PMID: 

Environ Int. 2016 Dec ;97:100-107. Epub 2016 Nov 9. PMID: 27835750

Abstract Title: 

Inferring the 1985-2014 impact of mobile phone use on selected brain cancer subtypes using Bayesian structural time series and synthetic controls.

Abstract: 

BACKGROUND: Mobile phone use has been increasing rapidly in the past decades and, in parallel, so has the annual incidence of certain types of brain cancers. However, it remains unclear whether this correlation is coincidental or whether use of mobile phones may cause the development, promotion or progression of specific cancers. The 1985-2014 incidence of selected brain cancer subtypes in England were analyzed and compared to counterfactual 'synthetic control' timeseries.METHODS: Annual 1985-2014 incidence of malignant glioma, glioblastoma multiforme, and malignant neoplasms of the temporal and parietal lobes in England were modelled based on population-level covariates using Bayesian structural time series models assuming 5,10 and 15year minimal latency periods. Post-latency counterfactual 'synthetic England' timeseries were nowcast based on covariate trends. The impact of mobile phone use was inferred from differences between measured and modelled time series.RESULTS: There is no evidence of an increase in malignant glioma, glioblastoma multiforme, or malignant neoplasms of the parietal lobe not predicted in the 'synthetic England' time series. Malignant neoplasms of the temporal lobe however, have increased faster than expected. A latency period of 10years reflected the earliest latency period when this was measurable and related to mobile phone penetration rates, and indicated an additional increase of 35% (95% Credible Interval 9%:59%) during 2005-2014; corresponding to an additional 188 (95%CI 48-324) cases annually.CONCLUSIONS: A causal factor, of which mobile phone use (and possibly other wireless equipment) is in agreement with the hypothesized temporal association, is related to an increased risk of developing malignant neoplasms in the temporal lobe.

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PMID: 

Gulf J Oncolog. 2016 Jan ;1(20):71-8. PMID: 27050182

Abstract Title: 

Mobile Phone Use and the Risk of Parotid Gland Tumors: A Retrospective Case-Control Study.

Abstract: 

BACKGROUND: Mobile phones are integral part of the modern lifestyle. As they emit radio frequency electromagnetic field, their role in carcinogenesis needs to be ascertained. The goal of this study was to investigate the association between the use of cellular phones and the risk for parotid gland tumors.MATERIALS AND METHODS: A total of 26 patients diagnosed with parotid gland tumors and 61 healthy controls were enrolled through a hospital-based retrospective case-control study. The patients were referred and admitted to a tertiary hospital from January 1996 to March 2013.RESULTS: The Odds of exposure were 3.47 times higher among patients compared to their controls. 95% CI suggested that the true Odds Ratio (OR) at the population level could be somewhere between 1.3 and 9.23 and so the observed OR was statistically significant at 5% level of significance.CONCLUSIONS: Overall, an association between the exposure of cellular phone use for more than 1 hour daily and parotid tumor was observed. This association should be interpreted with caution because of the relatively small sample size.

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PMID: 

Indian J Otolaryngol Head Neck Surg. 2013 Dec ;65(Suppl 3):645-9. Epub 2013 Sep 7. PMID: 24427730

Abstract Title: 

Auditory Brainstem Responses and EMFs Generated by Mobile Phones.

Abstract: 

There has been a manifold increase in the number of mobile phone users throughout the world with the current number of users exceeding 2 billion. However this advancement in technology like many others is accompanied by a progressive increase in the frequency and intensity of electromagnetic waves without consideration of the health consequences. The aim of our study was to advance our understanding of the potential adverse effects of GSM mobile phones on auditory brainstem responses (ABRs). 60 subjects were selected for the study and divided into three groups of 20 each based on their usage of mobile phones. Their ABRs were recorded and analysed for latency of waves I-V as well as interpeak latencies I-III, I-V and III-V (in ms). Results revealed no significant difference in the ABR parameters between group A (control group) and group B (subjects using mobile phones for maximum 30 min/day for 5 years). However the latency of waves was significantly prolonged in group C (subjects using mobile phones for 10 years for a maximum of 30 min/day) as compared to the control group. Based on our findings we concluded that long term exposure to mobile phones may affect conduction in the peripheral portion of the auditory pathway. However more research needs to be done to study the long term effects of mobile phones particularly of newer technologies like smart phones and 3G.

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PMID: 

Biol Pharm Bull. 2013 ;36(8):1375-9. PMID: 23902981

Abstract Title: 

Effect of eriodictyol on the development of atopic dermatitis-like lesions in ICR mice.

