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In this research, we will apply photoacoustic spectroscopy and evaluate bread added with turmeric (Curcuma longa Linnaeus) at different concentrations in relation to wheat flour weight (0, 1.25, 2.5, 5, and 10%). The amplitude of the photoacoustic signal was related to measures of antioxidant activity and evaluation of the sanitary quality and also, the texture, color, and sensory acceptability of the breads. It is shown that (i) the photoacoustic signal produced by bread significantly increases with the turmeric concentration, such that it raises more than 100% for a concentration of 10% at the wavelengths of 428 and 515 nm. (ii) The bread antioxidant activity is directly proportional to the level of photoacoustic signal at 515 nm and its value increases from 73.21 to 91.73%, when the concentration increases from 0 to 10%. (iii) The sanitary quality of bread added with 2.5% of turmeric is relatively higher than the ones obtained for other lower concentrations. No fungal colonies were observed in bread mixed with 2.5%, 5%, and 10%, after 6 days of storage. (iv) The addition of turmeric powder for bread making can slow down their textural changes (hardness, elasticity, cohesiveness, resilience, and chewiness) during storage. (v) Bread at 2.5 and 5% of turmeric concentration showed the yellowest color, while the one with a 10% concentration exhibited the most reddish color. Finally, through principal component analysis, it was possible to demonstrate that a concentration of either 5 or 10% of turmeric added to wheat flour could be used to improve its sanitary quality and antioxidant activity. [ABSTRACT FROM AUTHOR]

Curcumin, the active component of Curcuma longa L. (Zingiberaceae), exhibits a wide variety of biological activities including vasodilation and anti-inflammation. The relaxant effect of curcumin in tracheal smooth muscle (TSM) was not examined so far, thus, this study was designed to assess the relaxant effect of curcumin on rat TSM and examine the underlying mechanism(s) responsible for this effect. TSM was contracted by KCl (60 mM) or methacholine (10 μM), and cumulative concentrations of curcumin (12.5, 25, 50, and 100 mg/mL) or theophylline (0.2, 0.4, 0.6, and 0.8 mM, as positive control) were added to organ bath. The relaxant effect of curcumin was examined in non-incubated or incubated tissues with atropine (1 μM), chlorpheniramine (1 μM), indomethacin (1 μM), and papaverine (100 μM). In non-incubated TSM, curcumin showed significant relaxant effects on KCl-induced contraction in a concentration-dependent manner (p < 0.001 for all concentrations). The relaxant effects of curcumin 12.5, 25, and 50 mg/mL were significantly lower in atropine-incubated tissue compared to non-incubated TSM (p < 0.05 to p < 0.001). A significant difference was observed in EC50 between atropine-incubated (48.10 ± 2.55) and non-incubated (41.65 ± 1.81) tissues (p < 0.05). Theophylline showed a significant relaxant effect on both KCl and methacholine-induced contraction in a concentration-dependent manner (p < 0.001 for all cases). The results indicated a relatively potent relaxant effect of curcumin on TSM, which was less marked than the effect of theophylline. Calcium channel blocking and/or potassium channel opening properties of curcumin may be responsible for TSM relaxation. [ABSTRACT FROM AUTHOR]

Chronic low back pain (cLBP) that cannot be attributable to a specific pathoanatomical change is associated with high personal and societal costs. Still, the underlying mechanism that causes and sustains such a phenotype is largely unknown. Emerging evidence suggests that epigenetic changes play a role in chronic pain conditions. Using reduced representation bisulfite sequencing (RRBS), we evaluated DNA methylation profiles of adults with non-specific cLBP (n = 50) and pain-free controls (n = 48). We identified 28,325 hypermethylated and 36,936 hypomethylated CpG sites (p < 0.05). After correcting for multiple testing, we identified 159 DMRs (q < 0.01and methylation difference > 10%), the majority of which were located in CpG island (50%) and promoter regions (48%) on the associated genes. The genes associated with the differentially methylated regions were highly enriched in biological processes that have previously been implicated in immune signaling, endochondral ossification, and G-protein coupled transmissions. Our findings support inflammatory alterations and the role of bone maturation in cLBP. This study suggests that epigenetic regulation has an important role in the pathophysiology of non-specific cLBP and a basis for future studies in biomarker development and targeted interventions. [ABSTRACT FROM AUTHOR]

Poisonous animals imply a risk to human life, because their venom is a complex mixture of low molecular weight components, peptides and proteins. Hornets use the venom for self-defence, to repel intruders and to capture prey, but they can cause poisoning and allergic reactions to people. In particular, they seem to be a health problem in the countries where they are native due to their sting, which in the most severe cases can lead to severe or fatal systemic anaphylaxis. But this situation is being an emerging problem for new countries and continents because hornet incursions are increasing in the global change scenario, such as in Europe and America. Furthermore, 55 detailed cases of hornet sting were found in 27 papers during the current review where 36.4% died due to, mainly, a multi-organ failure, where renal failure and liver dysfunction were the most common complications. Moreover, the great taxonomic, ecological diversity, geographical distribution and the wide spectrum of pathophysiological symptoms of hornets have been the focus of new research. Considering this, the present systematic review summarizes the current knowledge about the components of Vespa venom and the epidemiology of its sting to serve as reference for the new research focused on the development of techniques for diagnosis, new drugs and treatments of its sting. [ABSTRACT FROM AUTHOR]

