy partly reflects the limited perception of migraine pathophysiology. Genetics seems to explain only to a minor extent the susceptibility and pathophysiological aspects of migraine. While the role of genetics in migraine has been extensively studied in the past, the interest in studying the role of gene regulatory mechanisms in migraine pathophysiology is recently evolving. A better understanding of the causes and consequences of migraine-associated epigenetic changes could help to better understand migraine risk, pathogenesis, development, course, diagnosis, and prognosis. Additionally, it could be a promising avenue to discover new therapeutic targets for migraine treatment and monitoring. In this review, we summarize the state of the art regarding epigenetic findings in relation to migraine pathogenesis and potential therapeutic targets, with a focus on DNA methylation, histone acetylation, and microRNA-dependent regulation. Several genes and their methylation patterns such as CALCA (migraine symptoms and age of migraine onset), RAMP1, NPTX2, and SH2D5 (migraine chronification) and microRNA molecules such as miR-34a-5p and miR-382-5p (treatment response) seem especially worthy of further study regarding their role in migraine pathogenesis, course, and therapy. Additionally, changes in genes including COMT, GIT2, ZNF234, and SOCS1 have been linked to migraine progression to medication overuse headache (MOH), and several microRNA molecules such as let-7a-5p, let-7b-5p, let-7f-5p, miR-155, miR-126, let-7g, hsa-miR-34a-5p, hsa-miR-375, miR-181a, let-7b, miR-22, and miR-155-5p have been implicated with migraine pathophysiology. Epigenetic changes could be a potential tool for a better understanding of migraine pathophysiology and the identification of new therapeutic possibilities. However, further studies with larger sample sizes are needed to verify these early findings and to be able to establish epigenetic targets as disease predictors or therapeutic targets