Cancer chemopreventive effects and cytotoxic activities of the triterpene acids from the resin of Boswellia carteri.

Posted on January 16, 2013 by Maurice Preter MD

Biol Pharm Bull. 2006 Sep;29(9):1976-9.

Cancer chemopreventive effects and cytotoxic activities of the triterpene acids from the resin of Boswellia carteri.

Akihisa T, Tabata K, Banno N, Tokuda H, Nishimura R, Nakamura Y, Kimura Y, Yasukawa K, Suzuki T.

Source

College of Science and Technology, Nihon University, Tokyo, Japan. akihisa@chem.cst.nihon-u.ac.jp

Erratum in

Biol Pharm Bull. 2006 Dec;29(12):2536. Nishihara, Reiko [corrected to Nishimura, Reiko].

Abstract

Fifteen triterpene acids, viz., seven of the beta-boswellic acids (ursane-type) (1-7), two of the alpha-boswellic acids (oleanane-type) (8, 9), two of the lupeolic acids (lupane-type) (10, 11), and four of the tirucallane-type (12-14, 16), and two cembrane-type diterpenes (17, 18), isolated from the MeOH extract of the resin of Boswellia carteri (Burseraceae), together with a triterpene acid 15 (the acetyl derivative of 14), were examined for their inhibitory effects on the induction of Epstein-Barr virus early antigen (EBV-EA) by 12-O-tetradecanoylphorbol-13-acetate (TPA) in Raji cells and on activation of (+/-)-(E)-methyl-2[(E)-hydroxyimino]-5-nitro-6-methoxy-3-hexemide (NOR 1), a nitrogen oxide (NO) donor, and cytotoxic activities against three human neuroblastoma cell lines, IMR-32, NB-39, and SK-N-SH in vitro. On evaluation against the EBV-EA activation induced by TPA, seven compounds, 2, 10, 11, and 13-16, showed potent inhibitory effects on EBV-EA induction. Upon evaluation against activation of NOR 1, five compounds, 7, 13, and 14-16, showed potent inhibitory effects. Further, fifteen compounds, 1-7, 9-11, 13-15, 17, and 18, exhibited potent cytotoxic activities with IC(50) values of 4.1-82.4 muM against all of the three human neuroblastoma cells tested.

PMID:

16946522

[PubMed – indexed for MEDLINE]

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Selenium and the thyroid: a close-knit connection.

Posted on January 16, 2013 by Maurice Preter MD
J Clin Endocrinol Metab. 2010 Dec;95(12):5180-8. doi: 10.1210/jc.2010-0191. Epub 2010 Sep 1.

Selenium and the thyroid: a close-knit connection.

Duntas LH.

Source

Endocrine Unit, Evgenidion Hospital, University of Athens, 20 Papadiamantopoulou Street 115 28 Athens, Greece. ledunt@otenet.gr

Abstract

CONTEXT:

The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and thyroid function. It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease.

EVIDENCE ACQUISITION:

Clinical reports as well as a large number of biochemical articles linking selenium to thyroid have been considered. Interventional, prospective, randomized, controlled studies, including large observational studies, supplementing selenium in autoimmune thyroid disease, together with review articles published in Medline and Pubmed have undergone scrutiny. The methodological differences and variety of results emerging from these trials have been analyzed.

EVIDENCE SYNTHESIS:

Evidence in support of selenium supplementation in thyroid autoimmune disease is evaluated, the results herein presented demonstrating the potential effectiveness of selenium in reducing the antithyroid peroxidase titer and improving the echostructure in the ultrasound examination. However, considerable discord remains as to who should comprise target groups for selenium treatment, who will most benefit from such treatment, the precise impact of the basal antithyroid peroxidase level, and the effect of disease duration on the treatment outcome. Clearly, further in-depth studies and evaluation are required concerning the mechanism of action of selenium as well as the choice of supplements or dietary intake.

CONCLUSIONS:

Maintenance of “selenostasis” via optimal intake not only aids preservation of general health but also contributes substantially to the prevention of thyroid disease.

PMID:
20810577
[PubMed – indexed for MEDLINE]

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Association between immediate initiation of intramuscular interferon beta-1a at the time of a clinically isolated syndrome and long-term outcomes: a 10-year follow-up of the Controlled High-Risk Avonex Multiple Sclerosis Prevention Study in Ongoing Neurological Surveillance.

Posted on January 16, 2013 by Maurice Preter MD

Arch Neurol. 2012 Feb;69(2):183-90. doi: 10.1001/archneurol.2011.1426. Epub 2011 Oct 10.

Association between immediate initiation of intramuscular interferon beta-1a at the time of a clinically isolated syndrome and long-term outcomes: a 10-year follow-up of the Controlled High-Risk Avonex Multiple Sclerosis Prevention Study in Ongoing Neurological Surveillance.

Kinkel RP, Dontchev M, Kollman C, Skaramagas TT, O’Connor PW, Simon JH; Controlled High-Risk Avonex Multiple Sclerosis Prevention Study in Ongoing Neurological Surveillance Investigators.

Collaborators (24)

Source

Multiple Sclerosis Center, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave, KS 211, Boston, MA 02215, USA. rkinkel@bidmc.harvard.edu

Abstract

OBJECTIVE:

To determine whether immediate initiation of treatment at the time of a clinically isolated syndrome in patients at high risk for clinically definite multiple sclerosis alters disease course over 10 years.

DESIGN:

Prospective follow-up study.

SETTING:

Twenty-four Controlled High-Risk Subjects Avonex Multiple Sclerosis Prevention Study (CHAMPS) sites in the United States and Canada.

