References: Hair growth and hair loss
Eur J Dermatol. 2002 Nov-Dec;12(6):565-8.
Subclinical speckled perifollicular melanosis of the scalp.
Petit L, Claudine, Pierard-Franchimont, Saint Leger D, Loussouarn G, Pierard GE.
Department of Dermatopathology, University Medical Center Sart Tilman and Sauveniere, B-4000 Liege, Belgium.
Based on the clinical presentation of some skin pigmentation disorders it is thought that a bicompartmental functional system exists in the epidermal melanocyte population. It corresponds to the perifollicular and interfollicular compartments, respectively. The present study was undertaken looking for the presence of such a system on scalp unaffected by pigmentary disorders. The scalps of 100 men with incipient to severe androgenic alopecia were examined using a videocamera equipped with an internal ultraviolet light-emitting unit. The face, trunk and limbs were similarly examined in 45 of these adults and in 13 children of both sexes. In 92 men, a subclinical hypermelanosis was found as a speckled pattern centered on every single follicle. With increasing baldness severity, another epidermal hyperpigmentation pattern involving the interfollicular area was superimposed to the perifollicular pattern. These stereotyped patterns of subclinical melanoderma were also disclosed on the face of adults, but not in children. In addition, the spotty perifollicular pattern was discrete or not apparent on the other parts of the body. It is concluded that the perifollicular subclinical melanotic pattern is a regional characteristic of cephalic skin, perhaps related to the local production of melanocortins, particularly alpha-MSH by the pilosebaceous unit.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12459529&dopt=Abstract
Gan To Kagaku Ryoho. 2002 Nov;29(11):1935-42.
[Combined chemoendocrine therapy using adriamycin, cyclophosphamide and high dose toremifene in patients with recurrent breast cancer]
[Article in Japanese]
Wada N, Kobayashi H, Oka S, Ando J, Tamura H.
Dept. of Surgery, Ashikaga Red Cross Hospital.
We studied a new chemoendocrine therapy against recurrent breast cancer in order to evaluate its efficacy and toxicity. Sixteen eligible patients were treated with the therapy consisting of adriamycin/cyclophosphamide (AC) plus toremifene (TOR). Adriamycin (20 mg/m2) was administered intravenously on days 1 and 8, and cyclophosphamide (100 mg/body) was given orally on days 1 to 14 every 4 weeks. TOR (120 mg/day) was given orally daily. The median age of the patients was 52 years; 6 were premenopausal and 10 postmenopausal. As post-operative adjuvant therapy, anthracycline chemotherapy and tamoxifen were given to 4 and 9 patients, respectively. AC therapy was administered for 8.5 cycles (median). Four complete responses (25%), 8 partial responses (37.5%), 4 no change (25%) (including 2 long NC), and 2 progressive disease (12.5%) were obtained, for an overall response rate of 62.5%. The median duration of time to progression and survival were 13.2 months (0.7-30.4 months) and 22.8 months (13.7-44.8 + months), respectively. The frequent toxicities were leukopenia, nausea/vomiting, and alopecia, but these were clinically well tolerated. Our results suggest that the addition of high dose TOR to AC therapy is useful in the treatment of recurrent breast cancer.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12465393&dopt=Abstract
Development. 2003 Jan;130(2):379-89.
'Cyclic alopecia' in Msx2 mutants: defects in hair cycling and hair shaft differentiation.
Ma L, Liu J, Wu T, Plikus M, Jiang TX, Bi Q, Liu YH, Muller-Rover S, Peters H, Sundberg JP, Maxson R, Maas RL, Chuong CM.
Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Msx2-deficient mice exhibit progressive hair loss, starting at P14 and followed by successive cycles of wavelike regrowth and loss. During the hair cycle, Msx2 deficiency shortens anagen phase, but prolongs catagen and telogen. Msx2-deficient hair shafts are structurally abnormal. Molecular analyses suggest a Bmp4/Bmp2/Msx2/Foxn1 acidic hair keratin pathway is involved. These structurally abnormal hairs are easily dislodged in catagen implying a precocious exogen. Deficiency in Msx2 helps to reveal the distinctive skin domains on the same mouse. Each domain cycles asynchronously - although hairs within each skin domain cycle in synchronized waves. Thus, the combinatorial defects in hair cycling and differentiation, together with concealed skin domains, account for the cyclic alopecia phenotype.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12466204&dopt=Abstract
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