PMID: 

Exp Anim. 2018 Nov 1 ;67(4):545-553. Epub 2018 Jul 31. PMID: 30068825

Abstract Title: 

Carnosol protects against renal ischemia-reperfusion injury in rats.

Abstract: 

Acute kidney injury, which is caused by renal ischemia-reperfusion injury (IRI), occurs in several clinical situations and causes severe renal damage. There is no effective therapeutic agent available for renal IRI at present. In this study, we performed an experiment based on an in vivo murine model of renal IRI to examine the effect of carnosol. Thirty Sprague-Dawley rats were randomized into three groups (10 rats in each group): the sham, IRI, and carnosol groups. Rats in the carnosol group were injected intravenously with 3 mg/kg of carnosol, and those in the sham and IRI groups were injected intravenously with 10% dimethyl sulfoxide 1 h before ischemia. Rats were sacrificed after 24 h of reperfusion. The blood and kidneys were harvested, renal function was assessed, and histologic evaluation was performed to analyze renal injury. A renal myeloperoxidase activity assay, in-situ apoptosis examination, enzyme-linked immunosorbent assay, immunohistochemical assay, and western blot were also performed. Carnosol pretreatment significantly reduced renal dysfunction and histologic damage induced by renal IRI. Carnosol pretreatment suppressed renal inflammatory cell infiltration and pro-inflammatory cytokine expression. In addition, carnosol markedly inhibited apoptotic tubular cell death, caspase-3 activation, and activation of the p38 pathway. Carnosol pretreatment protects rats against renal IRI by inhibiting inflammation and apoptosis. Although future investigation is needed, carnosol may be a potential therapeutic agent for preventing renal IRI.

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PMID: 

J Psychosom Res. 2010 Jan ;68(1):37-45. PMID: 20004299

Abstract Title: 

Symptoms, personality traits, and stress in people with mobile phone-related symptoms and electromagnetic hypersensitivity.

Abstract: 

OBJECTIVE: Some people report symptoms that they associate with electromagnetic field (EMF) exposure. These symptoms may be related to specific EMF sources or to electrical equipment in general (perceived electromagnetic hypersensitivity, EHS). Research and clinical observations suggest a difference between mobile phone (MP)-related symptoms and EHS with respect to symptom prevalence, psychological factors, and health prognosis. This study assessed prevalence of EMF-related and EMF-nonrelated symptoms, anxiety, depression, somatization, exhaustion, and stress in people with MP-related symptoms or EHS versus a population-based sample and a control sample without EMF-related symptoms.METHODS: Forty-five participants with MP-related symptoms and 71 with EHS were compared with a population-based sample (n=106) and a control group (n=63) using self-report questionnaires.RESULTS: The EHS group reported more symptoms than the MP group, both EMF-related and EMF-nonrelated. The MP group reported a high prevalence of somatosensory symptoms, whereas the EHS group reported more neurasthenic symptoms. As to self-reported personality traits and stress, the case groups differed only on somatization and listlessness in a direct comparison. In comparison with the reference groups, the MP group showed increased levels of exhaustion and depression but not of anxiety, somatization, and stress; the EHS group showed increased levels for all of the conditions except for stress.CONCLUSION: The findings support the idea of a difference between people with symptoms related to specific EMF sources and people with general EHS with respect to symptoms and anxiety, depression, somatization, exhaustion, and stress. The differences are likely to be important in the management of patients.

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PMID: 

Oncotarget. 2018 Sep 28 ;9(76):34200-34212. Epub 2018 Feb 6. PMID: 30344937

Abstract Title: 

Carnosol suppresses patient-derived gastric tumor growth by targeting RSK2.

Abstract: 

Carnosol is a phenolic diterpene that is isolated from rosemary, sage, and oregano. It has been reported to possess anti-oxidant, anti-inflammatory, and anti-cancer properties. However, the molecular mechanism of carnosol's activity against gastric cancer has not been investigated. Herein, we report that carnosol is an RSK2 inhibitor that attenuates gastric cancer growth. Carnosol reduced anchorage-dependent and -independent gastric cancer growth by inhibiting the RSKs-CREB signaling pathway. The results ofscreening and cell-based assays indicated that carnosol represses RSK2 activity and its downstream signaling. Carnosol increased the G2/M phase and decreased S phase cell cycle and also induced apoptosis through the activation of caspases 9 and 7 and inhibition of Bcl-xL expression. Notably, oral administration of carnosol suppressed patient-derived gastric tumor growth in anmouse model. Our findings suggest that carnosol is an RSK2 inhibitor that could be useful for treating gastric cancer.

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PMID: 

Arch Pharm Res. 2019 Mar ;42(3):274-283. Epub 2018 Nov 15. PMID: 30430364

Abstract Title: 

Inhibitory effect of Carnosol on UVB-induced inflammation via inhibition of STAT3.

