Relevant bibliographies by topics / Benign familial chronic pemphigus

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Benign familial chronic pemphigus'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Benign familial chronic pemphigus"

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Galimberti, Ricardo Luis, Alicia Maria Kowalczuk, Oscar Bianchi, Maria Victoria Boning, and Adelina Garcia Garcia. "Chronic Benign Familial Pemphigus." International Journal of Dermatology 27, no. 7 (September 1988): 495–500. http://dx.doi.org/10.1111/j.1365-4362.1988.tb00929.x.

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Sehgal, Virendra N., and Sanjiv Jain. "Chronic Familial Benign Pemphigus." Journal of Dermatology 21, no. 6 (June 1994): 382–88. http://dx.doi.org/10.1111/j.1346-8138.1994.tb01759.x.

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Steffen, Charles G. "Familial Benign Chronic Pemphigus." American Journal of Dermatopathology 9, no. 1 (February 1987): 58–73. http://dx.doi.org/10.1097/00000372-198702000-00012.

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Kurwa, A. R., and H. R. Vickers. "(20) Benign familial chronic pemphigus." British Journal of Dermatology 113, s29 (July 1985): 64. http://dx.doi.org/10.1111/j.1365-2133.1985.tb13035.x.

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Falto-Aizpurua, Leyre, Harleen Arora, Fleta Bray, and Jessica Cervantes. "Management of familial benign chronic pemphigus." Clinical, Cosmetic and Investigational Dermatology Volume 9 (September 2016): 281–90. http://dx.doi.org/10.2147/ccid.s89483.

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Takami, Yoshihiro, Yutaka Akutsu, Masako Suzuki, and Makoto Takahashi. "Familial Benign Chronic Pemphigus Generalized byPseudomonasInfection." Journal of Dermatology 13, no. 6 (December 1986): 474–76. http://dx.doi.org/10.1111/j.1346-8138.1986.tb02979.x.

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Parajuli, Niraj. "A recurrent intertrigo: benign familial chronic pemphigus." Journal of Chitwan Medical College 8, no. 2 (June 30, 2018): 63–65. http://dx.doi.org/10.3126/jcmc.v8i2.23741.

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Benign familial chronic pemphigus (BF CP) is an autosomal dominant disorder characterized by recurrent vesicles and plaques mostly over the intertriginous areas. The defect is in the AT P2C1 gene which leads to suprabasilar acantholysis. Pregnancy, physical trauma, excessive sweating, skin infections and exposure to ultraviolet radiation are the important trigger factors. Self-medications or over the counter treatment usually makes a delay in the proper diagnosis.
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Yordanova, Ivelina. "Familial benign chronic pemphigus (Hailey-Hailey disease)." Journal of IMAB - Annual Proceeding (Scientific Papers) 13, 1, no. 2007 (April 25, 2008): 56–58. http://dx.doi.org/10.5272/jimab.2007131.56.

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Dadban, A., and B. Guillot. "Oesophageal Involvement in Familial Benign Chronic Pemphigus." Acta Dermato-Venereologica 86, no. 3 (2006): 252–53. http://dx.doi.org/10.2340/00015555-0053.

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Kartamaa, Matti. "Familial Benign Chronic Pemphigus (Hailey-Hailey Disease)." Archives of Dermatology 128, no. 5 (May 1, 1992): 646. http://dx.doi.org/10.1001/archderm.1992.01680150076009.

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Dissertations / Theses on the topic "Benign familial chronic pemphigus"

1

Leinonen, P. (Pekka). "Calcium signaling in epithelium:special focus on Hailey-Hailey and Darier diseases, neurofibromatosis 1 and transitional cell carcinoma." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514290008.