Objective: To investigate complement(C) factors(F) and their activation fragments expression in OA joint tissues. Design: Immunohistochemistry and quantitative imaging were performed to analyze C3, C4, and CF (factor) B expression on osteochondral biopsies (43 patients) collected during arthroplasty. Isolated chondrocytes and synoviocytes, cartilage and synovial tissues obtained from surgical specimens of OA patients (15 patients) were cultured with or without IL-1β. Real time PCR for CFB, C3, and C4 was performed. Culture supernatants were analyzed for C3a, C5a, CFBa, and terminal complement complex (TCC) production. Results: In osteochondral biopsies, C factor expression was located in bone marrow, in a few subchondral bone cells and chondrocytes. C3 was the most expressed while factor C4 was the least expressed factor. Gene expression showed that all C factors analyzed were expressed both in chondrocytes and synoviocytes. In chondrocyte cultures and cartilage explants, CFB expression was significantly higher than C3 and C4. Furthermore, CFB, but not C3 and C4 expression was significantly induced by IL-1β. As to C activation factors, C3a was the most produced and CFBa was induced by IL-1β in synovial tissue. TCC production was undetectable in isolated chondrocytes and synoviocytes cell culture supernatants, whereas it was significantly augmented in cartilage explants. Conclusion: C factors were locally produced and activated in OA joint with the contribution of all tissues (cartilage, bone, and synovium). Our results support the involvement of innate immunity in OA and suggest an association between some C alternative pathway component and joint inflammation. [ABSTRACT FROM AUTHOR]

The solubility of curcumin in the pure water subcritical and water–ethanol solution (water + (5–10) % (v/v) ethanol) subcritical is investigated for the first time. The design approach taken from this study is the response surface methodology due to the Box Behnken. The experiments were performed in the temperature range of (90–150) °C, (0–10) volumetric percent of ethanol and the flow rate of (0.2–0.8) ml/min. As the pressure effect is ignored in the subcritical conditions, the pressure is constant in 2 MP in the experiments. All analyses were carried out employing the high-performance liquid chromatography apparatus. The curcumin solubility data were correlated with the dielectric constant of solvent mixture. Curcumin solubility modeling in subcritical conditions was done due to cubic-plus-association equation of state. The present study indicated that the rise in temperature and ethanol percentage cause an increase in curcumin solubility. Other important finding was by increasing the flow rate, curcumin solubility rate increased with a very mild slope. The optimum conditions for the curcumin solubility were in the water flow rate of 0.8 ml/min, 10% (v/v) of ethanol, and the temperature of 150 °C. [ABSTRACT FROM AUTHOR]

Objective: To compare the unilateral signs of knee osteoarthritis (KOA) 30 and 60 days after anterior cruciate ligament transection (ACLT). Pain, gait function, synovial fluid inflammation, and histopathological changes in the synovial membrane were analyzed, as well as the interaction between the variables. Materials and methods: Male Wistar rats (n = 32; 219.2 ± 18.6 g) were randomly distributed into four groups of eight animals each. Two groups were submitted to unilateral ACLT surgery to induce KOA and analyzed after 30 (KOA30) and 60 days (KOA60). Two control groups (without surgery) were also assessed after the same time periods (C30 and C60). All the groups were evaluated before ACLT from the least to most stressful tests (skin temperature, mechanical response threshold, gait test, thermal response threshold, and joint swelling), as well as 30 and 60 days after surgery. After euthanasia, the synovial fluid and synovial membrane were collected. Results: Thirty days after ACLT, KOA30 showed decrease paw print area and mechanical response threshold, higher joint swelling, skin temperature, leukocyte count, cytokine levels, and synovitis score. No differences were found between KOA30 and KOA60. Conclusion: Our data showed that 30 days after ACLT is sufficient to induce signs of KOA in rats, such as pain, functional impairment, and synovial inflammation, suggesting that a shorter time period can be used as an experimental model. [ABSTRACT FROM AUTHOR]

