The 3-Band Hubbard-Model versus the 1-Band Model for the high-Tc Cuprates: Pairing Dynamics, Superconductivity and the Ground-State Phase Diagram

One central challenge in high-$T_c$ superconductivity (SC) is to derive a detailed understanding for the specific role of the $Cu$-$d_{x^2-y^2}$ and $O$-$p_{x,y}$ orbital degrees of freedom. In most theoretical studies an effective one-band Hubbard (1BH) or t-J model has been used. Here, the physics is that of doping into a Mott-insulator, whereas the actual high-$T_c$ cuprates are doped charge-transfer insulators. To shed light on the related question, where the material-dependent physics enters, we compare the competing magnetic and superconducting phases in the ground state, the single- and two-particle excitations and, in particular, the pairing interaction and its dynamics in the three-band Hubbard (3BH) and 1BH-models. Using a cluster embedding scheme, i.e. the variational cluster approach (VCA), we find which frequencies are relevant for pairing in the two models as a function of interaction strength and doping: in the 3BH-models the interaction in the low- to optimal-doping regime is dominated by retarded pairing due to low-energy spin fluctuations with surprisingly little influence of inter-band (p-d charge) fluctuations. On the other hand, in the 1BH-model, in addition a part comes from "high-energy" excited states (Hubbard band), which may be identified with a non-retarded contribution. We find these differences between a charge-transfer and a Mott insulator to be renormalized away for the ground-state phase diagram of the 3BH- and 1BH-models, which are in close overall agreement, i.e. are "universal". On the other hand, we expect the differences - and thus, the material dependence to show up in the "non-universal" finite-T phase diagram ($T_c$-values).Comment: 17 pages, 9 figure

Cost effectiveness of a new combined immunosuppressive and antiviral regimen on the one-year follow-up of kidney transplant patients.

Background: Medical prescription after organ transplant must prevent both rejection and infectious complications. We assessed the 1-year effectiveness and cost of introducing a new combined regimen in kidney transplantation. Methods: Patients transplanted from January 2000 to March 2003 (Period 1) were compared to patients transplanted from April 2003 to July 2005 (Period 2). In period 1, patients were treated with Basiliximab, Cyclosporin, steroids and Mycophenolate (MMF) or Azathioprine. Prophylaxis with Valacyclovir was prescribed only in CMV D+/R- patients. In period 2, immunosuppressive drugs were Basiliximab, Tacrolimus, steroids and MMF. A 3-month universal CMV prophylaxis with Valganciclovir was used. Medical charts of outpatient visits allowed identifying drug, laboratory and radiological tests use, and hospital information system causes of hospitalisation and length of stay (LOS) over the first year after transplant. Patients with incomplete costs data were excluded. Results: 53 patients were analysed in period 1, and 60 in period 2. CMV serostatus patterns were not significantly different between the 2 periods. Over 12 months, acute rejection decreased from 22 patients (42%) in period 1 to 4 patients (7%) in period 2 (p&lt;0.001), and CMV infection from 25 patients (47%) to 9 patients (15%, p&lt;0.001). Average total rehospitalisation LOS decreased from 28±19 to 20±11 days (p&lt;0.007). Average outpatient visits decreased from 49±10 to 39±8 (p&lt;0.001). Average immunosuppression and CMV prophylaxis costs increased from US 18,362±6,546 to 24,637±5,457 (p<0.001), while average graft rejection costs decreased form US 4,135±9,164 to 585±2,850 (p=0.005), and average CMV treatment costs from US$2,043±5,545 to 91±293 (p=0.008). Average outpatient visits costs decreased from US$ 7,619±1,549 to 6,074±1,043 (p&lt;0.001), and other hospital costs from US$3,801±6,519 to 1,196±3,146 (p=0.007). Altogether, average 1-year treatment costs decreased from US$ 35,961±14,916 to 32,584±6,211 (p=0.115). Cost-effectiveness ratios to avoid graft rejection and CMV infection decreased from US$61,482±9,292 to 34,911± 1,639 (p=0.006) and US$ 68,070±11,122 to 39,899±2,650 (p=0.015), respectively. Conclusion: The new combined regimen administered in period 2 was significantly more effective. Its additional cost was more than offset by savings linked with complications avoidance

Effect of [F-18]FMISO stratified dose-escalation on local control in FaDu hSCC in nude mice

Objective: To investigate the effect of radiation dose-escalation on local control in hypoxic versus non-hypoxic hypoxic tumours defined using [F-18]fluoromisonidazole ([F-18]FMISO) PET. Materials and methods: FaDu human squamous cell carcinomas (hSCCs) growing subcutaneously in nude mice were subjected to [F-18]FMISO PET before irradiation with single doses of 25 or 35 Gy under normal blood flow conditions. [F-18]FMISO hypoxic volume (HV) and maximum standardised uptake value (SUVmax) were used to quantify tracer uptake. The animals were followed up for at least 120 days after irradiation. The endpoints were permanent local tumour control and time to local recurrence. Results: HV varied between 38 and 291 mm(3) (median 105 mm(3)). Non-hypoxic tumours (HV below median) showed significantly better local control after single dose irradiation than hypoxic tumours (HV above median) (p = 0.046). The effect of dose was significant and not different in non-hypoxic and in hypoxic tumours (HR= 0.82 [95% Cl 0.71; 0.93], p = 0.002 and HR= 0.86 [0.78; 0.95], p = 0.001, respectively). Dose escalation resulted in an incremental increase of local tumour control from low-dose hypoxic, over low-dose non-hypoxic and high-dose hypoxic to high-dose non-hypoxic tumours. SUVmax did not reveal significant association with local control at any dose level. Conclusions: The negative effect of [F-18]FMISO HV on permanent local tumour control supports the prognostic value of the pre-treatment [F-18]FMISO HV. Making the assumption that variable [F-18]FMISO uptake in different FaDu tumours which all have the same genetic background may serve as an experimental model of intratumoural heterogeneity, the data support the concept of dose-escalation with inhomogeneous dose distribution based on pre-treatment [F-18]FMISO uptake. This result needs to be confirmed in other tumour models and using fractionated radiotherapy schedules