8 Breneman D, Bronsky EA, Bruce S et al. Cetirizine and astemizole therapy for chronic idiopathic urticaria: a double-blind, placebocontrolled, comparative trial. J Am Acad Dermatol 1995; 33 (2 pt 1):192-8. 9 Kocatürk E, Kavala M, Kural E et al. Autologous serum skin test vs autologous plasma skin test in patients with chronic urticaria: evaluation of reproducibility, sensitivity and specificity and relationship with disease activity, quality of life and anti-thyroid antibodies. Eur J Dermatol 2011; 21:339-43. 10 Godse KV. Autologous serum skin test at various dilutions. Indian J Dermatol 2011; 56:352-3.B.I. and E.G. contributed equally to this work.
Thermoreversible gelation of poly(vinylidene fluoride) (PVDF) in propylene carbonate (PC) solutions at relatively low concentrations (0.5-3.5 wt.%) has been studied in terms of the gelation time (or rate) as a function of temperature and polymer concentration. A master curve could be made for the gelation time -temperature curves using the temperature shift based on the difference in the gel melting temperature (T m g ) at different PVDF concentrations. The apparent activation energy of gelation was estimated to be proportional to (T m g 2 T) 21.8 . The gel melting enthalpy (DH m g ) determined from the modified Eldrige -Ferry equation was 18.67 kJ/mol. In dried gel films many spherulites connected by tie molecules were observed by scanning electron microscopy (SEM). From the wide angle x-ray diffraction (WAXD) measurement, crystallites from PVDF gels were found to consist only of the g-type crystal with the TTTGTTTḠ conformation, irrespective of the polymer concentration. As judged from the results 741 ORDER REPRINTS obtained, the gelation of PVDF in PC seems to proceed mainly via liquid-liquid phase separation (even if followed by crystallization in the final stage) within the concentration range covered.
In psoriasis, tazarotene acts by modulating the three main pathogenic features: abnormal differentiation, hyperproliferation of keratinocytes, and inflammation. 3 As with other topical retinoids, adverse events with tazarotene are limited to local effects, most frequently being erythema, pruritus, burning/stinging and, rarely, pyogenic granuloma in patients with psoriasis. 4 However, retinoids are not known to cause depigmentation. Topical use of retinoic acid (RA) produces improvement in hyperpigmentation by reducing the number of functioning melanocytes and/or in inhibiting their ability to synthesize melanin. 5 Retinoids are potent inhibitors of mammalian GSTs (glutathione-s-transferase) and this makes cells more susceptible to the cytotoxic effects of chemicals. 6 We do not have the exact explanation for this observation besides the above-mentioned biochemical mechanisms or the local irritation and erythema following tazarotene causing depigmentation by Koebnerization. The occurrence of vitiligo within an area treated with tazarotene does not illustrate definite direct cause but probably does indicate the need for vigilance to see whether this association occurs again. Clinicians should be aware of potential pigmentary changes, particularly when using tazarotene on areas of skin that are readily visible or in patients of vitiligo for treatment of other dermatoses. We suggest that this rare but important observation should be considered as a potential side-effect of tazarotene. Mays S. The pathogenesis of psoriasis and the mechanism of action of tazarotene. J Am Acad Dermatol 1998; 39: S129-S133. 4 Weinstein GD, Krueger GG, Lowe NJ et al. Tazarotene gel, a new retinoid, for topical therapy of psoriasis. vehicle-controlled study of safety, efficacy, and duration of therapeutic effect. J Am Acad Dermatol 1997; 37: 85-92. 5 Kligman AM, Willis I. A new formula for depigmenting human skin. Arch Dermatol 1975; 111: 40-48. 6 Kasraee B, Handjani F, Aslani FS. Enhancement of the depigmenting effect of hydroquinone and 4-hydroxyanisole by all-trans-retinoic acid (tretinoin): the impairment of glutathione-dependent cytoprotection? Dermatology 2003; 206: 289-291.
This study was undertaken to investigate the immunohistochemical characterization of different subpopulations of macrophages and dendritic cells (DCs) of the spleen, thymus, tongue and heart in cyclophosphamide (CY)-induced immunosuppressed rat. After CY treatment, remarkably, ED1+, ED2+ and ED3+ macrophage subpopulations, in general exhibited signs of cellular activation such as an increase in number and size of cell, and an upregulation of the ED1, ED2 and ED3 reactive surface molecule expression in all the organs studied, except for some macrophage subpopulations including ED1+ macrophages in the non-lymphoid tissues. Subpopulations of DCs showed a differential sensitivity to CY. Lymphoid DCs were more sensitive to CY than non-lymphoid interstitial DCs. CY induced a conspicuous upregulation of intercellular adhesion molecule-1 (ICAM-1) expression in the vascular endothelial cells, splenic marginal zone and thymic cortex. In this study, we demonstrated the in vivo effects of CY treatment on subpopulations of macrophages and DCs as well as on ICAM-1 expression in the rat spleen, thymus, tongue and heart. Moreover, our results shed more light on the activation effects of CY on certain subpopulations of macrophages, on the differential sensitivity of DCs to CY between the immature and mature ones, on the functional role of different subpopulations of macrophages, and on the significance of upregulated ICAM-1 expression in the splenic marginal zone and thymic cortex after CY treatment.
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