Validity of the rigid band picture for the t-J model

We present an exact diagonalization study of the doping dependence of the single particle Green's function in 16, 18 and 20 site clusters of t-J model. We find evidence for rigid-band behaviour starting from the half-filled case: upon doping, the topmost states of the quasiparticle band observed in the photoemisson spectrum at half-filling cross the chemical potential and reappear as the lowermost states of the inverse photoemission spectrum. Features in the inverse photoemission spectra which are inconsistent with rigid-band behaviour are shown to originate from the nontrivial point group symmetry of the ground state with two holes, which enforces different selection rules than at half-filling. Deviations from rigid band behaviour which lead to the formation of the `large Fermi surface' in the momentum distribution occur only at energies far from the chemical potential. A Luttinger Fermi surface and a nearest neighbor hopping band do not exist.Comment: Remarks: Revtex file + 7 figures attached as compressed postscript files Figures can also be obtained by ordinary mail on reques

Bogoliubov Quasiparticle Excitations in the Two-Dimensional t-J Model

Using a proposed numerical technique for calculating anomalous Green's functions characteristic of superconductivity, we show that the low-lying excitations in a wide parameter and doping region of the two-dimensional $t$$-$$J$ model are well described by the picture of dressed Bogoliubov quasiparticles in the BCS pairing theory. The pairing occurs predominantly in $d_{x^2-y^2}$-wave channel and the energy gap has a size $\Delta_d$$\simeq$$0.15J$$-0.27J$ between quarter and half fillings. Opening of the superconducting gap in the photoemission and inverse-photoemission spectrum is demonstrated.Comment: 6 pages, RevTe

Patched homologue 1 mutations in four Japanese families with basal cell nevus syndrome

AIM: To search for patched homologue 1 (PTCH1) mutations in four families with basal cell nevus syndrome (BCNS). METHODS: Mutation analysis of PTCH1 in unrelated Japanese families affected with BCNS was carried out by direct sequencing. RESULTS: Six novel PTCH1 mutations, 833G→A in exon 6, 1415C→A and 1451G→T in exon 10, 2798delC in exon 17, 2918–2925dupAGTTCCCT in exon 18 and 3956C→A in exon 23, were identified. CONCLUSIONS: Among the six PTCH1 mutations, two frameshift mutations (2798delC and 2918–2925dupAGTTCCCT) and one nonsense mutation (833G→A) are predicted to lead to premature termination of PTCH1 protein translation. Three simultaneous mutations, 1415C→A (A472D) and 1451G→T (G484V) in exon 10, and 3956G→A (R1319H) in exon 23, were found on one allele in only affected members in one family and none of them were found among 90 unrelated healthy Japanese. The three mutations on one chromosome may have resulted from errors in the recombinational repair process and this is the first report on the PTCH1 mutations due to such a mechanism