Realtime gas emission monitoring at hazardous sites using a distributed point-source sensing infrastructure

This paper describes a distributed point-source monitoring platform for gas level and leakage detection in hazardous environments. The platform, based on a wireless sensor network (WSN) architecture, is organised into sub-networks to be positioned in the plant’s critical areas; each sub-net includes a gateway unit wirelessly connected to the WSN nodes, hence providing an easily deployable, stand-alone infrastructure featuring a high degree of scalability and reconfigurability. Furthermore, the system provides automated calibration routines which can be accomplished by non-specialized maintenance operators without system reliability reduction issues. Internet connectivity is provided via TCP/IP over GPRS (Internet standard protocols over mobile networks) gateways at a one-minute sampling rate. Environmental and process data are forwarded to a remote server and made available to authenticated users through a user interface that provides data rendering in various formats and multi-sensor data fusion. The platform is able to provide real-time plant management with an effective; accurate tool for immediate warning in case of critical events

Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Acai Berries and Pistachios and Cashews as Natural Food Sources

Inflammation is a biological reaction to oxidative stress in which cell starts producing proteins, enzymes, and other substances to restore homeostasis, while oxidative stress could be intrinsically a biochemical imbalance of the physiologically redox status of the intracellular environment. The nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway, which controls the transcription of numerous antioxidant genes that protect cellular homeostasis and detoxification genes that process and eliminate all toxic compounds and substances before they can cause damage. The Nrf2 pathway is the heart of the daily biological response to oxidative stress. Transient activation of Nrf2 by diet can upregulate antioxidant enzymes to protect cells against oxidative stress inducers. In this chapter, we summarize the effects of some novel foods in the regulation of the Nrf2/ARE pathway and its cellular mechanisms

A novel composite formulation of palmitoylethanolamide and quercetin decreases inflammation and relieves pain in inflammatory and osteoarthritic pain models

Background: Osteoarthritis (OA) is a common progressive joint disease in dogs and cats. The goal of OA treatment is to reduce inflammation, minimize pain, and maintain joint function. Currently, non-steroidal anti-inflammatory drugs (e.g., meloxicam) are the cornerstone of treatment for OA pain, but side effects with long-term use pose important challenges to veterinary practitioners when dealing with OA pain. Palmitoylethanolamide (PEA) is a naturally-occurring fatty acid amide, locally produced on demand by tissues in response to stress. PEA endogenous levels change during inflammatory and painful conditions, including OA, i.e., they are typically increased during acute conditions and decreased in chronic inflammation. Systemic treatment with PEA has anti-inflammatory and pain-relieving effects in several disorders, yet data are lacking in OA. Here we tested a new composite, i.e., PEA co-ultramicronized with the natural antioxidant quercetin (PEA-Q), administered orally in two different rat models of inflammatory and OA pain, namely carrageenan paw oedema and sodium monoiodoacetate (MIA)-induced OA. Oral treatment with meloxicam was used as benchmark. Results: PEA-Q decreased inflammatory and hyperalgesic responses induced by carrageenan injection, as shown by: (i) paw oedema reduction, (ii) decreased severity in histological inflammatory score, (iii) reduced activity of myeloperoxidase, i.e., a marker of inflammatory cell infiltration, and (iv) decreased thermal hyperalgesia. Overall PEA-Q showed superior effects compared to meloxicam. In MIA-treated animals, PEA-Q exerted the following effects: (i) reduced mechanical allodynia and improved locomotor function, (ii) protected cartilage against MIA-induced histological damage, and (iii) counteracted the increased serum concentration of tumor necrosis factor alpha, interleukin 1 beta, metalloproteases 1, 3, 9 and nerve growth factor. The magnitude of these effects was comparable to, or even greater than, those of meloxicam. Conclusion: The present findings shed new light on some of the inflammatory and nociceptive pathways and mediators targeted by PEA-Q and confirm its anti-inflammatory and pain-relieving effects in rodent OA pain models. The translatability of these observations to canine and feline OA pain is currently under investigation

Treatment With a Flavonoid-Rich Fraction of Bergamot Juice Improved Lipopolysaccharide-Induced Periodontitis in Rats

Objective: In this study, we investigated the effects of a flavonoid-rich fraction of Bergamot juice (BJe) in rats subjected to experimental periodontitis induced by a single intragingival injection of lipopolysaccharides (LPS).Main Methods: Periodontitis was induced by a single intragingival injection of 1 μl LPS (10 μg/μl) derived from Salmonella typhimurium in sterile saline solution. The injection was made in the mesolateral side at the interdental papilla between the first and the second molar. Fourteen days after LPS injection, we performed radiographic analyses and then we surgically removed the gingivomucosal tissue surrounding the mandibular first molar for histological, immunohistochemical and molecular analysis.Results: LPS significantly induced oedema, tissue damage and increased neutrophil infiltration. At molecular level, we found increased NF-κB translocation as well as raised both TNF-α and IL-1β expression, other than modulation of apoptosis-associated proteins. Moreover, the increased myeloperoxidase activity was associated with up-regulation of adhesion molecules. Immunohistochemical analysis for nitrotyrosine and poly ADP-ribose displayed an intense staining in the gingivomucosal tissue. Oral administration of BJe for 14 consecutive days reduced tissue injury and several markers of gingival inflammation including nuclear NF-κB translocation, cytokines expression, myeloperoxidase activity and the expression of some adhesion molecules such as ICAM and P-selectin. BJe also decreased both nitrosative stress and PARP positive staining. Moreover, it caused down-regulation of Bax and up-regulation of Bcl-2 expression.Conclusion: Our findings demonstrate that BJe improves LPS-induced periodontitis in rats by reducing the typical markers of inflammation, thus suggesting its potential in the treatment of periodontal diseases

