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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.
Dermatology 2002;205(4):374-7
Hair pain (trichodynia): frequency and relationship to hair loss and patient gender.
Background: Patients complaining of hair loss frequently claim that their hair has become painful. Objective and Methods: The aim of the study was to evaluate the frequency of this phenomenon and its relationship to hair loss. Patients seeking advice for hair loss either spontaneously reported or were questioned about painful sensations of the scalp. Hair loss activity was quantified by a hair pull, daily count and wash test. Telogen percentage was obtained by a hair pluck. The scalp surface was examined by dermatoscopy. Results: Of 403 examined patients, 20% of women and 9% of men reported hair pain, irrespective of the cause and activity of hair loss. A minority presented scalp telangiectasia. This strongly correlated with hair pain. Conclusions: Hair pain (trichodynia) affects a significant proportion of patients complaining of hair loss and may increase the anxiety. The symptom neither allows discrimination of the cause nor correlates with the activity of hair loss. A higher prevalence of female patients might be connected to gender-related differences in pain perception in relation to anxiety. The role of vasoactive neuropeptides in the interaction between the central nervous system and skin reactivity is discussed. In the absence of any correlation with quantitative parameters of hair loss or specific morphologic changes of the scalp, management remains empiric and tailored to the individual.
Dermatol Surg 2002 Oct;28(10):873-93
The art of repair in surgical hair restoration--part II: the tactics of repair.
BACKGROUND: As patient awareness of new hair transplantation techniques grows, the repair of improperly planned or poorly executed procedures becomes an increasingly important part of surgical hair restoration. OBJECTIVE: Part II of this series is written to serve as a practical guide for surgeons who perform repairs in their daily practices. It focuses on specific repair techniques. METHODS: The repairs are performed by excision with reimplantation and/or by camouflage. Follicular unit transplantation is used for the restorative aspects of the procedure. RESULTS: Using punch or linear excision techniques allows the surgeon to relocate poorly planted grafts to areas that are more appropriate. The key elements of camouflage include creating a deep zone of follicular units, angling grafts in their natural direction, and using forward and side weighting of grafts to increase the appearance of fullness. In special situations, removal of grafts without reimplantation can be accomplished using lasers or electrolysis. CONCLUSION: Meticulous surgical techniques and optimal utilization of a limited hair supply will enable the surgeon to achieve the best possible cosmetic results for patients requiring repairs
Ann Dermatol Venereol 2002 May;129(5 Pt 2):787-92
Hormonal interaction and hair growth
Androgenetic alopecia (AGA) is the most common form of hair loss in men and women. This continuous process results in a form of alopecia that follows a definite pattern in those individuals who are genetically predisposed. Although clinically different, the pathogenetic pathways leading to this type of hair loss are thought to be similar in both sexes. A genetic predisposition is a feature of AGA, but the predisposing genes are still unknown. Our understanding, however, of the hormonal effects on hair growth is far more advanced. AGA can be defined as a dihydrotestosterone (DHT)-dependent process with continuous miniaturization of sensitive hair follicles. So far, we do not understand the molecular steps involved in androgen-dependent beard growth versus androgen-dependent hair loss. However, the local androgen metabolism plays a central role in the intrafollicular conversion of weak androgens, such as DHEAS, to more potent androgens such as T or DHT within the hair follicle. The dermal papilla plays a central role by exhibiting an array of important steroidogenic isoenzymes. Provided that the dermal papilla (DP) cell triggers and regulates the growth of hair follicles, this physiological role may be reflected by metabolic differences, which could account for differences in androgen sensitivity as observed in hair follicles from different body sites, and in conditions such as male pattern baldness. The observation of STS, 17beta-HSD, 3beta-HSD, 3alpha-HSD and type 2 5alpha-R-activity within the DP could be a clue to understanding the regulation of androgen action in the human hair follicle by local androgen modification on target cell level. Hence, some of the intrafollicular steroidogenic enzymes would be potential pharmaceutical targets for the treatment of AGA or hirsutism.
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