Abstract: 

Ultraviolet B (UVB) irradiation causes sunburn, inflammatory responses, dysregulation of immune function, oxidative stress, DNA damage and photocarcinogenesis on skin. Rosemary (Rosmarinus officinalis L.) has been reported to inhibit inflammation. Carnosol, a major component of Rosemary, has prominent anti-inflammatory effects. However, its protective effect on UVB-induced inflammatory skin responses has not yet been reported. Here, we investigated the effectiveness of carnosol on UVB-induced inflammation. We examined the anti-inflammation effect of topical application of carnosol (0.05 µg/cm) on UVB (540 mJ/cm, for 3 successive days)-induced skin inflammation in HR1 mice. Topical application of carnosol inhibited UVB-induced erythema, epidermal thickness, inflammatory responses in HR1 mice. Carnosol reduced the level of Immunoglobulin-E and IL-1β in blood serum of UVB-induced mice. Carnosol also significantly inhibited the UVB-induced expression of inflammatory marker protein (iNOS and COX-2) in back skin of mice. In addition, carnosol treated skin decreased activation of STAT3, a transcriptional factor regulating inflammatory genes. Ourstudy suggested that carnosol has protective effects on skin inflammatory skin damages by UVB.

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PMID: 

Front Immunol. 2018 ;9:1807. Epub 2018 Aug 13. PMID: 30150982

Abstract Title: 

Carnosol Modulates Th17 Cell Differentiation and Microglial Switch in Experimental Autoimmune Encephalomyelitis.

Abstract: 

Medicinal plants as a rich pool for developing novel small molecule therapeutic medicine have been used for thousands of years. Carnosol as a bioactive diterpene compound originated from(Rosemary) and, herbs extensively applied in traditional medicine for the treatment of multiple autoimmune diseases (1). In this study, we investigated the therapeutic effects and molecule mechanism of carnosol in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Carnosol treatment significantly alleviated clinical development in the myelin oligodendrocyte glycoprotein (MOG) peptide-induced EAE model, markedly decreased inflammatory cell infiltration into the central nervous system and reduced demyelination. Further, carnosol inhibited Th17 cell differentiation and signal transducer and activator of transcription 3 phosphorylation, and blocked transcription factor NF-κB nuclear translocation. In the passive-EAE model, carnosol treatment also significantly prevented Th17 cell pathogenicity. Moreover, carnosol exerted its therapeutic effects in the chronic stage of EAE, and, remarkably, switched the phenotypes of infiltrated macrophage/microglia. Taken together, our results show that carnosol has enormous potential for development as a therapeutic agent for autoimmune diseases such as MS.

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Whether you’ve heard something on the news, seen mention of it on television, or are simply searching for a natural alternative to treat an ongoing health condition or frustration, CBD oil has likely come to your attention.

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Source: https://www.cbdcentral.com

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PMID: 

Cancer Epidemiol. 2011 Oct ;35(5):453-64. Epub 2011 Aug 23. PMID: 21862434

Abstract Title: 

Acoustic neuroma risk in relation to mobile telephone use: results of the INTERPHONE international case-control study.

Abstract: 

BACKGROUND: The rapid increase in mobile telephone use has generated concern about possible health risks of radiofrequency electromagnetic fields from these devices.METHODS: A case-control study of 1105 patients with newly diagnosed acoustic neuroma (vestibular schwannoma) and 2145 controls was conducted in 13 countries using a common protocol. Past mobile phone use was assessed by personal interview. In the primary analysis, exposure time was censored at one year before the reference date (date of diagnosis for cases and date of diagnosis of the matched case for controls); analyses censoring exposure at five years before the reference date were also done to allow for a possible longer latent period.RESULTS: The odds ratio (OR) of acoustic neuroma with ever having been a regular mobile phone user was 0.85 (95% confidence interval 0.69-1.04). The OR for≥10 years after first regular mobile phone use was 0.76 (0.52-1.11). There was no trend of increasing ORs with increasing cumulative call time or cumulative number of calls, with the lowest OR (0.48 (0.30-0.78)) observed in the 9th decile of cumulative call time. In the 10th decile (≥1640 h) ofcumulative call time, the OR was 1.32 (0.88-1.97); there were, however, implausible values of reported use in those with ≥1640 h of accumulated mobile phone use. With censoring at 5 years before the reference date the OR for ≥10 years after first regular mobile phone use was 0.83 (0.58-1.19) andfor ≥1640 h of cumulative call time it was 2.79 (1.51-5.16), but again with no trend in the lower nine deciles and with the lowest OR in the 9th decile. In general, ORs were not greater in subjects who reported usual phone use on the same side of the head as their tumour than in those who reported it on the opposite side, but it was greater in those in the 10th decile of cumulative hours of use.CONCLUSIONS: There was no increase in risk of acoustic neuroma with ever regular use of a mobile phone or for users who began regular use 10 years or more before the reference date. Elevated odds ratios observed at the highest level of cumulative call time could be due to chance, reporting bias or a causal effect. As acoustic neuroma is usually a slowly growing tumour, the interval between introduction of mobile phones and occurrence of the tumour might have been too short to observe an effect, if there is one.