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Abstract This study utilized normal and defective epithelial cell cultures and epidermal skin samples to examine intra- and intercellular calcium signaling. The main interests of this thesis were Hailey-Hailey disease (HHD), Darier disease (DD), neurofibromatosis 1 (NF1) and transitional cell carcinoma (TCC). HHD and DD diseases are rare autosomal dominant skin disorders characterized by dissociation of epidermal keratinocytes (acantholysis) at the suprabasal layer of the epidermis. HHD and DD diseases are caused by mutations in the genes encoding the calcium pumps in the Golgi apparatus (hSPCA1) and endoplasmic reticulum (SERCA2b), respectively. Due to these mutations calcium uptake into the Golgi apparatus or ER is diminished, which is believed to cause abnormal cell junction protein processing and dissociation of keratinocytes. This study utilized electron probe microanalysis (EPMA) and demonstrated for the first time that lesional areas of HHD and DD and non-lesional areas of DD epidermis display abnormally low calcium content in the basal cell layer. Furthermore, ATP mediated calcium signaling was impaired in cultured HHD and DD keratinocytes and epidermal ATP receptor localization was disrupted. In conclusion, these results suggest that the low calcium content in the basal cell layer is the reason for suprabasal ruptures in HHD but not necessarily in DD lesions, and that abnormal ATP receptor localization contributes to the calcium signaling defects. NF1 deficient keratinocytes display abnormally low resting cytosolic calcium levels and it has been suggested that the calcium concentration in the lumen of the endoplasmic reticulum is decreased. This study demonstrated that NF1 keratinocytes rely mostly on ATP mediated calcium signaling while normal keratinocytes rely mostly on gap junctional intercellular communication (GJIC). Studies with TCC cells have demonstrated that gap junctions participate in intercellular calcium wave propagation. This thesis demonstrated that the ATP mediated pathway was also operational in calcium wave propagation in normal uroepithelial and TCC cell cultures. Furthermore, impaired calcium wave propagation in the TCC cell culture could be improved through PKC α/βI –isoenzyme inhibition with Gö6976. Gö6976 treatment increased connexin 26 clustering at plasma membrane but did not alter expression level of the protein. This thesis contains a wide repertoire of calcium detection techniques including a new cutting-edge technology for elemental calcium detection of epidermal samples. These techniques can be used for molecular specific analysis of calcium signaling in epithelial cells.
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Book chapters on the topic "Benign familial chronic pemphigus"

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Desnick, Robert J., Orlando Guntinas-Lichius, George W. Padberg, Gustav Schonfeld, Xiaobo Lin, Maurizio Averna, Pin Yue, et al. "Familial Benign Chronic Pemphigus." In Encyclopedia of Molecular Mechanisms of Disease, 631. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8663.

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Hall, Anthony. "Hailey-Hailey Disease (Familial Benign Chronic Pemphigus)." In Atlas of Male Genital Dermatology, 129–31. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99750-6_39.

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Salavastru, Carmen Maria, and George-Sorin Tiplica. "Hailey-Hailey Disease (Familial Benign Pemphigus)." In European Handbook of Dermatological Treatments, 335–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45139-7_35.

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Gloster, Hugh Morris, Lauren E. Gebauer, and Rachel L. Mistur. "Hailey-Hailey Disease (Benign Familial Pemphigus)." In Absolute Dermatology Review, 73. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-03218-4_23.

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"Familial benign chronic pemphigus." In Dermatology Therapy, 234–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_1051.

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"Familial benign pemphigus." In Dermatology Therapy, 235. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_1052.

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O’Toole, Edel. "Tumours of the skin." In Oxford Textbook of Medicine, edited by Roderick J. Hay, 5732–42. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0563.

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A variety of tumours, both benign and malignant, are found in skin. Benign skin lesions, such as seborrhoeic keratoses and skin tags, are often just a cosmetic nuisance, but some benign skin lesions can be a component of diseases with serious medical consequences (e.g. neurofibromatosis or LEOPARD syndrome). Skin cancer is the most common human cancer and its incidence continues to increase. It most commonly affects older, fair-skinned individuals who have had either acute intermittent exposure to ultraviolet light or chronic ultraviolet light exposure. Organ transplant recipients have a 200-fold increased risk of squamous cell carcinoma. About 2% of patients who develop skin cancer have a genetic predisposition, for example, Gorlin’s syndrome in basal cell carcinoma and familial melanoma syndromes in malignant melanoma. Mutations in the PTCH gene cause Gorlin’s syndrome, and loss of heterozygosity at that locus is also present in most sporadic basal cell carcinoma.
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Journal articles
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