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Phic CTCLs from pseudoT-cell lymphomas, which may also present with a solitary plaque or nodule.129 Prognosis and predictive factors. These lymphomas have a rather favorable prognosis, with an estimated 5-year survival of approximately 60% to 80% Table 2 ; .2, 4, 5, Particularly, cases presenting with a solitary or localized skin lesions seem to have an excellent prognosis.11 Therapy. In patients with solitary localized skin lesions, surgical excision or radiotherapy is the preferred mode of treatment. Cyclophosphamide as single-agent therapy and interferon alpha have been reported effective in patients with more generalized skin disease.128 However, the optimal treatment for this group has still to be defined. Primary cutaneous peripheral T-cell lymphoma, unspecified. Definition. The designation PTL, unspecified, is maintained for cutaneous T-cell lymphomas that do not fit into any of the better defined subtypes of CTCL. Hence, other categories of T-cell lymphoma must be excluded. These include the 3 provisional entities described earlier. Clinical features. Patients are commonly adults, who present with solitary, localized, or more frequently generalized nodules or tumors.2, 4, 10, 11 No sites of predilection have been recorded. Histopathology. Skin lesions show nodular or diffuse infiltrates with variable numbers of medium- to large-sized pleomorphic or immunoblast-like T cells. Epidermotropism is generally mild or absent. Large neoplastic cells represent at least 30% of the total tumor cell population.10 Immunophenotype. Most cases show an aberrant CD4 T-cell phenotype with variable loss of panT-cell antigens. CD30 staining is negative or restricted to a few scattered tumor cells. Rare cases may show coexpression of CD56. Expression of cytotoxic proteins is uncommon.11 Prognosis and predictive factors. The prognosis is generally poor, with 5-year survival rates of less than 20% Table 2 ; .2, 4, 5, No statistical differences in survival were found between cases presenting with solitary localized lesions and cases presenting with generalized skin lesions.11 Treatment. Patients should be treated with multiagent chemotherapy.
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Figure 5. a ; Doseeffect relationship of human menopausal gonadotrophin HMG ; standard, recombinant human follicle stimulating hormone r-hFSH ; , Metrodin Ares-Serono, Switzerland ; and Metrodin HP Ares-Serono ; on rat ovary weight. FSH preparations were diluted in phosphate-buffered saline at pH 7.2 to final concentrations of 0.25, 0.5, 1, and 4 IU FSH ml. Samples were each administered to groups of five rats given s.c. injections of 0.5 ml rat, twice daily, for 3 consecutive days, yielding final cumulative doses of 0.75, 1.5, 3, and 12 IU FSH rat. A total dose of 40 IU human chorionic gonadotrophin HCG ; was also administered to each animal. Animals were killed 72 h after the first administration, the ovaries were then removed, dissected free of surrounding tissue and weighed. The cumulated mean results of two independent experiments are reported. b ; Timeeffect relationship of HMG standard, r-hFSH, Metrodin and Metrodin HP on rat ovary weight. FSH was diluted to a final concentration of 1 IU phosphate-buffered saline, pH 7.2, containing 13.3 IU ml HCG. Samples were each administered to groups of five rats by giving s.c. injections of 0.5 ml rat, twice daily for 1, 2, 3 or 4 consecutive days, yielding final cumulative doses of 1, 2, 3 and 4 IU FSH rat, respectively. Additional groups of rats received HCG containing buffer with the same modalities and served as control. The ovaries from experimental groups were removed and weighed out at 24, 48, 72 and 96 h after the first injection. The cumulated results of two independent experiments are reported and toremifene.
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EXPERIMENTAL PROCEDURES Adduct Formation. Tolmetin glucuronide 1.5 , umol ; , isolated and purified as previously described 11 ; , and HSA essentially fatty acid free, Sigma ; 0.45 gmol ; were incubated in 1 ml 0.1 M sodium phosphate buffer pH 7.4 ; in the presence of excess sodium cyanoborohydride NaCNBH3, 20 , umol ; to trap any imine formed. After 6 hr at 37C, the reaction was stopped by centrifugal filtration through a 30-kDa-cutoff membrane and the retained solution was rinsed with water. A control experiment was performed under the same conditions but with 1.5 gmol of tolmetin instead of tolmetin glucuronide. Trypsin Digestion. Twenty nmol of the reacted protein mixture was reduced with dithiothreitol 6 gmol; 60 min at 60C under argon ; , alkylated with sodium iodoacetate 10 , umol; 30 min at room temperature ; in 100 , ul of 6 guanidine hydrochloride 100 mM Tris 1 mM EDTA, pH 8.3, and subsequently dialyzed against 50 mM ammonium bicarbonate buffer pH 8.0 ; in a Bethesda Research Laboratories microdialysis apparatus equipped with a 6-kDa-cutoff membrane. The dialyzed protein was then treated with 2% wt wt ; trypsin L-1-tosylamido-2-phenylethyl chloromethyl ketonetreated; Sigma; type XIII ; for 4 hr at 37C. Protein concentrations were determined colorimetrically by using a kit Pierce ; . HPLC. The tryptic fragments were separated by reversed phase chromatography on a Beckman HPLC system using a Vydac protein and peptide C18 column 250 x 4.6 mm ; . Elution was performed with a linear gradient from 99% solvent A [0.1% vol vol ; trifluoroacetic acid in water] to 45% solvent B 0.08% trifluoroacetic acid in acetonitrile ; within 90 min at a flow rate of 1 ml min. The elution was monitored at a wavelength of 215 nm for peptides and 313 nm.
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31. Guadano-Ferraz A, Escamez MJ, Rausell E, Bernal J 1999 Expression of type 2 iodothyronine deiodinase in hypothyroid rat brain indicates an important role of thyroid hormone in the development of specific primary sensory systems. J Neurosci 19: 3430 3439 Dumitrescu A, Liao X, Lado-Abeal J, Moeller L, Brockmann K, Refetoff S 2004 Abstract presented at the 76th ATA meeting on the mechanism producing the unusual thyroid phenotype in defects of the MCT8 gene. Thyroid 14: 761 33. Kohrle J, Jakob F, Contempre B, Dumont JE 2005 Selenium, the thyroid, and the endocrine system. Endocr Rev 26: 944 984 Biebermann H, Ambrugger P, Tarnow P, von Moers A, Schweizer U, Grueters A 2005 Extended clinical phenotype, endocrine investigations and functional studies of a loss-of-function mutation A150V in the thyroid hormone specific transporter MCT8. Eur J Endocrinol 153: 359 366
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