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Alopecia, hair loss abstracts ||
Ann Dermatol Venereol. 2002 Oct;129(10 Pt 1):1168-71.
[Trichothiodystrophy and congenital heart disease in two sisters]
[Article in French]
Mazereeuw-Hautier J, Pech JH, Heitz F, Bonafe JL.
Service de dermatologie, Centre hospitalier de Toulouse Rangueil, 1, avenue Jean Poulhes, 31403 Toulouse Cedex 4.
INTRODUCTION: Trichothiodystrophy refers to a heterogeneous group of autosomal recessive genodermatosis of unknown etiology. Patients with trichothiodystrophy have alopecia with typical hair dysplasia ("tiger-tail"), and abnormally low sulfur content. Numerous unrelated neuroectodermal defects have been observed in trichothiodystrophy. We report here trichothiodystrophy and congenital heart disease in two sisters. CASES REPORT: Two sisters were born as collodion babies and presented ichthyosis and alopecia. The diagnosis of trichothiodystrophy was confirmed by polarizing microscopy of hair and low sulfur content. Both had congenital heart disease. DISCUSSION: Cardiovascular defects have rarely been reported in trichothiodystrophy. The association trichothiodystrophy - congenital heart disease has never been described. The low incidence of both conditions suggests that these abnormalities are linked etiologically rather than by chance. Abnormal Notch signaling, or contiguous gene deletion syndrome could lead to combined phenotype as observed in our family.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12442133&dopt=Abstract
Cancer Epidemiol Biomarkers Prev. 2002 Jun;11(6):549-53.
Androgenetic alopecia and prostate cancer: findings from an Australian case-control study.
Giles GG, Severi G, Sinclair R, English DR, McCredie MR, Johnson W, Boyle P, Hopper JL.
Cancer Epidemiology Centre, Anti-Cancer Council of Victoria, Melbourne, VIC 3053 Australia.
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.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12050096&dopt=Abstract
Genes Dev. 2002 Jun 1;16(11):1412-22.
Keratin 17 null mice exhibit age- and strain-dependent alopecia.
McGowan KM, Tong X, Colucci-Guyon E, Langa F, Babinet C, Coulombe PA.
Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Onset of type I keratin 17 (K17) synthesis marks the adoption of an appendageal fate within embryonic ectoderm, and its expression persists in specific cell types within mature hair, glands, and nail. We report that K17 null mice develop severe alopecia during the first week postbirth, correlating with hair fragility, alterations in follicular histology, and apoptosis in matrix cells. These alterations are incompletely penetrant and normalize starting with the first postnatal cycle. Absence of a hair phenotype correlates with a genetic strain-dependent compensation by related keratins, including K16. These findings reveal a crucial role for K17 in the structural integrity of the first hair produced and the survival of hair-producing cells. Given that identical inherited mutations in this gene can cause either pachyonychia congenita or steatocystoma multiplex, the features of this mouse model suggest that this clinical heterogeneity arises from a cell type-specific, genetically determined compensation by related keratins.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12050118&dopt=Abstract
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