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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.


Cancer Epidemiol Biomarkers Prev 2002 Jun;11(6):549-53

Androgenetic alopecia and prostate cancer: findings from an Australian case-control study.


The purpose of this study was to examine the relationship between androgenetic alopecia (AA) and prostate cancer with particular emphasis on early age at diagnosis and higher grade tumors. We conducted an age-stratified, population-based case-control study in Australia of men who were diagnosed before 70 years of age during 1994-1997 with histopathology-confirmed adenocarcinoma of the prostate, excluding well-differentiated tumors. Controls were selected from the electoral rolls, and the frequency was matched on age. After excluding subjects with missing values, the analysis was based on 1446 cases and 1390 controls of whom direct observations were made of their pattern of AA during face-to-face interviews. Our data suggest an association between prostate cancer and vertex baldness; compared with men who had no balding, the adjusted odds ratio (OR) was 1.54 (1.19-2.00). No associations were found between prostate cancer and frontal baldness or when frontal baldness was present concurrently with vertex baldness. The ORs were 0.98 (0.79-1.23) and 1.14 (0.90-1.45), respectively. The highest ORs were for high-grade disease in men 60-69 years of age: 1.80 (1.02-3.16) for frontal baldness; 2.91 (1.59-5.32) for vertex baldness; and 1.95 (1.10-3.45) for frontal and vertex baldness. This association between the pattern of AA and prostate cancer points to shared androgen pathways that are worthy of additional investigation.


Am Fam Physician. 2003 Mar 1;67(5):1007-14.

Alopecia in women.


Alopecia can be divided into disorders in which the hair follicle is normal but the cycling of hair growth is abnormal and disorders in which the hair follicle is damaged. Androgenetic alopecia is the most common cause of hair loss in women. Other disorders include alopecia areata, telogen effluvium, cicatricial alopecia, and traumatic alopecias. The diagnosis is usually based on a thorough history and a focused physical examination. In some patients, selected laboratory tests or punch biopsy may be necessary. Topically administered minoxidil is labeled for the treatment of androgenetic alopecia in women. Corticosteroids and other agents are typically used in women with alopecia areata. Telogen effluvium is often a self-limited disorder. Because alopecia can be devastating to women, management should include an assessment for psychologic effects.


Hum Genet. 2003 Apr;112(4):400-3. Epub 2003 Feb 14.

Notch4, a non-HLA gene in the MHC is strongly associated with the most severe form of alopecia areata.


Alopecia areata (AA) is a disorder primarily affecting the hair and nails in which associated autoimmune or atopic disease is common. Genetically, it is a complex trait with evidence of a role for genes of the major histocompatibility complex (MHC), the interleukin-1 cluster and chromosome 21 in the pathogenesis. The strongest association is with HLA class II alleles, although whether this indicates a direct contribution to the pathogenesis or results merely from linkage disequilibrium with nearby disease genes is unknown. Notch4 is a recently defined gene in the HLA class III region. Notch signalling is a direct determinant of keratinocyte growth arrest and entry into differentiation. A possible role for Notch in hair growth has been indicated by transgenic mouse findings that activation of the Notch pathway in the hair cortex leads to aberrant differentiation of adjacent hair-shaft layers. Notch4 is therefore a plausible candidate gene for AA. We have examined two polymorphisms in the coding sequence of the Notch4 gene at positions +1297 and +3063 in a case-control study of 116 AA patients and 142 ethnically matched, healthy control subjects. The initial analysis showed a significant association of AA in the overall data set with the Notch4(T+1297C) polymorphism (P<0.001) but not with Notch4(A+3063G). To confirm this association, we genotyped an additional 62 patients and found that the risk for disease was higher in Notch4(+1297C) homozygotes [odds ratio (OR) 3.43 (1.63, 7.19)] than in heterozygotes [OR 2.58 (1.57, 4.24)]. On classifying the patients by severity of disease, the association appeared to be confined to the severest form (alopecia universalis) [OR 4.02 (1.64, 9.88), P=0.0014]. These results support previous findings showing that different HLA susceptibility alleles are associated with mild and severe AA.


Seeing is believing. Learning by anecdotal observations is an old way of science. It is not reasonable to stop taking daily food and herbal supplements altogether just because of scietific/clinical support: our life must go on until we have better understandings of food and herb. There are two merits that Hair Million enjoys: Firstly, Hair Million is relatively inexpensive, and secondly, it is made only of edible herbs that are known to be safe when consumed in regular quantities. Propecia is a clincally validated prescription medication for hair loss.








Related Web resources:


  • What is hair?
  • Curly Hair
  • Biology of hair growth and development.
  • The phenomenon of hair loss.
  • Methods and treatments for hair loss and baldness.
  • Drugs and hair transplantation surgery for hair loss and baldness.
  • Hair loss linked to other health problems.
  • Baldness by choice and fashion.
  • Alopecia info.
  • Alopecia treatment info.
  • Alopecia treatment info.
  • Hair care info.
  • Hair loss and alopecia research articles: abstracts and source links.



    DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.





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