Background
Many breast cancer survivors experience fatigue, mood, and sleep disturbances.
Purpose
To compare a Meditative Movement practice, Qigong/Tai Chi Easy (QG/TCE), with sham Qigong (SQG), testing effects of meditation/breath aspects of QG/TCE on breast cancer survivors' persistent fatigue and other symptoms.
Methods
A double-blind, randomized controlled trial tested 12-weeks of QG/TCE versus SQG on fatigue, depression and sleep among 87 post-menopausal, fatigued breast cancer survivors, Stage 0-III, age 40–75.
Results
Fatigue decreased significantly in the QG/TCE group compared to control at post-intervention (p = 0.005) and 3 month follow-up (p = 0.024), but not depression and sleep quality. Improvement occurred over time for both interventions in depression and sleep quality (all p < 0.05).
Conclusions
QG/TCE showed significant improvement over time compared to SQG for fatigue, but not depression or sleep. Both QG/TCE and SQG showed improvement for two prevalent symptoms among breast cancer survivors, depression and sleep dysfunction.
The colorectal mucosa of pre-symptomatic individuals with familial adenomatous polyposis (FAP) contains elevated levels of the proliferation-associated polyamines. The Min mouse, like humans with FAP, expresses an abnormal genotype for the APC tumor suppressor gene. In order to determine how APC mutation influences intestinal tissue polyamine content, we measured steady-state RNA levels of ornithine decarboxylase (ODC), the first enzyme in polyamine synthesis, antizyme (AZ), a protein which negatively regulates ODC, and the spermidine/spermine N(1)-acetyltransferase (SSAT), the first enzyme in polyamine catabolism. RNA content was increased 6- to 8-fold in both the small intestine and colon for ODC, decreased significantly in the small intestine but not the colon for AZ and was not statistically different in either intestinal tissue for SSAT in Min mice compared with normal littermates. Consistent with the changes in ODC and AZ gene expression, small intestinal, but not colonic, polyamine content was elevated in Min mice compared with normal littermates. Treatment of Min mice with the specific ODC inhibitor difluoromethylornithine (DFMO) suppressed small intestinal, but not colonic, polyamine content and tumor number. These data indicate that small intestinal tissue polyamine content is elevated in Min mice by a mechanism involving APC-dependent changes in ODC and AZ RNA. Further, ODC enzyme activity, which is influenced by both ODC and AZ RNA levels and inhibited by DFMO, is consequential for small intestinal tumorigenesis in this model. In the FAP population, DFMO may be of value in the chemoprevention of small intestinal adenocarcinoma that remains a risk following colectomy.
The prehospital mGCS appears have good discriminatory power and is equivalent to the prehospital tGCS for predicting intubation and survival to hospital discharge in this trauma population as a whole, those with ISS ≥ 16, or TBI.
A chemopreventive effect of aspirin (ASA) on lung cancer risk is supported by epidemiologic and preclinical studies. We conducted a randomized, doubleblinded study in current heavy smokers to compare modulating effects of intermittent versus continuous low-dose ASA on nasal epithelium gene expression and arachidonic acid (ARA) metabolism. Fifty-four participants were randomized to intermittent (ASA 81 mg daily for one week/placebo for one week) or continuous (ASA 81 mg daily) for 12 weeks. Lowdose ASA suppressed urinary prostaglandin E2 metabolite (PGEM; change of À4.55 AE 11.52 from baseline 15.44 AE 13.79 ng/mg creatinine for arms combined, P ¼ 0.02), a surrogate of COX-mediated ARA metabolism, but had minimal effects on nasal gene expression of nasal or bronchial gene-expression signatures associated with smoking, lung cancer, and chronic obstructive pulmonary disease. Suppression of urinary PGEM correlated with favorable changes in a smoking-associated gene signature (P < 0.01). Gene set enrichment analysis (GSEA) showed that ASA intervention led to 1,079 enriched gene sets from the Canonical Pathways within the Molecular Signatures Database. In conclusion, low-dose ASA had minimal effects on known carcinogenesis gene signatures in nasal epithelium of current smokers but results in wide-ranging genomic changes in the nasal epithelium, demonstrating utility of nasal brushings as a surrogate to measure gene-expression responses to chemoprevention. PGEM may serve as a marker for smoking-associated gene-expression changes and systemic inflammation. Future studies should focus on NSAIDs or agent combinations with broader inhibition of pro-inflammatory ARA metabolism to shift gene signatures in an anti-carcinogenic direction.
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