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1.
Cureus ; 15(8): e43424, 2023 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-37706133

RESUMO

Myofascial pain is a common problem resulting in musculoskeletal pain characterized by myofascial trigger points. These trigger points can cause substantial discomfort and functional limitations. This meta-analysis aims to assess the effectiveness and safety of trigger point injections versus medical management alone in treating acute onset myofascial pain. A thorough search was conducted across four databases, namely, PubMed, SCOPUS, Web of Science (WOS), and Cochrane Library, to identify randomized controlled trials that compared the effectiveness of trigger point injections versus medical management for the treatment of acute myofascial pain. The search encompassed articles published from the databases' inception until June 2023. The relevant data were extracted and analyzed using the standardized mean difference (SMD) and 95% confidence interval (CI). Of the 1151 records identified, four met the inclusion criteria for the systematic review, and all were included in the meta-analysis. The analysis of four randomized controlled trials (RCTs) showed that trigger point injections were effective in reducing pain scores compared to medical treatment (SMD = -2.09 (95% CI: -3.34 to -0.85, P = 0.001)). The data revealed a negative standardized mean difference, which was significant and consistent in favor of trigger point injections. Overall, these findings highlight the beneficial impact of trigger point injections in reducing acute myofascial pain when compared to isolated medical management.

2.
Clin Pract Cases Emerg Med ; 6(2): 180-182, 2022 May.
Artigo em Inglês | MEDLINE | ID: mdl-35701362

RESUMO

CASE PRESENTATION: An 88-year-old female presented to the emergency department (ED) with complaints of painful vision loss four days after an intravitreal injection for her neovascular macular degeneration. Her right eye visual acuity was markedly diminished with an absence of red reflex. A point-of-care ocular ultrasound was performed and demonstrated hyperechoic vitreous debris concerning for endophthalmitis. DISCUSSION: Endophthalmitis is an infection of the vitreous or aqueous humors commonly caused by exogenous sources, such as inoculation of bacteria into the eye from surgery, injections, or trauma. It is an ophthalmologic emergency as it is a vision-threatening infection. Although a rare complication, post-surgery or post-injection are the leading causes of endophthalmitis. Point-of-care ocular ultrasound findings suggestive of endophthalmitis, such as hyperechoic vitreous debris, aid in the timely diagnosis and treatment of patients in the ED.

3.
J Biol Chem ; 288(23): 16937-16948, 2013 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-23599427

RESUMO

We previously found that BDNF-dependent retrograde trafficking is impaired in AD transgenic mouse neurons. Utilizing a novel microfluidic culture chamber, we demonstrate that Aß oligomers compromise BDNF-mediated retrograde transport by impairing endosomal vesicle velocities, resulting in impaired downstream signaling driven by BDNF/TrkB, including ERK5 activation, and CREB-dependent gene regulation. Our data suggest that a key mechanism mediating the deficit involves ubiquitin C-terminal hydrolase L1 (UCH-L1), a deubiquitinating enzyme that functions to regulate cellular ubiquitin. Aß-induced deficits in BDNF trafficking and signaling are mimicked by LDN (an inhibitor of UCH-L1) and can be reversed by increasing cellular UCH-L1 levels, demonstrated here using a transducible TAT-UCH-L1 strategy. Finally, our data reveal that UCH-L1 mRNA levels are decreased in the hippocampi of AD brains. Taken together, our data implicate that UCH-L1 is important for regulating neurotrophin receptor sorting to signaling endosomes and supporting retrograde transport. Further, our results support the idea that in AD, Aß may down-regulate UCH-L1 in the AD brain, which in turn impairs BDNF/TrkB-mediated retrograde signaling, compromising synaptic plasticity and neuronal survival.


Assuntos
Doença de Alzheimer/metabolismo , Peptídeos beta-Amiloides/metabolismo , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Hipocampo/metabolismo , Ubiquitina Tiolesterase/metabolismo , Doença de Alzheimer/genética , Doença de Alzheimer/patologia , Peptídeos beta-Amiloides/genética , Animais , Fator Neurotrófico Derivado do Encéfalo/genética , Sobrevivência Celular/genética , Hipocampo/patologia , Humanos , Camundongos , Camundongos Transgênicos , Plasticidade Neuronal/genética , Neurônios/metabolismo , Neurônios/patologia , Transporte Proteico/genética , Ratos , Receptor trkB/genética , Receptor trkB/metabolismo , Transdução de Sinais/genética , Ubiquitina/genética , Ubiquitina/metabolismo , Ubiquitina Tiolesterase/genética
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