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"Skeletal Muscle Strength as a Predictor of All-Cause Mortality in Healthy Men," "Strength, but not Muscle Mass, Is Associated With Mortality in the Health, Aging and Body Composition Study Cohort," "Decreased Muscle and Increased Central Adiposity are Independently Related to Mortality in Older Men," etc.

Dysfunctional cortico-limbic brain activity associated with anger may be normalized by nicotine. Cortico-limbic brain activity associated with anger may be susceptible to nicotine and, thus, may contribute to smoking initiation and nicotine addiction. Functional imaging studies on regional brain activity in response to nicotine and smoking have documented the involvement of cortico-limbic structures such as the prefrontal cortex (including the dorsolateral prefrontal cortex, inferior frontal, medial frontal, and orbitofrontal gyri), cingulate, thalamus, and amygdala

Molecular immunological approaches to biotherapy of human cancers--a review, hypothesis and implications.\nBecker Y.\nAnticancer Res. 2006 Mar-Apr;26(2A):1113-34. Review.\nPMID: 16619514 \n\nPolarized Th1 cells produce interleukin (IL)-2, IL-12 and interferon (IFN)-gamma, and polarized Th2 cells and the hematopoietic cells produce IL-4, IL-5, IL-6, IL-10 and IL-13. In healthy individuals there is a Th1/Th2 cytokine balance, but during microbial-induced inflammation the pathogens induce an overproduction of the Th2 cytokines that inhibit the adaptive immune response against the pathogen. A review of studies on the Th1/Th2 cytokine balance in humans harboring different tumor types revealed that tumor cells induce increased Th2 cytokine levels in patients' sera that can serve as indicators for the existence of tumors. I\n

"There are very few large, well-designed human studies testing the health effects of DHEA supplements. For example, there is not enough scientific evidence to rate the effectiveness of DHEA supplements in treating adrenal insufficiency, metabolic syndrome, depression, HIV/AIDS, Addison's disease, chronic fatigue syndrome, menopausal symptoms, heart disease, breast cancer, infertility, diabetes, or Parkinson's disease according to the National Institutes of Health (NIH). In addition, there isn't enough evidence to support the use of DHEA supplements as an anti-aging remedy or weight-loss aid. The NIH also cautions that DHEA supplements appear to be ineffective for boosting libido, enhancing muscle strength in elderly people, protecting against Alzheimer's disease and improving thinking in healthy older people."

Vitamin D, nervous system and aging.\nP. Tuohimaa, T. Keisala, A. Minasyan, J. Cachat and A. Kalueff. .\nPsychoneuroendocrinology, Volume 34, Supplement 1, December 2009, Pages S278-S286\n NEUROACTIVE STEROIDS: EFFECTS and MECHANISMS ofACTION\n \n\nReview of vitamin D3, its active metabolites, and their functioning in the central nervous system (CNS), especially in relation to nervous system pathologies and aging. The vitamin D3 endocrine system consists of 3 active calcipherol hormones: calcidiol (25OHD3), 1α-calcitriol (1α,25(OH)2D3) and 24-calcitriol (24,25(OH)2D3). The impact of the calcipherol hormone system on aging, health and disease is discussed. Low serum calcidiol concentrations are associated with an increased risk of several chronic diseases including osteoporosis, cancer, diabetes, autoimmune disorders, hypertension, atherosclerosis, and muscle weakness ~ all of which can be considered aging-related diseases. The relationship of many of these diseases and aging-related changes in physiology show a U-shaped response curve to serum calcidiol concentrations. Clinical data suggest that vitamin D3 insufficiency is associated with an increased risk of several CNS diseases, including multiple sclerosis, Alzheimers, Parkinsons, seasonal affective disorder (SAD), and schizophrenia. In line with this, recent animal and human studies suggest that vitamin D insufficiency is associated with abnormal development and functioning of the CNS. * Overall, imbalances in the calcipherol system appear to cause abnormal function, including premature aging, of the CNS. *

We found that 5% imiquimod cream is an effective treatment option for superficial and nodular basal cell carcinomas, giving a clearance rate of 89.5% at an average of 39 months of follow up.

Raasch B. Clinical, Cosmetic and Investigational Dermatology. 9 June 2009.  There is reasonable evidence that the use of imiquimod for small (<2 cm) superficial BCC that occur other than on the face provides  outcomes only marginally less satisfactory t

Composite clearance rates (combined clinical and histological assessments) for the 5 and 7x/week imiquimod groups were 75% and 73%, respectively. Histological clearance rates for the 5 and 7x/week imiquimod groups were 82% and 79%, respectively. Increasing severity of erythema, erosion, and scabbing/crusting was associated with higher clearance rates. CONCLUSION: Imiquimod appears to be safe and effective for the treatment of sBCC when compared with vehicle cream. The difference in clearance rates between the two imiquimod dosing groups was not significant. The 5x/week regimen is recommended.

The initial sBCC clearance rate was 90% (12-week post treatment), whereas the proportion of subjects who were clinically clear at 2 years (current time point) was estimated to be 79.4%.

Clinical clearance rate at 1 and 2 years were 89% and 85%, respectively.

Clinical clearance rate at 1, 2 and 3 years were 94, 76 and 70%, respectively. We conclude that imiquimod seems to be an appropriate therapeutic alternative for the treatment of recurrent BCC in patients with associated co-morbidities.

The precise mechanism of the anti-tumor effect of imiquimod in BCC is not known. It has been postulated that ultraviolet radiation induces mutations in the tumor-suppressor genes and alters the immuno-surveillance, so that tumor cells escape from cytotoxic T cells and apoptosis.[1] Th-2 cytokines, that downregulate tumor surveillance, are raised in BCC.[1],[5] Imiquimod acts on toll-like receptor-7 (TLR-7) present on dendritic cells, macrophages and monocytes and induces expression of interferons, Th-1 cytokines (IL-1, IL-6, IL-10 and IL-12), tumor necrosis factor-a and G-CSF, thereby counteracting Th2 cytokines and promoting tumor surveillance.[1],[5] It also enhances the activity of natural killer cells and epidermal Langerhans' cells. The tumor regression is achieved probably by induction of Fas receptors on the tumor cells resulting in their apoptosis.[10]

For patients without comorbidities, the overall cure rate was 73%. For these patients, the cure rates were 85.7% for superficial and nodular BCC, 88% for superficial BCC, 57% for Bowen's disease, 50% for nodular BCC, and 50% for aggressive BCC.