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PMID: 

Int J Epidemiol. 2010 Jun ;39(3):675-94. Epub 2010 May 17. PMID: 20483835

Abstract Title: 

Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study.

Abstract: 

BACKGROUND: The rapid increase in mobile telephone use has generated concern about possible health risks related to radiofrequency electromagnetic fields from this technology.METHODS: An interview-based case-control study with 2708 glioma and 2409 meningioma cases and matched controls was conducted in 13 countries using a common protocol.RESULTS: A reduced odds ratio (OR) related to ever having been a regular mobile phone user was seen for glioma [OR 0.81; 95% confidence interval (CI) 0.70-0.94] and meningioma (OR 0.79; 95% CI 0.68-0.91), possibly reflecting participation bias or other methodological limitations. No elevated OR was observed>or =10 years after first phone use (glioma: OR 0.98; 95% CI 0.76-1.26; meningioma: OR 0.83; 95% CI 0.61-1.14). ORs wereor =1640 h, the OR was 1.40 (95% CI 1.03-1.89) for glioma, and 1.15 (95% CI 0.81-1.62) for meningioma; but there are implausible values of reported use in this group. ORs for glioma tended to be greater in the temporal lobe than in other lobes of the brain, but the CIs around the lobe-specific estimates were wide. ORs for glioma tended to be greater in subjects who reported usual phone use on the same side of the head as their tumour than on the opposite side.CONCLUSIONS: Overall, no increase in risk of glioma or meningioma was observed with use of mobile phones. There were suggestions of an increased risk of glioma at the highest exposure levels, but biases and error prevent a causal interpretation. The possible effects of long-term heavy use of mobile phones require further investigation.

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PMID: 

N Engl J Med. 2001 Jan 11 ;344(2):79-86. PMID: 11150357

Abstract Title: 

Cellular-telephone use and brain tumors.

Abstract: 

BACKGROUND: Concern has arisen that the use of hand-held cellular telephones might cause brain tumors. If such a risk does exist, the matter would be of considerable public health importance, given the rapid increase worldwide in the use of these devices.METHODS: We examined the use of cellular telephones in a case-control study of intracranial tumors of the nervous system conducted between 1994 and 1998. We enrolled 782 patients through hospitals in Phoenix, Arizona; Boston; and Pittsburgh; 489 had histologically confirmed glioma, 197 had meningioma, and 96 had acoustic neuroma. The 799 controls were patients admitted to the same hospitals as the patients with brain tumors for a variety of nonmalignant conditions.RESULTS: As compared with never, or very rarely, having used a cellular telephone, the relative risks associated with a cumulative use of a cellular telephone for more than 100 hours were 0.9 for glioma (95 percent confidence interval, 0.5 to 1.6), 0.7 for meningioma (95 percent confidence interval, 0.3 to 1.7), 1.4 for acoustic neuroma (95 percent confidence interval, 0.6 to 3.5), and 1.0 for all types of tumors combined (95 percent confidence interval, 0.6 to 1.5). There was no evidence that the risks were higher among persons who used cellular telephones for 60 or more minutes per day or regularly for five or more years. Tumors did not occur disproportionately often on the side of head on which the telephone was typically used.CONCLUSIONS: These data do not support the hypothesis that the recent use of hand-held cellular telephones causes brain tumors, but they are not sufficient to evaluate the risks among long-term, heavy users and for potentially long induction periods.

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PMID: 

Neuro Oncol. 2010 Nov ;12(11):1147-51. Epub 2010 Jul 16. PMID: 20639214

Abstract Title: 

Brain cancer incidence trends in relation to cellular telephone use in the United States.

Abstract: 

The use of cellular telephones has grown explosively during the past two decades, and there are now more than 279 million wireless subscribers in the United States. If cellular phone use causes brain cancer, as some suggest, the potential public health implications could be considerable. One might expect the effects of such a prevalent exposure to be reflected in general population incidence rates, unless the induction period is very long or confined to very long-term users. To address this issue, we examined temporal trends in brain cancer incidence rates in the United States, using data collected by the Surveillance, Epidemiology, and End Results (SEER) Program. Log-linear models were used to estimate the annual percent change in rates among whites. With the exception of the 20-29-year age group, the trends for 1992-2006 were downward or flat. Among those aged 20-29 years, there was a statistically significant increasing trend between 1992 and 2006 among females but not among males. The recent trend in 20-29-year-old women was driven by a rising incidence of frontal lobe cancers. No increases were apparent for temporal or parietal lobe cancers, or cancers of the cerebellum, which involve the parts of the brain that would be more highly exposed to radiofrequency radiation from cellular phones. Frontal lobe cancer rates also rose among 20-29-year-old males, but the increase began earlier than among females and before cell phone use was highly prevalent. Overall, these incidence data do not provide support to the view that cellular phone use causes brain cancer.

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