Joint pain is a distressing symptom of arthritis, and it is frequently persistent even after treatments which reduce local inflammation. Continuous production of algogenic factors activate/sensitize nociceptors in the joint structures and contribute to persistent pain, a challenging and difficult condition to treat. TNF is a crucial cytokine for the pathogenesis of several rheumatic diseases, and its inhibition is a mainstay of treatment to control joint symptoms, including pain. Here, we sought to investigate the inflammatory changes and the role of TNF in dorsal root ganglia (DRG) during persistent hypernociception after the resolution of acute joint inflammation. Using a model of antigen-induced arthritis, the peak of joint inflammation occurred 12–24 h after local antigen injection and was characterized by an intense influx of neutrophils, pro-inflammatory cytokine production, and joint damage. We found that inflammatory parameters in the joint returned to basal levels between 6 and 8 days after antigen-challenge, characterizing the resolving phase of joint inflammation. Mechanical hyperalgesia was persistent up to 14 days after joint insult. The persistent nociception was associated with the inflammatory status of DRG after cessation of acute joint inflammation. The late state of neuroinflammation in the ipsilateral side was evidenced by gene expression of TNF, TNFR2, IL-6, IL-1β, CXCL2, COX2, and iNOS in lumbar DRG (L3-L5) and leukocyte adhesion in the lumbar intumescent vessels between days 6 and 8. Moreover, there were signs of resident macrophage activation in DRG, as evidenced by an increase in Iba1-positive cells. Intrathecal or systemic injection of etanercept, an agent clinically utilized for TNF neutralization, at day 7 post arthritis induction, alleviated the persistent joint hyperalgesia by specific action in DRG. Our data suggest that neuroinflammation in DRG after the resolution of acute joint inflammation drives continuous neural sensitization resulting in persistent joint nociception in a TNF-dependent mechanism. [ABSTRACT FROM AUTHOR]

Introduction: Neurodegeneration is the term describing the death of neurons both in the central nervous system and periphery. When affecting the central nervous system, it is responsible for diseases like Alzheimer's disease, Parkinson's disease, Huntington's disorders, amyotrophic lateral sclerosis, and other less frequent pathologies. There are several common pathophysiological elements that are shared in the neurodegenerative diseases. The common denominators are oxidative stress (OS) and inflammatory responses. Unluckily, these conditions are difficult to treat. Because of the burden caused by the progression of these diseases and the simultaneous lack of efficacious treatment, therapeutic approaches that could target the interception of development of the neurodegeneration are being widely investigated. This review aims to highlight the most recent proposed novelties, as most of the previous approaches have failed. Therefore, older approaches may currently be used by healthcare professionals and are not being presented.Methods: This review was based on an electronic search of existing literature, using PubMed as primary source for important review articles, and important randomized clinical trials, published in the last 5 years. Reference lists from the most recent reviews, as well as additional sources of primary literature and references cited by relevant articles, were used.Results: Eighteen natural pharmaceutical substances and 24 extracted or recombinant products, and artificial agents that can be used against OS, inflammation, and neurodegeneration were identified. After presenting the most common neurodegenerative diseases and mentioning some of the basic mechanisms that lead to neuronal loss, this paper presents up to date information that could encourage the development of better therapeutic strategies.Conclusions: This review shares the new potential pharmaceutical and not pharmaceutical options that have been recently introduced regarding OS and inflammatory responses in neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Purpose: The complex nature of cancer-induced bone pain (CIBP) has led to investigation into cancer-targeted therapies. This has involved targeting glutamate release from the tumor, secreted as a byproduct of antioxidant responses and metabolic disruption. Cancer cells undergo many metabolic changes that result in increased glutamine metabolism and subsequently the production of glutamate. Glutaminase (GLS) is the enzyme that mediates the conversion of glutamine to glutamate and has been shown to be upregulated in many cancer types including malignancies of the breast. This enzyme, therefore, represents another potential therapeutic target for CIBP, one that lies upstream of glutamate secretion. Methods: A recently developed inhibitor of GLS, CB-839, was tested in an animal model of CIBP induced by intrafemoral MDA-MB-231 xenografts. CIBP behaviors were assessed using Dynamic Weight Bearing and Dynamic Plantar Aesthesiometer readings of mechanical hyperalgesia and allodynia. Results: CB-839 failed to modulate any of the associated nociceptive behaviors induced by intrafemoral MDA-MB-231 tumor growth. Further investigation in vitro revealed the sensitivity of the drug is dependent on the metabolic flexibility of the cell line being tested which can be modulated by cell culture environment. Conclusion: Adaptation to metabolic disturbances may explain the failure of CB-839 to exhibit any significant effects in vivo and the metabolic flexibility of the cell line tested should be considered for future investigations studying the metabolic effects of glutaminase inhibition. [ABSTRACT FROM AUTHOR]

The central nervous system (CNS) constitutively expresses complement (C) membrane receptors and complement proteins, including the component C5a. This is a crucial terminal effector of the C cascade, mostly involved in pain and neuroinflammatory conditions. Aberrant activation of C5a protein and its receptor C5aR has been reported to play a critical role in neurodegenerative diseases, with important clinical consequences. Here we have investigated the effects of DF3016A, a novel selective C5aR antagonist, able to penetrate the blood-brain barrier (BBB), on cortical neurons exposed to oxygen-glucose deprivation-reoxygenation (OGD/R), a neuroinflammation-related process. We demonstrated that a mild ischemic insult induces an early upregulation of C5aR associated with the over-production of pro-inflammatory cytokines and the over-expression of the transcriptional regulatory factor miR-181. Furthermore, we report the first experimental evidence of the effect of DF3016A, modulating complement component C5a, on neurons in a model of injury. Interestingly, DF3016A protects neuronal viability by restoring intracellular calcium levels, thus opposing the increase in pro-inflammatory cytokine levels and miR-181 expression. Based on our results, we suggest that DF3016A is a novel C5aR antagonist promoting protective effects against OGD/R-induced damage that could be a new therapeutic approach to controlling CNS neuroinflammatory conditions. [ABSTRACT FROM AUTHOR]

