References: Hair growth and hair loss
dent.tokushima-u.ac.jp
Cepharanthin is one of the biscoclaurine alkaloids widely used for treatment of many acute and chronic diseases; snakebite, bronchial asthma, alopecia areata, leukopenia during radiation therapy or anticancer treatment. Recently, it has been reported that cepharanthin exerts antitumour effects by increasing immunological competence of the host or apoptosis-inducing activity. In this study, we examined the antitumour effects of cepharanthin against a human adenosquamous cell carcinoma cell line (TYS). Treatment of TYS cells with cepharanthin (10 approximately 20 microg/ml) resulted in a significant suppression of cell growth. Moreover, it was found by the flow cytometry analysis, nick end labelling or agarose gel electrophoresis, that G1 arrest and DNA fragmentation occurred in cepharanthin-treated cells. In addition, it was detected that induction of p21(WAF1) protein and activation of caspase 3 protype, which is one of Interleukin-1beta converting enzyme (ICE) family proteases, were detected by Western blotting. The TYS tumour-bearing nude mice were treated with cepharanthin, which was administered subcutaneously (20 mg/kg/day). The cepharanthin treatment results in a significant suppression of tumour growth and an induction of apoptosis. These findings suggest that cepharanthin induces G1 arrest via expression of p21(WAF1) and apoptosis through caspase 3.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11590074&dopt=Abstract
Med Cutan Ibero Lat Am. 1976;4(6):401-13.
[Skin manifestations in patients with renal chronic renal failure on regular hemodyalysis]
[Article in Spanish]
Griffon-Euvrard S, Bustamante R, Thiovolet J.
The authors studied the skin disorders in 50 hemodialyzed patients. Pruritus appears to be the main dermatological feature by the frequency of its occurrence and by its unpleasant and even intolerable effects. This sign is more frequent among long time dialyzed patients and seems to be due to 2 factors: high urea blood concentration and secondary hyperparathyroidism. Calcinosis cutis is less frequent than pruritus. It seems to have the same origin and can be considered in the more general picture of the metastatic calcinosis in patients with renal failure and secondary hyperparathyroidism. Hypermelanosis, exceptional in the chronic renal insufficiency patients before hemodialysis, is present in 41% of our group. It is more obvious in the long time dialyzed patients. The nail disorders are mostly the absence of lunula (30%), related to the anaemia, and the half and half nail (36%) that seems specific of the severe azotaemia. Skin dryness (30%) and ichthyosis (10%) can be related to the pruritus. Alopecia, drug reactions and prurigo seems to have a particular indidence. Two patients presented bullous eruptions localized in sunlight exposed areas of skin. The clinical, histological and immunological aspect was identical to that observed in the Porphyria Cutanea Tarda but all the porphyrin levels in the urine and faeces were normal.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1035395&dopt=Abstract
Hum Mol Genet. 2001 Sep 15;10(19):2171-9.
A recurrent deletion in the ubiquitously expressed NEMO (IKK-gamma) gene accounts for the vast majority of incontinentia pigmenti mutations.
Aradhya S, Woffendin H, Jakins T, Bardaro T, Esposito T, Smahi A, Shaw C, Levy M, Munnich A, D'Urso M, Lewis RA, Kenwrick S, Nelson DL.
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.
Incontinentia pigmenti (IP) is an X-linked dominant disorder characterized by abnormal skin pigmentation, retinal detachment, anodontia, alopecia, nail dystrophy and central nervous system defects. This disorder segregates as a male lethal disorder and causes skewed X-inactivation in female patients. IP is caused by mutations in a gene called NEMO, which encodes a regulatory component of the IkappaB kinase complex required to activate the NF-kappaB pathway. Here we report the identification of 277 mutations in 357 unrelated IP patients. An identical genomic deletion within NEMO accounted for 90% of the identified mutations. The remaining mutations were small duplications, substitutions and deletions. Nearly all NEMO mutations caused frameshift and premature protein truncation, which are predicted to eliminate NEMO function and cause cell lethality. Examination of families transmitting the recurrent deletion revealed that the rearrangement occurred in the paternal germline in most cases, indicating that it arises predominantly by intrachromosomal misalignment during meiosis. Expression analysis of human and mouse NEMO/Nemo showed that the gene becomes active early during embryogenesis and is expressed ubiquitously. These data confirm the involvement of NEMO in IP and will help elucidate the mechanism underlying the manifestation of this disorder and the in vivo function of NEMO. Based on these and other recent findings, we propose a model to explain the pathogenesis of this complex disorder.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11590134&dopt=Abstract
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