PARTICIPANTS:

A total of 81 patients originally randomly assigned to receive intramuscular interferon beta-1a (the immediate-treatment group) and 74 patients originally randomly assigned to receive placebo (the delayed-treatment group). All patients were from CHAMPS.

INTERVENTION:

For the immediate-treatment group, treatment was initiated within a month after the onset of a clinically isolated syndrome, and for the delayed-treatment group, treatment was initiated a median of 30 months (interquartile range, 24-35 months) after CHAMPS randomization.

MAIN OUTCOME MEASURES:

Rate of developing clinically definite multiple sclerosis, annualized relapse rate, disease course classification, disability measures, and magnetic resonance imaging measures.

RESULTS:

The immediate-treatment group showed a lower 10-year rate of clinically definite multiple sclerosis (unadjusted hazard ratio, 0.64 [95% CI, 0.48-0.87]; P = .004) and a lower annualized relapse rate between years 5 and 10 (P = .03). There was no differential effect on disability, magnetic resonance imaging T2-weighted lesions, or the proportion of patients developing progressive disease at 10 years. Few patients reached the Expanded Disability Status Scale milestone scores of 4.0 or greater (9% of patients) or 6.0 or greater (6% of patients).

CONCLUSIONS:

Immediate initiation of intramuscular interferon beta-1a at the time of a clinically isolated syndrome in high-risk patients reduces relapse rates over 10 years but does not improve disability outcomes compared with a control group that also initiated therapy relatively early in the disease course.

TRIAL REGISTRATION:

clinicaltrials.gov Identifier: NCT00179478.

PMID:

21987393

[PubMed – indexed for MEDLINE]

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Cancer risk in multiple sclerosis: findings from British Columbia, Canada.

Posted on January 16, 2013 by Maurice Preter MD
Good news but probably offset by use of immune-modulating/suppressive interventions (especially of cellular immunity) for MS. Do neurologists explain that to their patients?
Another study to be done.
Brain. 2012 Oct;135(Pt 10):2973-9. doi: 10.1093/brain/aws148. Epub 2012 Jun 21.

Cancer risk in multiple sclerosis: findings from British Columbia, Canada.

Kingwell E, Bajdik C, Phillips N, Zhu F, Oger J, Hashimoto S, Tremlett H.

Source

Division of Neurology, Faculty of Medicine, Multiple Sclerosis Program, University of British Columbia, Vancouver, British Columbia, Canada. elainejk@mail.ubc.ca

Abstract

Findings regarding cancer risk in people with multiple sclerosis have been inconsistent and few studies have explored the possibility of diagnostic neglect. The influence of a relapsing-onset versus primary progressive course on cancer risk is unknown. We examined cancer risk and tumour size at diagnosis in a cohort of patients with multiple sclerosis compared to the general population and we explored the influence of disease course. Clinical data of patients with multiple sclerosis residing in British Columbia, Canada who visited a British Columbia multiple sclerosis clinic from 1980 to 2004 were linked to provincial cancer registry, vital statistics and health registration data. Patients were followed for incident cancers between onset of multiple sclerosis, and the earlier of emigration, death or study end (31 December 2007). Cancer incidence was compared with that in the age-, sex- and calendar year-matched population of British Columbia. Tumour size at diagnosis of breast, prostate, colorectal and lung cancers were compared with population controls, matched for cancer site, sex, age and calendar year at cancer diagnosis, using the stratified Wilcoxon test. There were 6820 patients included, with 110 666 person-years of follow-up. The standardized incidence ratio for all cancers was 0.86 (95% confidence interval: 0.78-0.94). Colorectal cancer risk was also significantly reduced (standardized incidence ratio: 0.56; 95% confidence interval: 0.37-0.81). Risk reductions were similar by sex and for relapsing-onset and primary progressive multiple sclerosis. Tumour size was larger than expected in the cohort (P = 0.04). Overall cancer risk was lower in patients with multiple sclerosis than in the age-, sex- and calendar year matched general population. The larger tumour sizes at cancer diagnosis suggested diagnostic neglect; this could have major implications for the health, well-being and longevity of people with multiple sclerosis.

PMID:
22730559
[PubMed – indexed for MEDLINE]
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Modifiable factors influencing relapses and disability in multiple sclerosis.

Posted on January 16, 2013 by Maurice Preter MD

Mult Scler. 2010 Jul;16(7):773-85. doi: 10.1177/1352458510367721. Epub 2010 May 18.

Modifiable factors influencing relapses and disability in multiple sclerosis.

D’hooghe MB, Nagels G, Bissay V, De Keyser J.

Source

National Center For Multiple Sclerosis, Melsbroek, Belgium. marie.dhooghe@ms-centrum.be

Abstract

A growing body of literature indicates that the natural course of multiple sclerosis can be influenced by a number of factors. Strong evidence suggests that relapses can be triggered by infections, the postpartum period and stressful life events. Vaccinations against influenza, hepatitis B and tetanus appear to be safe. Surgery, general and epidural anaesthesia, and physical trauma are not associated with an increased risk of relapses. Factors that have been associated with a reduced relapse rate are pregnancy, exclusive breastfeeding, sunlight exposure and higher vitamin D levels. A number of medications, including hormonal fertility treatment, seem to be able to trigger relapses. Factors that may worsen progression of disability include stressful life events, radiotherapy to the head, low levels of physical activity and low vitamin D levels. Strong evidence suggests that smoking promotes disease progression, both clinically and on brain magnetic resonance imaging. There is no evidence for an increased progression of disability following childbirth in women with multiple sclerosis. Moderate alcohol intake and exercise might have a neuroprotective effect, but this needs to be confirmed.

PMID:

20483884

[PubMed – indexed for MEDLINE]

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