Copyright of Enfermagem Brasil is the property of Atlantica Editora and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Limb length inequality results from many types of musculoskeletal disorders. Asymmetric weight bearing from a limb length discrepancy of less than 2% can have debilitating consequences such as back problems and early-onset osteoarthritis. Existing treatments include invasive surgeries and/or drug regimens that are often only partially effective. As a noninvasive alternative, we previously developed a once daily limb-heating model using targeted heat on one side of the body for 2 weeks to unilaterally increase bone length by up to 1.5% in growing mice. In this study, we applied heat for 1 week to determine whether these small differences in limb length are functionally significant, assessed by changes in hindlimb weight bearing. We tested the hypothesis that heat-induced limb length asymmetry has a functional impact on weight bearing in mouse hindlimbs. Female 3-week-old C57BL/6 mice (N = 12 total) were treated with targeted intermittent heat for 7 days (40 C for 40 min/day). High-resolution x-ray (N = 6) and hindlimb weight bearing data (N = 8) were acquired at the start and end of the experiments. There were no significant left-right differences in starting tibial length or hindlimb weight bearing. After 1-week heat exposure, tibiae (t = 7.7, p < 0.001) and femora (t = 11.5, p < 0.001) were ~1 and 1.4% longer, respectively, on the heat-treated sides (40 C) compared to the non-treated contralateral sides (30 C). Tibial elongation rate was over 6% greater (t = 5.19, p < 0.001). Hindlimb weight bearing was nearly 20% greater (t = 11.9, p < 0.001) and significantly correlated with the increase in tibial elongation rate on the heat-treated side (R2 = 0.82, p < 0.01). These results support the hypothesis that even a small limb length discrepancy can cause imbalanced weight distribution in healthy mice. The increase in bone elongation rate generated by localized heat could be a way to equalize limb length and weight bearing asymmetry caused by disease or trauma, leading to new approaches with better outcomes by using heat to lengthen limbs and reduce costly side effects of more invasive interventions. [ABSTRACT FROM AUTHOR]

Accumulating evidence demonstrates that complement activation is involved in the pathogenesis of osteoarthritis (OA). However, the intimate complement regulation and cross talk with other signaling pathways in joint-associated tissues remain incompletely understood. Recent insights are summarized and discussed here, to put together a more comprehensive picture of complement involvement in OA pathogenesis. Complement is regulated by several catabolic and inflammatory mediators playing a key role in OA. It seems to be involved in many processes observed during OA development and progression, such as extracellular cartilage matrix (ECM) degradation, chondrocyte and synoviocyte inflammatory responses, cell lysis, synovitis, disbalanced bone remodeling, osteophyte formation, and stem cell recruitment, as well as cartilage angiogenesis. In reverse, complement can be activated by various ECM components and their cleavage products, which are released during OA-associated cartilage degradation. There are, however, some other cartilage ECM components that can inhibit complement, underlining the diverse effects of ECM on the complement activation. It is hypothesized that complement might also be directly activated by mechanical stress, thereby contributing to OA. The question arises whether keeping the complement activation in balance could represent a future therapeutic strategy in OA treatment and in the prevention of its progression. [ABSTRACT FROM AUTHOR]

Candida albicans biofilms play a key role in denture stomatitis, one of the most common oral pathologies in elderly people. Because biofilms are highly resistant to antifungals, new pharmacological strategies are needed. Aspirin and nitric oxide-donor molecules have both shown antibiofilm effects on C. albicans, making them promising candidates for treatment. In this study, we evaluated the antifungal/antibiofilm effect of a nitric-oxide releasing aspirin (NO-ASA) on C. albicans isolates from denture stomatitis patients in vitro. Disk diffusion assays showed that while NO-ASA had no antifungal effect, the drug potentiated fluconazole inhibition zone diameters, increasing the effect of fluconazole by 20–30% (p<0.05). The effect of NO-ASA on the morphogenesis of C. albicans was evaluated using light microscopy after inducing hyphae formation. For all clinical strains assayed, 125 μM NO-ASA significantly decreased the number of filamentous cells present (p<0.01). Adhesion to abiotic surfaces, a critical event for biofilm formation, was evaluated in 96-well polystyrene plates using crystal violet assay; 125 μM NO-ASA significantly inhibited adhesion. Biofilms were observed with scanning electron microscopy (SEM) and quantified using XTT reduction assay. NO-ASA decreased biofilm formation (IC50 ranging from 300 μM to 700 μM), consistent with SEM findings of altered biofilm microarchitecture. PGE2 and carboxy-PTIO (an NO scavenger) both blocked the antibiofilm effects of NO-ASA, suggesting that the efficacy of NO-ASA may be associated with both inhibition of PGE2 synthesis and release of NO. NO-ASA is a promising novel antibiofilm agent for treating fluconazole-resistant strains of C. albicans. [ABSTRACT FROM AUTHOR]

