ABSTRACT
A comparative synthetic, structural, and thermochemical study on a series of chelate complexes containing the fragment (eta 5-C5Me5)Ir [(eta 5-C5Me5)Ir(TsNCH2CH2NTs) (1), (eta 5-C5Me5)Ir(TsNCH2CO2) (2), (eta 5-C5Me5)Ir(CO2CO2) (3)] was performed to clarify the roles of carboxylato and sulfonamido ligands. Whereas 1 and 2 are monomeric in solution and in the solid state, 3 appears to exist as an oligomer or polymer, (3)n, which can be broken up by addition of a ligand L such as a phosphine, CO, or 2-methoxypyridine to form (eta 5-C5Me5)Ir(L)(CO2CO2) (6). The synthesis of (3)n from [(eta 5-C5Me5)IrCl(mu-Cl)]2 required the use of silver oxalate in CH3CN, but if other solvents were used, the bridging oxalato complex (eta 5-C5Me5)IrCl(mu-eta 2-eta 2-C2O4)ClIr(eta 5-C5Me5) (7) was obtained and identified by X-ray diffraction. Enthalpies for reaction of THF-soluble monomers 1 and 2 with PMe3 were determined to be -28.7(0.5) and -28.5(0.4) kcal mol-1, respectively. The oligomerization behavior of 3 may be a result of reduced sigma- or pi-donation of carboxylato ligands compared to N-tosylamido ligands, because the values for nu CO in oxalato and bissulfonamido complexes 6-CO and (eta 5-C5Me5)Ir(CO)(TsNCH2CH2NTs) (4-CO) were 2064 and 2042 cm-1, respectively.
ABSTRACT
The results of treatment were reviewed in 16 patients (10 male and six female) who had Ewing's sarcoma of the foot from 1954 through 1992. Mean age was 17 years (range, 10-42 years). The tumor involved the metatarsals (six patients), phalanges (four), calcaneus (three), navicular (one), talus (one), and calcaneus and phalanx (one). Seven patients had metastatic disease at the time of diagnosis, and only one of these patients survived. None of the patients with pulmonary metastasis at presentation survived. Nine patients had localized disease at the time of diagnosis, and eight survived. In the overall series, nine of the 16 patients were alive at followup (eight survived at least 5 years). Diagnosis was established at an average of 14 months from the onset of symptoms: 7 months in forefoot tumors and 22 months in hindfoot tumors. None of the six patients who had a resection had local failure. Seven of the 10 patients with forefoot lesions survived, and two of the six patients with hindfoot lesions survived. Treatment of Ewing's sarcoma of the foot by local control with radiation or operation and systemic control with chemotherapy is recommended. Survival appears to be better in patients who present with localized disease and forefoot lesions. Survival is worse in patients who present with metastatic disease. Surgical treatment appears to have an important role in local control and survival.
Subject(s)
Bone Neoplasms/therapy , Foot Bones/pathology , Foot Diseases/therapy , Sarcoma, Ewing/therapy , Adolescent , Adult , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Bone Neoplasms/diagnosis , Bone Neoplasms/drug therapy , Bone Neoplasms/radiotherapy , Bone Neoplasms/surgery , Calcaneus/pathology , Child , Combined Modality Therapy , Female , Follow-Up Studies , Foot Diseases/diagnosis , Foot Diseases/drug therapy , Foot Diseases/radiotherapy , Foot Diseases/surgery , Forefoot, Human/pathology , Humans , Lung Neoplasms/secondary , Male , Metatarsal Bones/pathology , Neoplasm Recurrence, Local/pathology , Prognosis , Radiotherapy Dosage , Retrospective Studies , Sarcoma, Ewing/diagnosis , Sarcoma, Ewing/drug therapy , Sarcoma, Ewing/radiotherapy , Sarcoma, Ewing/secondary , Sarcoma, Ewing/surgery , Survival Rate , Tarsal Bones/pathology , Toes/pathologyABSTRACT
Retinol or retinoic acid is required for insulin release. Retinoids increase transglutaminase activity, and transglutaminase has been implicated in islet insulin release. To examine whether transglutaminase could mediate effects of retinoids on insulin secretion, we measured (i) transglutaminase activity in islets from rats deficient in vitamin A or repleted with retinol or retinoic acid, (ii) transglutaminase activity in RINm5F and INS-1 insulin-secreting cells cultured in retinol or retinoic acid, (iii) mRNA for transglutaminase in RINm5F and INS-1 cells, and (iv) insulin secretion from INS-1 cells in response to retinoic acid. Islets from rats repleted with retinol or retinoic acid showed more than twice the transglutaminase activity of islets from vitamin A deficient rats. Retinoic acid increased RINm5F cells and INS-1 cell transglutaminase activity. Retinol did not increase transglutaminase activity. Transglutaminase mRNA was detected in INS-1 cells but not in RINm5F cells. Retinoic acid increased insulin secretion from INS-1 cells as observed previously in RINm5F cells. In conclusion, retinoic acid increases transglutaminase activity in both rat islets and two insulin-secreting from INS-1 cells. Transglutaminase is a candidate for mediating retinoid-induced changes in insulin secretion.