Abstract: 

Atopic dermatitis (AD) is a chronic, allergic, and inflammatory skin disease associated with eczema and dermatitis symptoms. Our previous studies have reported that eriodictyol extract inhibits immunoglobulin E (IgE)/Ag-induced type I hypersensitivity by suppressing the activation of proinflammatory cytokines, such as interleukin-4 (IL-4), and the expression of ceramide kinase. In this study, we investigated the inhibitory effect of eriodictyol on 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin lesions in ICR mice. Treatment with 2 mg/mL eriodictyol for DNCB-induced AD-like skin lesions in ICR mice improved scratching behavior and skin severity score. Histological analysis demonstrated that thickening of the skin lesions were significantly reduced in the eriodictyol-treated group. Also, eriodictyol suppressed the DNCB-mediated elevation of IgE serum levels. These results suggest that eriodictyol may be a potential therapeutic resource for AD and an adjunctive agent to control itchiness in AD.

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PMID: 

Neurochem Res. 2015 Jul ;40(7):1463-71. Epub 2015 May 21. PMID: 25994859

Abstract Title: 

Eriodictyol Attenuatesβ-Amyloid 25-35 Peptide-Induced Oxidative Cell Death in Primary Cultured Neurons by Activation of Nrf2.

Abstract: 

Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). Eriodictyol, a flavonoid isolated from the Chinese herb Dracocephalum rupestre, has long been established as an antioxidant. The present study was designed to investigate the effect of eriodictyol onβ-amyloid 25-35 peptide (Aβ25-35)-induced oxidative cell death in primary neurons and to explore the role of the nuclear factor erythroid-2-related factor 2/antioxidant response element (Nrf2/ARE) pathway in this process. For this purpose, primary cultures of cortical neurons were exposed to 15 μM Aβ25-35 in the absence or presence of eriodictyol (20, 40 and 80 μM). The results revealed that Aβ25-35-induced cytotoxicity and apoptotic characteristics such as activation of JNK/p38 apoptotic signaling pathway were effectively attenuated by eriodictyol pretreatment. Eriodictyol treatment also resulted in an increase in Nrf2 protein levels and subsequent activation of ARE pathway genes in primary cultured neurons. The protective effects of eriodictyol were attenuated by RNA interference-mediated knockdown of Nrf2 expression. Taken together, these results clearly demonstrate that eriodictyol protects neurons against Aβ25-35-induced cell death partially through Nrf2/ARE signaling pathway, which further supports that eriodictyol might be a promising novel therapeutic agent for AD.

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PMID: 

Int J Mol Sci. 2015 Jun 26 ;16(7):14526-39. Epub 2015 Jun 26. PMID: 26132561

Abstract Title: 

Eriodictyol Protects Endothelial Cells against Oxidative Stress-Induced Cell Death through Modulating ERK/Nrf2/ARE-Dependent Heme Oxygenase-1 Expression.

Abstract: 

The pathophysiology of cardiovascular diseases is complex and may involve oxidative stress-related pathways. Eriodictyol is a flavonoid present in citrus fruits that demonstrates anti-inflammatory, anti-cancer, neurotrophic, and antioxidant effects in a range of pathophysiological conditions including vascular diseases. Because oxidative stress plays a key role in the pathogenesis of cardiovascular disease, the present study was designed to verify whether eriodictyol has therapeutic potential. Upregulation of heme oxygenase-1 (HO-1), a phase II detoxifying enzyme, in endothelial cells is considered to be helpful in cardiovascular disease. In this study, human umbilical vein endothelial cells (HUVECs) treated with eriodictyol showed the upregulation of HO-1 through extracellular-regulated kinase (ERK)/nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathways. Further, eriodictyol treatment provided protection against hydrogen peroxide-provoked cell death. This protective effect was eliminated by treatment with a specific inhibitor of HO-1 and RNA interference-mediated knockdown of HO-1 expression. These data demonstrate that eriodictyol induces ERK/Nrf2/ARE-mediated HO-1 upregulation in human endothelial cells, which is directly associated with its vascular protection against oxidative stress-related endothelial injury, and propose that targeting the upregulation of HO-1 is a promising approach for therapeutic intervention in cardiovascular disease.

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PMID: 

Exp Cell Res. 2015 Dec 10 ;339(2):380-8. Epub 2015 Oct 9. PMID: 26450448

Abstract Title: 

Eriodicyol inhibits osteoclast differentiation and ovariectomy-induced bone loss in vivo.

Abstract: 

Osteoclasts are responsible for bone erosion in diseases such as osteoporosis and rheumatoid arthritis. In the present study, we investigate the effects of eriodictyol, a flavonoid found naturally in citrus fruits, on the receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation using mouse bone marrow macrophages (BMMs). Eriodictyol inhibited RANKL-induced osteoclast formation in a dose-dependent manner without cytotoxicity. In addition, eriodictyol suppressed bone resorption activity of differentiated osteoclasts. The inhibitory effect of eriodictyol was associated with impaired activation of multiple signaling events downstream of RANK, including extracellular signal-regulated kinase, p38, and c-Jun terminal kinase phosphorylation, followed by decreased nuclear factor of activated T cells (NFAT)c1 expression. Ectopicoverexpression of a constitutively active form of NFATc1 completely rescued the anti-osteoclastogenic effect of eriodictyol, suggesting that the anti-osteoclastogenic effect was mainly attributed to the reduction in NFATc1 expression. Consistent with the in vitro anti-osteoclastogenic effect, eriodictyol suppressed lipopolysaccharide-induced osteoclast formation in the calvarial model and ovariectomy-induced bone loss in vivo. Taken together, our data demonstrate that eriodictyol is a new therapeutic agent with the potential to prevent bone destructive diseases by reducing both osteoclast differentiation and function.