Certain non-steroidal anti-inflammatory drugs can inhibit fungal growth, fungal prostaglandin E2 production, and enzyme activation. This study aims to investigate the antifungal effect of nimesulide against pathogenic filamentous fungi and yeast. The experiments detailed below were also designed to investigate whether the action is dependent on E2 fungal prostaglandins. Our data showed that nimesulide exhibited potent antifungal activity, mainly against Trichophyton mentagrophytes (ATCC 9533) and Cryptococcus neoformans with MIC values of 2 and 62 μg/mL, respectively. This drug was also able to inhibit the growth of clinic isolates of filamentous fungi, such as Aspergillus fumigatus, and dermatophytes, such as T. rubrum, T. mentagrophytes, Epidermophyton floccosum, Microsporum canis, and M. gypseum, with MIC values ranging from 112 to 770 μg/mL. Our data also showed that the inhibition of fungal growth by nimesulide was mediated by a mechanism dependent on PGE2, which led to the inhibition of essential fungal enzymes. Thus, we concluded that nimesulide exerts a fungicidal effect against pathogenic filamentous fungi and yeast, involving the inhibition of fungal prostaglandins and fungal enzymes important to the fungal growth and colonization. [ABSTRACT FROM AUTHOR]

Background: Chrysobalanus icaco is a medicinal plant commonly used to treat fungal infections in Brazilian Amazonian region. Objective: This work aimed to evaluate the antifungal activity of the hydroalcoholic extract of C. icaco (HECi) against oral clinical isolates of Candida spp. and to determine the pharmacognostic parameters of the herbal drug and the phytochemical characteristics of HECi. Materials and Methods: The pharmacognostic characterization was performed using pharmacopoeial techniques. Phytochemical screening, total flavonoid content, and high-performance liquid chromatography (HPLC) analysis were used to investigate the chemical composition of the HECi. A broth microdilution method was used to determine the antifungal activity of the extract against 11 oral clinical isolates of Candida spp. Results: Herbal drug presented parameters which were within the limits set forth in current Brazilian legislation. A high amount of flavonoid content (132,959.33 ± 12,598.23 µg quercetin equivalent/g of extract) was found in HECi. Flavonoids such as myricetin and rutin were detected in the extract by HPLC analyses. HECi showed antifungal activity against oral isolates of Candida albicans and Candida parapsilosis (minimum inhibitory concentrations [MIC] 3.12 and 6.25 mg/mL, respectively), and C. albicans American American Type Culture Collection (MIC <1.56 mg/mL). Conclusion: HECi was shown to possess antifungal activity against Candida species with clinical importance in the development of oral candidiasis, and these activities may be related to its chemical composition. The antifungal activity detected for C. icaco against Candida species with clinical importance in the development of oral candidiasis can be attributed to the presence of flavonoids in HECi, characterized by chromatographic and spectroscopic techniques. [ABSTRACT FROM AUTHOR]

Abstract: It has been proposed that complex regional pain syndrome (CRPS) is a posttraumatic autoimmune disease. Previously, we observed that B cells contribute to CRPS-like changes in a mouse tibia fracture model, and that early (<12 months duration) CRPS patient IgM antibodies have pronociceptive effects in the skin and spinal cord of muMT fracture mice lacking B cells. The current study evaluated the pronociceptive effects of intraplantar or intrathecal injections of early CRPS IgM (5 µg) in muMT fracture mice. Skin and lumbar spinal cord were collected for immunohistochemistry and polymerase chain reaction analyses. Wild-type mice exhibited postfracture increases in complement component C5a and its receptor expression in skin and spinal cord, predominantly on dermal macrophages and spinal microglia. Intraplantar IgM injection caused nociceptive sensitization in muMT fracture mice with increased complement component C1q and inflammatory cytokine expression, and these IgM effects were blocked by a C5a receptor antagonist (PMX53) or a global cytokine inhibitor (pentoxifylline). Intrathecal IgM injection also had pronociceptive effects with increased spinal cytokine expression, effects that were blocked by PMX53 or pentoxifylline treatment. Intrathecal injection of chronic (>12 months duration) CRPS patient IgM (but not IgG) caused nociceptive sensitization in muMT fracture mice, but intraplantar injection of chronic CRPS IgM or IgG had no effect. We postulate that CRPS IgM antibodies bind to neoantigens in the fracture limb skin and corresponding spinal cord to activate C5a complement signaling in macrophages and microglia, evoking proinflammatory cytokine expression contributing to nociceptive sensitization in the injured limb., (Copyright © 2021 Written work prepared by employees of the Federal Government as part of their official duties is, under the U.S. Copyright Act, a “work of the United States Government” for which copyright protection under Title 17 of the United States Code is not available. As such, copyright does not extend to the contributions of employees of the Federal Government.)

