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J Invest Dermatol 2002 Dec;119(6):1237-43
Loss of cell adhesion in Dsg3bal-Pas mice with homozygous deletion mutation (2079del14) in the desmoglein 3 gene.
Pemphigus encompasses a group of autoimmune blistering diseases with circulating pathogenic autoantibodies recognizing several proteins, including the desmosomal cadherin, desmoglein 3. Targeted disruption of the Dsg3 gene by homologous recombination (Dsg3tm1stan) in mouse results in fragility of the skin and oral mucous membranes, analogous to the human disease. In addition, the Dsg3tm1stan mice develop phenotypic runting and hair loss, identical to that of the mouse mutant, Dsg3bal-2J. The Dsg3bal-2J mice are homozygous for a 1 bp insertion (2275insT) in the Dsg3 gene resulting in a nonfunctional Dsg3 mRNA. In this study, we characterized an allelic mutation, Dsg3bal-Pas, with clinical features similar to those in Dsg3bal-2J. We have identified a 14 bp deletion in exon 13 of the Dsg3 gene resulting in a frameshift and premature termination codon 7 bp downstream from the site of the deletion and causing a truncation of the desmoglein 3 polypeptide by 199 amino acids, eliminating virtually all of the intracellular domain. We demonstrate that, although a Dsg3 mRNA transcript was detectable in Dsg3bal-Pas skin, the corresponding protein for desmoglein 3 was completely absent in the oral mucosal epithelium of homozygous Dsg3bal-Pas compared with that of +/Dsg3bal-Pas mice. No significant changes in the expression of desmogleins 1 and 2 were detected. To elucidate a potential mechanism causing loss of cell adhesion in the Dsg3bal-Pas mice, we generated a myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein and expressed it in keratinocytes. The myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein was found predominantly in the cytoplasm possibly due to increased proteolytic degradation. Cell surface staining was also detected but was jagged, not linear along the cell-cell border like that observed for the full-length desmoglein 3. The expression of the myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein resulted in a reduction in staining of other desmosomal proteins, including desmoglein 1 and 2, plakophilin 2, and plakoglobin. In addition, the cells expressing myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein underwent dramatic changes in cell morphology and exhibited striking extensive filopodia. Collectively, these data showed that the perturbation of desmoglein 3 found in the Dsg3bal-Pas mice resulted in disadhesion of keratinocytes manifested with blistering phenotype.
Rev Environ Health 2001 Jul-Sep;16(4):233-51
Adverse health effects of selenium in humans.
Epidemiologic studies and case reports have shown that chronic exposure to selenium compounds is associated with several adverse health effects in humans. An early toxic effect of selenium is on endocrine function, particularly on the synthesis of thyroid hormones following dietary exposure of around 300 micrograms Se/d, and on the metabolism of growth hormone and insulin-like growth factor-1. Other adverse effects of selenium exposure can be the impairment of natural killer cells activity and at higher levels, hepatotoxicity and gastrointestinal disturbances. Dermatologic effects, such as nail and hair loss and dermatitis, occur after exposure to high levels of environmental selenium. Assessing the toxicity and morbidity after long-term exposure to environmental selenium is difficult: neurotoxicity, particularly the degeneration of motor neurons leading to increased risk of amyotrophic lateral sclerosis, might occur after chronic exposure to both organic and inorganic selenium compounds. The results of laboratory investigations and cohort studies suggest that selenium species exhibit a bivalent effect in cancer, either increasing or decreasing risk. Current environmental selenium exposure limits appear to be inadequate for averting adverse health effects.
Cancer Pract 2001 Nov-Dec;9(6):283-9
Psychological sequelae and alopecia among women with cancer.
PURPOSE: This article reviews the relevant literature on treatment-induced alopecia in women with cancer and describes the development of a computer-assisted intervention to reduce distress associated with this side effect. DESCRIPTION OF PROGRAM: Alopecia has been cited as the most disturbing anticipated side effect by up to 58% of women preparing for chemotherapy, with 8% being at risk for avoiding treatment. Women with cancer who experience alopecia as a side effect, compared with women with cancer and no alopecia, report lower self-esteem, poorer body image, and lower quality of life. Although physicians' recommendations are the most influential factor on cancer treatment choice, body image and effects on sexuality are the next most influential factors. A study of a computer-imaging intervention, based on concepts related to guided imagery and anticipatory grief, has been launched in an effort to aid women in coping with anticipated treatment-related alopecia. RESULTS: While we are still waiting for final data collection and analysis from the computer intervention study, the feedback thus far has been positive. CLINICAL IMPLICATIONS: The intervention described here may prove to be effective in desensitizing women with cancer to hair loss and facilitating an adjustment to self-acceptance. As such, a higher quality of life during the difficult time of coping may be maintained. The development of a computer-imaging intervention offers an opportunity to integrate a standard psychosocial intervention, personalized for each patient, into the routine patient care in the oncology setting.
J Theor Biol 2002 Feb 7;214(3):469-79
The follicular automaton model: effect of stochasticity and of synchronization of hair cycles.
Human scalp hair consists of a set of about 10(5)follicles which progress independently through developmental cycles. Each hair follicle successively goes through the anagen (A), catagen (C), telogen (T) and latency (L) phases that correspond, respectively, to growth, arrest and hair shedding before a new anagen phase is initiated. Long-term experimental observations in a group of ten male, alopecic and non-alopecic volunteers allowed determination of the characteristics of hair follicle cycles. On the basis of these observations, we previously proposed a follicular automaton model to simulate the dynamics of human hair cycles and the development of different patterns of alopecia [Halloy et al. (2000) Proc. Natl Acad. Sci. U.S.A.97, 8328-8333]. The automaton model is defined by a set of rules that govern the stochastic transitions of each follicle between the successive states A, T, L and the subsequent return to A. These transitions occur independently for each follicle, after time intervals given stochastically by a distribution characterized by a mean and a standard deviation. The follicular automaton model was shown to account both for the dynamical transitions observed in a single follicle, and for the behaviour of an ensemble of independently cycling follicles. Here, we extend these results and investigate additional properties of the model. We present a deterministic version of the follicular automaton. We show that numerical simulations of the stochastic version of the automaton yield steady-state level of follicles in the different phases which approach the levels predicted by the deterministic equations as the number of follicles progressively increases. Only the stochastic version can successfully reproduce the fluctuations of the fractions of follicles in each of the three phases, observed in small follicle populations. When the standard deviation is reduced or when the follicles become otherwise synchronized, e.g. by a periodic external signal inducing the transition of anagen follicles into telogen phase, large-amplitude oscillations occur in the fractions of follicles in the three phases. These oscillations are not observed in humans but are reminiscent of the phenomenon of moulting observed in a number of mammalian species.
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