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PMID: 

Exp Ther Med. 2015 Dec ;10(6):2259-2266. Epub 2015 Oct 23. PMID: 26668626

Abstract Title: 

Eriodictyol, a plant flavonoid, attenuates LPS-induced acute lung injury through its antioxidative and anti-inflammatory activity.

Abstract: 

Acute lung injury (ALI) is characterized by excessive inflammatory responses and oxidative injury in the lung tissue. It has been suggested that anti-inflammatory or antioxidative agents could have therapeutic effects in ALI, and eriodictyol has been reported to exhibit antioxidative and anti-inflammatory activity. The aim of the present study was to investigate the effect of eriodictyol on lipopolysaccharide (LPS)-induced ALI in a mouse model. The mice were divided into four groups: Phosphate-buffered saline-treated healthy control, LPS-induced ALI, vehicle-treated ALI (LPS + vehicle) and eriodictyol-treated ALI (LPS + eriodictyol). Eriodictyol (30 mg/kg) was administered orally once, 2 days before the induction of ALI. The data showed that eriodictyol pretreatment attenuated LPS-induced ALI through its antioxidative and anti-inflammatory activity. Furthermore, the eriodictyol pretreatment activated the nuclear factor erythroid-2-related factor 2 (Nrf2) pathway in the ALI mouse model, which attenuated the oxidative injury and inhibited the inflammatory cytokine expression in macrophages. In combination, the results of the present study demonstrated that eriodictyol could alleviate the LPS-induced lung injury in mice by regulating the Nrf2 pathway and inhibiting the expression of inflammatory cytokines in macrophages, suggesting that eriodictyol could be used as a potential drug for the treatment of LPS-induced lung injury.

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PMID: 

Eur J Pharmacol. 2016 Feb 5 ;772:124-30. Epub 2015 Dec 23. PMID: 26723515

Abstract Title: 

Eriodictyol attenuates cisplatin-induced kidney injury by inhibiting oxidative stress and inflammation.

Abstract: 

Eriodictyol, a flavonoid present in citrus fruits, has been reported to have antioxidant and anti-inflammatory effects. In this study, the protective effects of eriodictyol on cisplatin (CP)-induced kidney injury were detected. CP-induced kidney injury model was established by administration of CP (20mg/kg). The results showed that treatment of eriodictyol inhibited the production of blood urea nitrogen (BUN), creatinine, MDA, TBARS, reactive oxygen species (ROS), as well as the production of TNF-α, and IL-1β in kidney tissues induced by CP. Eriodictyol also up-regulated the activities of SOD, CAT, and GSH-PX decreased by CP. Furthermore, eriodictyol was found to up-regulate the expression of Nrf2/HO-1 and inhibited CP-induced NF-κB activation in kidney tissues. In conclusion, eriodictyolprotected against CP-induced kidney injury through activating Nrf2 and inhibiting NF-κB activation.

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PMID: 

Cell Stress Chaperones. 2016 09 ;21(5):773-81. Epub 2016 Jun 1. PMID: 27250501

Abstract Title: 

Investigation of immunomodulatory and anti-inflammatory effects of eriodictyol through its cellular anti-oxidant activity.

Abstract: 

Many studies have been performed to assess the potential utility of natural products as immunomodulatory agents to enhance host responses against infection or to ameliorate immune-based pathologies. To determine whether eriodictyol has immunomodulatory effects and clarify which types of immune effector cells are stimulated in vitro, we investigated the stimulatory effect of eriodictyol on spleen cells isolated from BALB/c mice. Eriodictyol significantly stimulated splenocyte proliferation. However, only B lymphocytes (not T lymphocytes) could be stimulated by eriodictyol in a dose-related manner. Studies assessing potential effect of eriodictyol on innate immunity reported that eriodictyol enhanced significantly the killing activity of natural killer (NK) cells, T lymphocytes, and macrophages. We also demonstrated that eriodictyol inhibited nitric oxide (NO) production and lysosomal enzyme activity in murine peritoneal macrophages cultured ex-vivo, suggesting a potential anti-inflammatory effect in situ. Eriodictyol revealed also a cellular anti-oxidant activity in splenocytes and macrophages. Furthermore, eriodictyol increased catalase activity in spleen cells. From this data, it can be concluded that eriodictyol exhibited an immunomodulatory effect that could be ascribed in part to a cytoprotective effect related to its anti-oxidant activity.

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