Objective: Factors affecting pain sensation are still being investigated. In this study, we aimed to examine the effects of sex, age, body mass index (BMI), somatosensory amplification, anxiety, and depression on the perception of pain. Methods: Venipuncture was performed on 140 healthy individuals. All the cases completed a sociodemographic data form, visual analog scale (VAS), Beck Anxiety Inventory (BAI), Beck Depression Inventory, and Somatosensory Amplification Scale. Height and weight were also measured. Results: When both the sexes were compared, there was no difference in terms of VAS, BMI, age, and Beck Depression Inventory, but Somatosensory Amplification Scale and BAI were found to be higher in females. A correlation was found among VAS points, BAI, and BMI. The results of a regression analysis show that the BAI score is a predictor for the VAS score. Conclusion: These results indicate that anxiety may be a predictor of pain, whereas sex, depression, somatosensory amplification, age, and weight do not appear to influence the perception of pain. [ABSTRACT FROM AUTHOR]

Sodium salicylate (NaS) and aspirin (ASA) are known to have a variety of effects on microorganisms, such as fungus ( C. albicans and C. neoformans), moreover, it have effects in leukocyte adhesion and migration in vitro. In this report, we investigated the effect of ASA and NaS in neutrophil migration and cytokine production in C. albicans-induced peritonitis murine model. For this, mice were treated intraperitoneally (i.p) or orally (po) with NaS or ASA; after they were stimulated i.p. with C. albicans, the cellular migration was evaluated 24 h after stimulation. NaS, in mice treated i.p., unlike ASA, was able to inhibit the neutrophil migration and proinflammatory cytokine production induced by C. albicans, such as TNF-α, IL-1, IFN-γ, IL-12, and IL-10, but did not alter the IL-4 levels in these animals. However, the po treatment with same the dose of NaS or ASA did not affect the influx of this cell for inflammatory site. These results suggest that the NaS inhibits cellular migration and proinflammatory cytokine by different anti-inflammatory mechanism compared to ASA. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate therapeutic potential of curcumin-loaded poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) PHBHHx nanoparticles (CUR-NPs) and concanavaline A conjugated curcumin-loaded NPs (ConA-CUR-NPs) for breast cancer treatment. The size and zeta potential of prepared NPs were about 228 ± 5 nm and −23.3 mV, respectively. The entrapment efficiencies of polymer/drug weight ratios, 1.25CUR-NPs, 2.5CUR-NPs, 5CUR-NPs, ConA-1.25CUR-NPs, ConA-2.5CUR-NPs and ConA-5CUR-NPs were found to be ≈68, 55, 45, 70, 60 and 51%, respectively. Optimized NPs formulations in the freeze-dried form were assessed with their short-term stability for 30 days of storage at 4 °C and 25 °C. Anticancer activity of ConA-CUR-NPs was proved by MTT assay and reconfirmed by double staining and flow cytometry results. The anticancer activity of ConA-CUR-NPs was measured in human breast cancer cells (MDA-MB 231)in vitro, and the results revealed that the ConA-CUR-NPs had better tumor cells decline activity. [ABSTRACT FROM PUBLISHER]

Context: Eupatorium triplinerve Vahl (Asteraceae), popularly known as Japana, is widely used in folk medicine, due its analgesic, anticoagulant, antianorexic, antiparasitic, anthelmintic, sedative, antifungal, and antibacterial properties. Objective: The present study evaluated the chemical composition and antimicrobial activity of E. triplinerve extracts from different parts of the plant and identified the extract with the highest antimicrobial potential. Materials and methods: Extracts were obtained by maceration of all parts of plant, and subjected to bioassay-guided fractionation of methanol extract by partition column chromatography. The major chemical groups, saponins, reducing sugars, alkaloids, steroids, triterpenoids, phenols, tannins, flavonoids, and others were screened by standard techniques. The antimicrobial activity of the different extracts was performed by microdilution assay and the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) values were reported. Results: Phytochemical screening of hydroalcoholic extract from all parts of E. triplinerve identified mainly steroids, coumarins, alkaloids, saponins, tannins, depsides and absence of polysaccharides and flavonoids. The methanol extract of leaves presented the highest content of coumarins and lower MIC values of 62 and 75 µg/mL against Enterococcus faecalis and Staphylococcus aureus, respectively. In addition, its non-polar fractions showed antimicrobial activity with MIC ranging from 16 to 125 µg/mL against Gram-negative bacteria, mainly Escherichia coli. Discussion and conclusion: Data showed that non-polar fractions of E. triplinerve methanolic extract has better antimicrobial activity and most likely depends on the presence of several compounds, such as depsidones, coumarins, saponins, and triterpenes on crude extract. The results can be exploited largely in research of new antibacterial agents. [ABSTRACT FROM AUTHOR]

