Universidade Estadual de Londrina

About: Universidade Estadual de Londrina is a education organization based out in Londrina, Brazil. It is known for research contribution in the topics: Population & Toxoplasma gondii. The organization has 13052 authors who have published 19291 publications receiving 212123 citations.

Characterization of chronic pain and analgesic approaches among community-dwelling elderly

Abstract: OBJECTIVE: To characterize chronic pain and analgesic approaches in community- dwelling elderly of the northern district of Londrina - Brazil. METHODS: Cross-sectional study with individuals 60 years old and more, resident in the local area of a Basic Health Unit (UBS) of Londrina, by home inquiry. Chronic pain was defined as pain lasting for six months or more. The elderly with pain, were questioned about characteristics of the pain as regards location, duration, frequency, intensity, improvement and worsening situations, as well as the impact of pain in the quality of life and also about analgesic approaches. RESULTS: One hundred and seventy two elderly were interviewed (101 women and 71 men). Presence of chronic pain was observed in 107 (62.%) of these 69.3% were female and 52.1% male (p = 0.004). The very old people, 80-year-old or more (p=0.01) and the depressive elderly (p=0.0008) presented higher frequency of chronic pain. Most prevalent pains were in the legs and back, with 31.2% each, and the majority of elderly referred to continuous, daily high intensity pain. Regarding analgesic approaches, the pharmacologic method was mentioned by 86 elderly (80.4%) and simple analgesic (32.6%) was the most used. CONCLUSION: Facts show that there is a high predominance of chronic pain in the population of elderly, mainly in women, in very old people and in depressive individuals.

The specialised pro-resolving lipid mediator maresin 1 reduces inflammatory pain with a long-lasting analgesic effect.

Abstract: Background and purpose Maresin 1 (MaR1) is a specialised pro-resolving lipid mediator with anti-inflammatory and analgesic activities. In this study, we addressed the modulation of peripheral and spinal cord cells by MaR1 in the context of inflammatory pain. Experimental approach Mice were treated with MaR1 before intraplantar injection of carrageenan or complete Freund's adjuvant (CFA). Mechanical hyperalgesia was assessed using the electronic von Frey and thermal hyperalgesia using a hot plate. Spinal cytokine production and NF-κB activation were determined by ELISA and astrocytes and microglia activation by RT-qPCR and immunofluorescence. CGRP release by dorsal root ganglia (DRG) neurons was determined by EIA. Neutrophil and macrophage recruitment were determined by immunofluorescence, flow cytometry, and colorimetric methods. Trpv1 and Nav1.8 expression and calcium imaging of DRG neurons were determined by RT-qPCR and Fluo-4AM respectively. Key results MaR1 reduced carrageenan- and CFA-induced mechanical and thermal hyperalgesia and neutrophil and macrophage recruitment proximal to CGRP+ fibres in the paw skin. Moreover, MaR1 reduced NF-κB activation, IL-1β and TNF-α production, and spinal cord glial cells activation. In the DRG, MaR1 reduced CFA-induced Nav1.8 and Trpv1 mRNA expression and calcium influx and capsaicin-induced release of CGRP by DRG neurons. Conclusions and implications MaR1 reduced DRG neurons activation and CGRP release explaining, at least in part, its analgesic and anti-inflammatory effects. The enduring analgesic and anti-inflammatory effects and also post-treatment activity of MaR1 suggest that specialised pro-resolving lipid mediators have potential as a new class of drugs for the treatment of inflammatory pain.

Reduction in Plasma Levels of Inflammatory and Oxidative Stress Indicators After Roux-En-Y Gastric Bypass

Abstract: Background Obesity is considered to be associated with high levels of oxidative stress and inflammation. Anticipated weight loss secondary to bariatric surgery may offer an opportunity to evaluate this association. We studied a few markers of oxidative stress and inflammation in 20 obese patients submitted to Roux-en-Y gastric bypass (RYGBP).

Acetic acid- and phenyl-p-benzoquinone-induced overt pain-like behavior depends on spinal activation of MAP kinases, PI3K and microglia in mice

Abstract: The acetic acid and phenyl-p-benzoquinone are easy and fast screening models to access the activity of novel candidates as analgesic drugs and their mechanisms. These models induce a characteristic and quantifiable overt pain-like behavior described as writhing response or abdominal contortions. The knowledge of the mechanisms involved in the chosen model is a crucial step forward demonstrating the mechanisms that the candidate drug would inhibit because the mechanisms triggered in that model will be addressed. Herein, it was investigated the role of spinal mitogen-activated protein (MAP) kinases ERK (extracellular signal-regulated kinase), JNK (Jun N-terminal Kinase) and p38, PI(3)K (phosphatidylinositol 3-kinase) and microglia in the writhing response induced by acetic acid and phenyl-p-benzoquinone, and flinch induced by formalin in mice. Acetic acid and phenyl-p-benzoquinone induced significant writhing response over 20 min. The nociceptive response in these models were significantly and in a dose-dependent manner reduced by intrathecal pre-treatment with ERK (PD98059), JNK (SB600125), p38 (SB202190) or PI(3)K (wortmannin) inhibitors. Furthermore, the co-treatment with MAP kinase and PI(3)K inhibitors, at doses that were ineffective as single treatment, significantly inhibited acetic acid- and phenyl-p-benzoquinone-induced nociception. The treatment with microglia inhibitors minocycline and fluorocitrate also diminished the nociceptive response. Similar results were obtained in the formalin test. Concluding, MAP kinases and PI(3)K are important spinal signaling kinases in acetic acid and phenyl-p-benzoquinone models of overt pain-like behavior and there is also activation of spinal microglia indicating that it is also important to determine whether drugs tested in these models also modulate such spinal mechanisms.