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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. *

New findings in rodents and human brain shed light on the mechanisms of major depressive disorder (MDD), uncovering over-expression of MKP-1 (mitogen-activated protein kinase [MAPK] phosphatase-1)...and identifying a new therapeutic target. MKP-1, also known as dual-specificity phosphatase-1 (DUSP1), is a member of a family of proteins that dephosphorylate both threonine and tyrosine residues and thereby serves as a key negative regulator of the MAPK cascade4, a major signaling pathway involved in neuronal plasticity, function and survival This study identifies MKP-1 as a key factor in MDD pathophysiology, and as a new target for therapeutic interventions.f Here we use whole-genome expression profiling of postmortem tissue and show significantly increased expression of mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1, encoded by DUSP1, but hereafter called MKP-1) in the hippocampal subfields of subjects with MDD compared to matched controls. MKP-1, also known as dual-specificity phosphatase-1 (DUSP1), is a member of a family of proteins that dephosphorylate both threonine and tyrosine residues and thereby serves as a key negative regulator of the MAPK cascade4, a major signaling pathway involved in neuronal plasticity, function and survival. We tested the role of altered MKP-1 expression in rat and mouse models of depression and found that increased hippocampal MKP-1 expression, as a result of stress or viral-mediated gene transfer, causes depressive behaviors. Conversely, chronic antidepressant treatment normalizes stress-induced MKP-1 expression and behavior, and mice lacking MKP-1 are resilient to stress. These postmortem and preclinical studies identify MKP-1 as a key factor in MDD pathophysiology and as a new target for therapeutic interventions.

"Women with low libido: correlation of decreased androgen levels with female sexual function index"

DAFLON 500 mg can be combined with any therapeutic agent; in fact no drug interactions have been reported. This point is very important, considering that patients can suffer concomitant diseases and may require other therapies. Even more, on long-term treatment compared with placebo, no evidence was found of any statistically significant variation in laboratory parameters, such as red cell count, hemoglobin, hematocrit, liver function (SGPT, SGOT), or other blood parameters

Medicine has increased the ranks of the elderly. Can it make old age any easier? The job of any doctor, Bludau later told me, is to support quality of life, by which he meant two things: as much freedom from the ravages of disease as possible, and the retention of enough function for active engagement in the world. Most doctors treat disease, and figure that the rest will take care of itself. And if it doesn't-if a patient is becoming infirm and heading toward a nursing home-well, that isn't really a medical problem, is it?

We describe how innate and adaptive immune cascades trigger the release of cytokines and chemokines, resulting in the initiation and progression of atherosclerosis. We discuss how cytokines have direct and indirect effects on myocardial function.

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

Symposium: Pleiotropic Actions of Vitamin D. Departments of Pediatrics/Pediatric Allergy & Immunology, University of California at San Diego (UCSD), La Jolla, CA. Jacques M. Lemire, Hans L. Spiegelberg, et al.

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