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171.
Michael D. Nelson Ryan Rosenberry Rita Barresi Evgeny I. Tsimerinov Florian Rader Xiu Tang O'Neil Mason Avery Schwartz Thomas Stabler Sarah Shidban Neigena Mobaligh Shomari Hogan Robert Elashoff Jason D. Allen Ronald G. Victor 《The Journal of physiology》2015,593(23):5183-5200
AbstractBecker muscular dystrophy (BMD) is a progressive X‐linked muscle wasting disease for which there is no treatment. BMD is caused by in‐frame mutations in the gene encoding dystrophin, a structural cytoskeletal protein that also targets other proteins to the sarcolemma. Among these is neuronal nitric oxide synthase mu (nNOSμ), which requires specific spectrin‐like repeats (SR16/17) in dystrophin''s rod domain and the adaptor protein α‐syntrophin for sarcolemmal targeting. When healthy skeletal muscle is exercised, sarcolemmal nNOSμ‐derived nitric oxide (NO) attenuates α‐adrenergic vasoconstriction, thus optimizing perfusion. In the mdx mouse model of dystrophinopathy, this protective mechanism (functional sympatholysis) is defective, resulting in functional muscle ischaemia. Treatment with a NO‐donating non‐steroidal anti‐inflammatory drug (NSAID) alleviates this ischaemia and improves the murine dystrophic phenotype. In the present study, we report that, in 13 men with BMD, sympatholysis is defective mainly in patients whose mutations disrupt sarcolemmal targeting of nNOSμ, with the vasoconstrictor response measured as a decrease in muscle oxygenation (near infrared spectroscopy) to reflex sympathetic activation. Then, in a single‐arm, open‐label trial in 11 BMD patients and a double‐blind, placebo‐controlled cross‐over trial in six patients, we show that acute treatment with oral sodium nitrate, an inorganic NO donor without a NSIAD moiety, restores sympatholysis and improves post‐exercise hyperaemia (Doppler ultrasound). By contrast, sodium nitrate improves neither sympatholysis, nor hyperaemia in healthy controls. Thus, a simple NO donor recapitulates the vasoregulatory actions of sarcolemmal nNOS in BMD patients, and constitutes a putative novel therapy for this disease.
Abbreviations
- BMD
- Becker muscular dystrophy
- deoxyHb
- deoxyhaemoglobin
- deoxyMb
- deoxymyoglobin
- DMD
- Duchenne muscular dystrophy
- LBNP
- lower body negative pressure
- MVC
- maximal voluntary contraction
- NIRS
- near infrared spectroscopy
- NO
- nitric oxide
- NO2−
- nitrite
- NO3−
- nitrate
- nNOSμ
- neuronal nitric oxide synthase mu
- NSAID
- non‐steroidal anti‐inflammatory drug
- PDE5
- phosphodiesterase 5
- TLS
- total labile signal
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Yulia Ammour Olga Susova George Krasnov Eugenia Nikolaeva Vyacheslav Varachev Yulia Schetinina Marina Gavrilova Alexey Mitrofanov Anna Poletaeva Ali Bekyashev Evgeny Faizuloev Vitaly V. Zverev Oxana A. Svitich Tatiana V. Nasedkina 《Viruses》2022,14(11)
Glioblastoma multiforme (GBM) accounts for almost half of all primary malignant brain tumors in adults and has a poor prognosis. Here we demonstrated the oncolytic potential of the L-16 vaccine strain of measles virus (MV) against primary human GBM cells and characterized the genetic patterns that determine the sensitivity of primary human GBM cells to oncolytic therapy. MV replicated in all GBM cells, and seven out of eight cell lines underwent complete or partial oncolysis. RNA-Seq analysis identified about 1200 differentially expressed genes (FDR < 0.05) with at least two-fold expression level change between MV-infected and uninfected cells. Among them, the most significant upregulation was observed for interferon response, apoptosis and cytokine signaling. One out of eight GBM cell lines was defective in type I interferon production and, thus, in the post-interferon response, other cells lacked expression of different cellular defense factors. Thus, none of the cell lines displayed induction of the total gene set necessary for effective inhibition of MV replication. In the resistant cells, we detected aberrant expression of metalloproteinase genes, particularly MMP3. Thus, such genes could be considered intriguing candidates for further study of factors responsible for cell sensitivity and resistance to L-16 MV infection. 相似文献
177.
Bolong Miao Alina Nikolaevna Isachkina Evgeny Viktorovich Shutov Alexander Alekseevich Selyutin Lyudmila Vladimirovna Kvitkova Valery Yuryevich Shilo Olga Nikolaevna Vetchinnikova Ilya Vyacheslavovich Alexandrov Dmitry Vladislavovich Perlin Alexander Vasilievich Zuev Igor Leonidovich Davydkin Tatyana Pavlovna Mironova Olga Mikhailovna Solovyova Alexey Pavlovich Tutin Alexey Mikhailovich Omelchenko Kriengsak Vareesangthip Nadezhda Georgievna Khadikova Man Li Xiang Li 《Medicine》2022,101(47)
178.
George E. Woody Evgeny Krupitsky Edwin Zvartau 《Journal of neuroimmune pharmacology》2016,11(3):401-407
Naltrexone is an antagonist that binds tightly to μ-opioid receptors and blocks the subjective and analgesic effects of opioids. It does not produce physiologic dependence and precipitates withdrawal if administered to an opioid dependent person, thus starting it must begin with detoxification. It was first available in the mid-1970s as a 50 mg tablet that blocked opioids for 24–36 h if taken daily, or every 2–3 days at higher doses - for example: 100 mg Monday and Wednesday, 150 mg on Friday. From a pharmacological perspective it worked very well and was hoped to be an effective treatment but results were disappointing due to low patient interest and high dropout followed by relapse. Interest in it waned but rose again in the late 1990’s when injecting opioid use and the rapid spread of HIV in the Russian Federation converged with an international interest in reducing the spread of HIV. One result was a series of meetings sponsored by the U.S. National Institute on Drug Abuse (NIDA) and Pavlov State Medical University in St. Petersburg, Russian Federation, on ways to reduce the spread of HIV in that country. Addiction treatment was a clear priority and discussions showed that naltrexone could have a role since agonist treatment is against Russian law but naltrexone is approved and the government funds over 25,000 beds for detoxification, which is the first step in starting naltrexone treatment. These meetings were followed by NIDA studies that showed better compliance to oral naltrexone than in prior U.S. studies with the expected reductions in HIV injecting risk for those that stayed in treatment. These events and findings provided a background and identified an infrastructure for the study that led to FDA approval of extended release injectable naltrexone for preventing relapse to opioid dependence. This paper will briefly review findings from these studies and end with comments on the potential role of extended release naltrexone as a meaningful addition to current pharmacotherapies for treating opiod dependence and reducing HIV risk. 相似文献
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HERMITAGE—a randomized controlled trial to reduce sexually transmitted infections and HIV risk behaviors among HIV‐infected Russian drinkers 下载免费PDF全文