Human Cryptic Host Defence Peptide {GVF}27 Exhibits Anti-Infective Properties against Biofilm Forming Members of the Burkholderia cepacia Complex

Therapeutic solutions to counter Burkholderia cepacia complex (Bcc) bacteria are challenging due to their intrinsically high level of antibiotic resistance. Bcc organisms display a variety of potential virulence factors, have a distinct lipopolysaccharide naturally implicated in antimicrobial resistance. and are able to form biofilms, which may further protect them from both host defence peptides (HDPs) and antibiotics. Here, we report the promising anti-biofilm and immunomodulatory activities of human HDP GVF27 on two of the most clinically relevant Bcc members, Burkholderia multivorans and Burkholderia cenocepacia. The effects of synthetic and labelled GVF27 were tested on B. cenocepacia and B. multivorans biofilms, at three different stages of formation, by confocal laser scanning microscopy (CLSM). Assays on bacterial cultures and on human monocytes challenged with B. cenocepacia LPS were also performed. GVF27 exerts, at different stages of formation, antibiofilm effects towards both Bcc strains, a significant propensity to function in combination with ciprofloxacin, a relevant affinity for LPSs isolated from B. cenocepacia as well as a good propensity to mitigate the release of pro-inflammatory cytokines in human cells pre-treated with the same endotoxin. Overall, all these findings contribute to the elucidation of the main features that a good therapeutic agent directed against these extremely leathery biofilm-forming bacteria should possess

protective effect of a new hyaluronic acid carnosine conjugate on the modulation of the inflammatory response in mice subjected to collagen induced arthritis

Abstract Several studies demonstrated the pharmacological actions of carnosine as well as hyaluronic acid (HA) during joint inflammation. In that regard, the aim of this study was to investigate the protective effect of a new HA -Carnosine conjugate (FidHycarn) on the modulation of the inflammatory response in mice subjected to collagen-induced arthritis (CIA). CIA was induced by two intradermal injections of 100 μl of an emulsion of collagen (CII) and complete Freund's adjuvant (CFA) at the base of the tail on day 0 and 21. At 35 day post CIA induction, the animals were sacrificed. CII injection caused erythema and edema in the hind paws, histological alterations with erosion of the joint cartilage as well as behavioral changes. Oral treatment with FidHycarn starting at the onset of arthritis (day 25) ameliorated the clinical signs, improved behavioral deficits as well as decreased histological and radiographic alterations. The degree of oxidative damage evaluated by inducible nitric oxide synthase (iNOS), nitrotyrosine, poly-ADP-ribose (PAR) expressions and malondialdehyde (MDA) levels, was also significantly reduced in Carnosine+HA association and FidHycarn treated mice. Moreover, the levels of proinflammatory cytokines and chemokines and cyclo-oxygenase COX-2 enzyme were also more significantly reduced by Carnosine+HA and FidHycarn compared to carnosine alone. However, interestingly, in some cases, the effects of FidHycarn were more important than Carnosine+HA association and not statistically different to methotrexate (MTX) used as positive control. Thus, the conjugation of Carnosine with HA (FidHycarn) could represent an interesting therapeutic strategy to combat arthritis disorders

Socioeconomic deprivation worsens the outcomes of Italian women with hormone receptor-positive breast cancer and decreases the possibility of receiving standard care.

BACKGROUND: Socioeconomic factors influence access to cancer care and survival. This study investigated the role of socioeconomic status on the risk of breast cancer recurrence and on the delivery of appropriate cancer care (sentinel lymph node biopsy and breast-conserving surgery plus radiotherapy), by patients' age and hormone receptor status. METHODS: 3,462 breast cancer cases diagnosed in 2003-2005 were selected from 7 Italian cancer registries and assigned to a socioeconomic tertile on the basis of the deprivation index of their census tract. Multivariable models were applied to assess the delivery of sentinel lymph node biopsy and of breast-conserving surgery plus radiotherapy within socioeconomic tertiles. RESULTS: In the 1,893 women younger than 65 years, the 5-year risk of recurrence was higher in the most deprived group than in the least deprived, but this difference was not significant (16.4% vs. 12.9%, log-rank p=0.08); no difference was seen in women ≥65 years. Among the 2,024 women with hormone receptor-positive cancer, the 5-year risk was significantly higher in the most deprived group than in the least deprived one (13.0% vs. 8.9%, p=0.04); no difference was seen in cases of hormone receptor-negative cancer. The most deprived women were less likely than the least deprived women to receive sentinel lymph node biopsy (adjusted odds ratio (ORa), 0.69; 95% CI, 0.56-0.86) and to undergo breast-conserving surgery plus radiotherapy (ORa=0.66; 95% CI, 0.51-0.86). Conclusions: Socioeconomic inequalities affect the risk of recurrence, among patients with hormone receptor-positive cancer, and the opportunity to receive standard care