Copyright of Boletín Latinoamericano y del Caribe de Plantas Medicinales y Aromáticas is the property of Universidad de Santiago de Chile and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Internalization of drugs by cancer cells is a crucial factor to impact cancer treatment effect. Curcumin, having inhibitory effect on a variety of cancers, was encapsulated into micelles of six-arm star-shape poly(?-caprolactone)-b-poly(2-methacryloyloxyethylphosphorylcholine) (6sPCL-PMPC) in order to enhance its concentration in blood and cellular uptake. Micelles and curcumin-loaded micelles were prepared by the solvent-evaporation method. Drug-loading content and drug-loading efficiency could be achieved as high as 18.9 and 98%. MTT results showed that these curcumin-loaded micelles displayed significant cell cytotoxicity, while these blank micelles were noncytotoxic. The curcumin-loaded 6sPCL-PMPC micelles showed higher efficiency to kill HeLa cells than that of curcumin-loaded PCL-PEG micelles. The cellular uptake study indicated that the curcumin encapsulated into 6sPCL-PMPC micelles was ingested more by HeLa cells than the curcumin encapsulated into PCL-PEG micelles. In conclusion, the micelles with phosphatidylcholine (PC) groups as their exterior can greatly enhance the uptake by HeLa cells and the cytotoxicity of curcumin due to excellent internalization by cancer cells. [ABSTRACT FROM PUBLISHER]

Background: cis-Diammineplatinum (II) dichloride (cisplatin) is the important anti-cancer agent useful in treatment of various cancers. Unfortunately, it can produce unwanted side effects in various tissues, including the liver. The present study investigated the possible protective role of curcumin and α-tocopherol against oxidative stress-induced hepatotoxicity in rats upon cisplatin treatment. Methods: Male Wistar rats were divided into five groups (n = 5). Saline and Cis groups, rats were intraperitoneal (i.p.) injected with normal saline and cisplatin [20 mg/kg body weight (b.w.)], respectively. Cis + α-tocopherol group, Cis + Cur group and Cis + α-tocopherol + Cur group, rats were pre-treated with a single dose of α-tocopherol (250 mg/kg b.w.), curcumin (200 mg/kg b.w.) and combined α-tocopherol with curcumin, respectively, for 24 h prior the administration of cisplatin. After 72 h of first injection, specimens were collected. Liver enzyme, lipid peroxidation biomarker, liver histopathology and gene expression of liver nicotinamide adenine dinucleotide phosphate (NADPH) oxidase were investigated. Results: Cisplatin revealed a significant increase of hepatic malondialdehyde (MDA) levels and a significant reduction of hepatic superoxide dismutase (SOD) and catalase activities compared to the saline group. It elicited a marked increase of the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and demonstrated the liver pathologies including liver congestion, disorganization of hepatic cords and ground glass appearance of hepatocytes. It also demonstrated a significant increase of NADPH oxidase gene expression compared to saline group. Pre-treatment with combined curcumin and α-tocopherol improved the liver enzymes, lipid peroxidation biomarker, liver histopathology and gene expression of liver NADPH oxidase in cisplatin-treated rats. Conclusions: The findings indicate that pre-treatment with combined curcumin and α-tocopherol can protect cisplatin-induced hepatotoxicity including the biochemical, histological and molecular aspects. The down-regulations of NADPH oxidase gene expression may be involved in abrogating oxidative stress via reduction of reactive oxygen species (ROS) production. [ABSTRACT FROM AUTHOR]

Candida albicans is the primary cause of systemic candidiasis, which has a high mortality rate. Unfortunately, the number of antifungal drugs available for treatment of Candida infections is limited, and there is an urgent need for development of new drugs and alternative therapeutic options. We investigated the combinatory effect of fluconazole (FLCZ) and 640 FDA-approved drugs in vitro. Ten drugs enhanced and 77 drugs attenuated the antifungal activity of FLCZ. Other drugs did not appear to alter the antifungal activity of FLCZ, although 17 drugs displayed potency equivalent to or greater than that of FLCZ. The 10 FLCZ-enhancing drugs included three inhibitors of 3-hydroxy-3-methyl-glutaryl-CoA reductase, whose synergistic activity had been reported previously. However, the antifungal effects of 3 FLCZ enhancers—artesunate, carvedilol, and bortezomib—were previously unknown. In addition, many drugs were found to attenuate the antifungal activity of FLCZ, including 17 cyclooxygenase (COX) inhibitors, 15 estrogen-related agents, vitamin A- and D-related compounds, antihypertensive drugs, and proton pump inhibitors. Although the clinical significance remains to be determined, analyses of molecular events responsible for synergy or antagonism could provide insight into more efficient use of existing antifungals and lead to novel therapies. [ABSTRACT FROM AUTHOR]

