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Disabling Consent, or Reconstructing Sexual Autonomy
Does a right to sexual autonomy criminalize the embellished pick-up line? Or does a right to sexual autonomy permit each and every consensual sex act, however life- threatening, or even life-ending? This Article defends (by reconstructing) sexual autonomy as the governing principle of modern rape law. Powerful criticisms of sexual autonomy otherwise normatively opposed share an antecedent assumption: that sexual autonomy can be read off and as first person present active (or passive) consent (Part I). This Article argues against the conflation of sexual autonomy with sexual consent. Instead, and in conversation with competing liberal and feminist political theoretic accounts of sexual autonomy, this Article defines sexual autonomy as the capability to codetermine sexual relations (Part II). By interfacing a revised concept of sexual autonomy against and alongside State v. Fourtin, a 2012 Connecticut Supreme Court decision overturning a conviction of sexual assault against a severely mentally and physically disabled woman (Part III), the Article proposes three possibilities for statutory reform: refurbishing consent; expanding restrictions on status relations; and applying an accommodation model of disability entitlements to sexual relations (Part IV). After synopsizing our interventions, the Conclusion reminds readers that our brief for sexual autonomy, relationally reconstructed, presumes and propounds the ordinariness, not the extraordinariness, of sex
Current problems in Stellar Pulsation Instabilities
Instabilities of pulsating variable stars, such as Cepheid variables, Cepheid masses, early-type variable stars, White Dwarfs, and Mira variables, are discussed
Ternary combination of irinotecan, fluorouracil-folinic acid and oxaliplatin: results on human colon cancer cell lines
A marked antitumour efficacy is currently obtained by oxaliplatin (LOHP)–fluorouracil (FU)–folinic acid (FA) combination and by CPT11–FU–FA combination. Logically, the triple association LOHP, CPT11 and FUFA will be soon tested in cancer patients. The aim of the present study was to compare two schedules combining SN38 (the active metabolite of CPT11, irinotecan) with FU–FA and LOHP. The two schedules differed by the SN38 position. The relative contribution of each drug in the resulting global cytotoxicity was evaluated. Two human colon cancer cell lines were used (WIDR and SW620 both p53 mutated). LOHP plus FA were applied for 2 h, just before a 48 h FU exposure. The SN38 sequence was applied for 24 h, starting either 48 h before LOHP-FA (schedule A), or just after LOHP-FA exposure (schedule B). Cytotoxicity was assessed by the 3-(4,5-demethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) test and drug interactions were analysed according to the Chou and Talalay method, based on the computation of a combination index (CI). The SN38 position significantly induces a shift from additivity-antagonism when SN38 was applied after LOHP, towards additivity-synergism when SN38 was applied first (P = 0.03). The relative contribution (RC) of each drug in the overall cytotoxicity of the triple combination was defined as the drug concentration giving 50% cell lethality (IC 50) of the double association without that drug divided by the IC 50 of the triple association. Whatever the SN38 position, the larger contribution was made by LOHP (median RC = 2.4) and the smaller by SN38 (median RC = 1.1). In addition, the contribution of FUFA was improved when SN38 was applied first (median RC = 2.2) as compared to the opposite schedule (median RC = 1.2). Results were in agreement between the two explored cell lines. The present data should be taken into account when establishing the rationale of future trials combining CPT11, LOHP and FU–FA. © 2001 Cancer Research Campaign http://www.bjcancer.co
Impact of thymidine phosphorylase surexpression on fluoropyrimidine activity and on tumour angiogenesis
Tumoral thymidine phosphorylase (TP) appears to play a dual role by being involved in neoangiogenesis and by activating 5FU prodrugs at the tumoral target site. The aim of the study was to investigate more thoroughly these potential physiological and pharmacological roles of TP. A rat carcinoma cell line (PROb) was transfected with TP/PD-ECGF in order to study the effect of the overexpression of this enzyme (1) on the sensitivity of cells to 5′DFUR and 5FU in vitro and (2) on tumour growth in vivo by using a syngenic tumour model in the BDIX rat (hepatic tumours, sub-cutaneous tumours). Cytotoxic effects of 5′DFUR, and to a lesser extent those of 5FU, were enhanced in TP clones as compared to control cells: there was a highly significant correlation between TP activity and in vitro sensitivity to 5’DFUR (r2= 0.91, P = 0.0002, n = 8) and, to a lesser extent, to 5FU (r2= 0.49, P = 0.053, n = 8). The impact of TP transfection on tumour growth was relatively modest and concerned only the initial stages of tumour expansion. Staining of TP tumours for endothelial (factor VIII) cells was always higher than controls. The staining ratio (TP/controls) tended to be reduced as tumours increased in size. The stability of TP expression was checked both in vitro (TP activity measurement) and in vivo (RT-PCR determinations) and there was no loss of TP expression over time which could be advanced to explain the progressive weakening of the impact of TP overexpression on both tumour growth and neoangiogenesis. © 2001 Cancer Research Campaign http://www.bjcancer.co
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