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Biomedical subjects

A Borras

Publications and source records attributed to A Borras.

9 recordsLinked to original sources
PubMed1997

Cyclosporin A-sensitive induction of the Epstein-Barr virus lytic switch is mediated via a novel pathway involving a MEF2 family member.

Induction of the Epstein-Barr virus (EBV) lytic cycle by crosslinking surface immunoglobulin is inhibited by the immunosuppressants cyclosporin A (CsA) and FK506. This correlates with the ability of CsA to inhibit Ca2+-dependent transcription of the lytic cycle switch gene BZLF1. It is shown here that CsA sensitivity maps to three sites (ZIA, ZIB and ZID) that bind the serum response factor-related protein MEF2D. A synthetic promoter containing multiple copies of a MEF2D site from Zp, in conjunction with a CREB/AP-1 site (ZII) from Zp, exhibits CsA-sensitive inducibility. Furthermore, the Zp MEF2D sites were functionally interchangeable with MEF2 sites derived from heterologous promoters. While no evidence of a NFAT family member binding to either the MEF2 or CREB/AP-1 sites was obtained, it could be demonstrated that CsA-sensitive induction of Zp was mediated by calcineurin and NFATc2 in synergy with either phorbol ester or especially with the EBV-induced Ca2+/calmodulin-dependent kinase type IV/Gr. These studies identify Zp as prototypic of a novel class of CsA-sensitive and NFAT-dependent promoters defined by the presence of MEF2 sites.

Binding Sites↗
PubMed1984

[Cytotoxicity in psoriasis].

The authors study three cytotoxicity system in psoriasis: direct cytotoxicity (DCC), antibodies mediated cytotoxicity (ADCC) and activated lymphocytes mediated cytotoxicity (PCC). The results of DCC and PCC are in the normal values, while ADCC are a somewhat increased, showing a hyperactivity of this system, which could explain some physiopathological phenomena of this disease. We consider this finding as secondary to an alteration of the immune system by dysbalance of B-T lymphocytes.

Adolescent↗
PubMed1983

[Epidermic and lymphocytary chalone receptors in psoriasis].

By Hondius-Boldingh. Laurence and Bullough, Laurence method, the activity of the epidermal chalone receptors was studied in 36 psoriasis and 36 healthy controls. The lymphocyte chalone receptors was also studied in 26 patients, by Garcia Giralt et al. and Lasalvia et al. method. The results showed that the epidermal chalone receptors are significantly decreased in the involved skin, and in a lesser degree in the uninvolved one of the patients with psoriasis. The lymphocyte chalone receptors were normal. This decreasing in the function of the epidermal chalone system by means of different "antireceptor factors", interrupt the physiological cell control of the epidermis. The absence of the chalone specific function, produces an intracelular disbalance which provokes, in particular, the high number of mitosis and the lack of terminal differentiation. These elements admit that in psoriasis there is an abnormal epidermopoyesis. Over a genetic disorder, multiple factors leading to a deffect of the cell membrane. These factors, acquired, local or systemic interfering with the receptors of membrane, would alter the cellular regulation induced my the chalones.

Adolescent↗
PubMed1983

[Epidermic chalone receptors in psoriasis treated with retinoid:Ro 10-9359].

The epidermic chalone receptor of skin with lesion and without lesion are studied on 20 patients with active psoriasis. The testlest were performed before and two month after oral treatment with RO 10-9359. Roche. The results show significant variation with an increased a the number of receptors after treatment. As these receptors are in the cell membrane, the authors consider that RO 10-9359 action in on the membrane and its surrounding, making in possible to the epithelial cell to begin its autoregulation, autocontrol and differentiation when the specific activity of the chalones become normal.

Adolescent↗
PubMed1983

[Antimelanin antibodies in vitiligo].

The circunlant antimelanin antibodies are studied in common or idiopathic vetiligo. The patients did not have other skin or systemic lesions. The results show the presence antimelanin antibodies in a very significant fashion. Based on these elements, the authors consider that this observation is very important and that in this disease the autoimmune mechanisms have a fundamental character. In vitiligo as in every autoimmune disease, the etiology can be multiple.

Adolescent↗
PubMed1982

[Phosphohexose isomerase in psoriasis].

--The authors study in psoriasis an enzyme of the glucolytic way, the Phospho-hexose-isomerase. --They find significant high levels in blood and damaged skin, while these were "normal" in healthy skin. --Phospho-hexose-isomerase acts as a biological marker in psoriasis, and acquires the significance of an active cellular proliferation. --The highest values are those of the erythrodermaes which become normal with clinical involution. --The authors suggest that psoriasis, by an exaggerated cellular division inhibition mechanism, metabolism is deviated in order to bring the energetic elements and substrate to form the new cell. --Phospho-hexose-isomerase is not specific of the malignant process.

Adolescent↗
PubMed1982

[Cytotoxicity in acne vulgaris].

Three cellular cytotoxic lymphocytary populations were studied in patients with different forms of inflammatory acne vulgaris: direct or spontaneous, antibodies dependent and phytohemagglutinine stimulated. To these was added "Propionibacterium acnes" from cultures of material extracted separately from comedones and pustules. The direct or spontaneous and antibodies dependent cytotoxicity were normal. The subpopulation responsible of the phytohemagglutinine stimulated cytotoxicity has shown a clear hyperactivity which was augmented by the addition of these bacteria. But this hyperactivity stimulation was selective for the "Propionibacterium acnes" from pustules and not for those from comedones. These findings could contribute to the knowledge of the immune cellular mechanisms in acne vulgaris inflammation provoked by these bacteria.

Acne Vulgaris↗