Background: Asaronaldehyde (2, 4, 5-trimethoxybeznaldehyde) is an active component of Acorus gramineus rhizome. This study aims to evaluate the anti-Candida efficacy of asaronaldehyde and its three structural isomers, namely, 2, 3, 4-trimethoxybenzaldehyde, 3, 4, 5-trimethoxybenzaldehyde, and 2, 4, 6- trimethoxybenzaldehyde. Methods: Susceptibility testing of test compounds was carried out using standard methodology (M27-A2) as per clinical and laboratory standards institute guidelines. Minimum fungicidal concentration (MFC) was determined as the lowest concentration of drug killing 99.9% of Candida cells. The effect on sterol profile was evaluated using the ergosterol quantitation method. Effects on morphogenesis, adhesion and biofilm formation in C. albicans were studied using germ-tube, adherence and biofilm formation assays respectively. Cytotoxicity of test compounds to human RBCs was determined by hemolysis assay. Results: 2, 4, 6-Trimethoxybenzaldehyde exhibited significant anti-Candida activity (P = 0.0412). Minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC) were established as 0.25 and 0.5 mg/mL, respectively. All of the test compounds showed significant inhibition of hyphal form transition in yeast at MIC/2 and MIC/4 values. 3, 4, 5-Trimethoxybenzaldehyde and 2, 4, 6-trimethoxybenzaldehyde inhibited adhesion and biofilms. A hemolytic assay of these compounds revealed that they were non-toxic at MIC values. Asaronaldehyde reduced sterol content. Conclusion: Asaronaldehyde and 2, 4, 6-trimethoxybenzaldehyde showed anti-Candida efficacy. [ABSTRACT FROM AUTHOR]

Abstract: Although most of what is known about the biology and function of arachidonic acid metabolites comes from the study of mammalian biology, these compounds can also be produced by lower eukaryotes, including yeasts and other fungi. It is also in this group of organisms that the least is known about the metabolic pathways leading to the production of these compounds as well as the functions of these compounds in the biology of fungi and yeasts. This review will deal with the discovery of oxylipins from polyunsaturated fatty acids, and more specifically the arachidonic acid derived eicosanoids, such as 3-hydroxy eicosatetraenoic acid, prostaglandin F2α and prostaglandin E2, in yeasts starting in the early 1990s. This review will also focus on what is known about the metabolic pathways and/or proteins involved in the production of these compounds in pathogenic yeasts. The possible roles of these compounds in the biology, including the pathology, of these organisms will be discussed. [ABSTRACT FROM AUTHOR]

Cryotherapy is a non-pharmacological treatment commonly used to control inflammation and improve function after acute traumas. However, there are no definitive findings about its effects on chronic joint diseases such as knee osteoarthritis (KOA). The aim of this study was to investigate the effects of clinical-like cryotherapy on functional impairment and synovial inflammation in a rat model of KOA generated by anterior cruciate ligament transection (ACLT). Thirty-two male Wistar rats were randomly divided into four groups (n = 8/group): Control, KOA, KOA + Cryotherapy and KOA + Placebo. The last two groups were submitted to the relevant interventions twice a day for five days (61 to 65), with each session lasting 20 min. Gait test, skin temperature, thermal response threshold and joint swelling were assessed in all groups before ACLT surgery, and pre (60th day) and post (66th day) intervention protocols. On day 66, the animals were euthanized and exsanguinated to remove the synovial membrane for histopathological examination and synovial fluid to determine the leukocyte count and cytokine concentration. After the intervention period (66th day), footprint area only increased in the KOA + Cryotherapy group (P = 0.004; 14%) when compared to KOA and KOA + Placebo, but did not differ from controls. Cryotherapy lowered the synovial fluid leukocyte count (P < 0.0001; ≥95.0%) and cytokine concentration (P < 0.0001; ≥55%) when compared to the KOA and Placebo groups. Synovial score and synovial fibrosis did not differ in the KOA groups. In conclusion, footprint patterns improved in rats with ACLT-induced KOA as a result of clinical-like cryotherapy, which also lowered the synovial fluid leukocyte count and inflammatory cytokine concentration in these rats. [ABSTRACT FROM AUTHOR]

Knee osteoarthritis (KOA) is associated with muscle weakness, but it is unclear which structures are involved in the muscle changes. This study assessed morphological alterations and the expression of genes and proteins linked to muscular atrophy and neuromuscular junctions (NMJs) in KOA, induced by anterior cruciate ligament transection (ACLT) in rats. Two groups of rats were assessed: control (without intervention) and KOA (ACLT surgery in the right knee). After 8 weeks, quadriceps, tibialis anterior (TA) and gastrocnemius muscles were analyzed (area of muscle fibers, NMJ, gene and protein expression). KOA group showed atrophy in quadriceps (15.7%) and TA (33%), with an increase in atrogin-1 and muscle RING-finger protein-1 (MuRF-1). KOA group showed quadriceps NMJ remodeling (reduction area and perimeter) and decrease in NMJ diameter in TA muscle. The expression of nicotinic acetylcholine receptor (nAChR) γ-nAChR increased and that of α-nAChR and muscle specific tyrosine kinase (MuSK) declined in the quadriceps, with a decrease in ε-nAChR in TA. MuRF-1 protein expression increased in quadriceps and TA, with no changes in neural cell adhesion molecule (NCAM). In conclusion, ACLT-induced KOA promotes NMJ remodeling and atrophy in quadriceps and TA muscles, associated with inflammatory signs and changes in muscle gene and protein expression. [ABSTRACT FROM AUTHOR]