Fractional quantization of the magnetic flux in cylindrical unconventional superconductors.

The magnetic flux threading a conventional superconducting ring is typically quantized in units of Φ0=hc/2e. The factor of 2 in the denominator of Φ0 originates from the existence of two different types of pairing states with minima of the free energy at even and odd multiples of Φ0. Here we show that spatially modulated pairing states exist with energy minima at fractional flux values, in particular, at multiples of Φ0/2. In such states, condensates with different center-of-mass momenta of the Cooper pairs coexist. The proposed mechanism for fractional flux quantization is discussed in the context of cuprate superconductors, where hc/4e flux periodicities were observed.

Quasiparticle anisotropy and pseudogap formation from the weak-coupling renormalization group point of view.

Using the one-loop functional renormalization group technique, we evaluate the self-energy in the weak-coupling regime of the 2D t-t(') Hubbard model. At van Hove (vH) band fillings and at low temperatures, the quasiparticle weight along the Fermi surface (FS) continuously vanishes on approaching the (pi,0) point where the quasiparticle concept is invalid. Away from vH band fillings the quasiparticle peak is formed inside an anisotropic pseudogap and the self-energy has the conventional Fermi-liquid characteristics near the Fermi level. The spectral weight of the quasiparticle features is reduced on parts of the FS between the near vicinity of hot spots and the FS points closest to (pi,0) and (0,pi).

Spin-charge separation in Aharonov-Bohm rings of interacting electrons.

We investigate the properties of strongly correlated electronic models on a flux-threaded ring connected to semi-infinite free-electron leads. The interference pattern of such an Aharonov-Bohm ring shows sharp dips at certain flux values, determined by the filling, which are a consequence of spin-charge separation in a nanoscopic system.

Detection of topological transitions by transport through molecules and nanodevices.

We analyze the phase transitions of an interacting electronic system weakly coupled to free-electron leads by considering its zero-bias conductance. This is expressed in terms of two effective impurity models for the cases with and without spin degeneracy. Using the half-filled ionic Hubbard ring, we demonstrate that the weight of the first conductance peak as a function of external flux or of the difference in gate voltages between even and odd sites allows one to identify the topological charge transition between a correlated insulator and a band insulator.

Human keratinocyte line HaCaT metabolizes 1alpha-hydroxyvitamin D3 and vitamin D3 to 1alpha,25-dihydroxyvitamin D3 (calcitriol).

Cultured human keratinocytes have the property to hydroxylate exogenous 25-hydroxyvitamin D3 (25OHD3) at the C-1alpha position thus producing 1alpha,25-dihydroxyvitamin D3 (1alpha,25(OH)2D3). In this study we investigated whether keratinocytes can also hydroxylate vitamin D3 and one of its metabolites at the C-25 position. We could demonstrate that HaCaT keratinocytes can metabolize 1alpha-hydroxyvitamin D3 (1alpha-OHD3) and vitamin D3 to 1alpha,25(OH)2D3. Identification of the generated product as 1alpha,25(OH)2D3 was based on its elution pattern in two different high performance liquid chromatography systems, on its specific binding in a calf thymus receptor assay and on its gas chromatography-mass spectrometry characteristics. The hydroxylation of vitamin D3 to 1alpha,25(OH)2D3 was dose- and time-dependent. Bovine serum albumin added up to 1.5% (w/v) to the culture medium greatly increased the hydroxylation rates. These results show that HaCaT cells have the capacity to hydroxylate vitamin D3 at the C-1/25 positions. The generation of endogenous 1alpha,25(OH)2D3 from vitamin D3 within the skin may indicate a novel pathway which is of importance for the regulation of epidermal cell growth and differentiation.

Transformation and degradation of leukotriene B4, 12-hydroxyeicosatetraenoic acid and 5-hydroxyeicosatetraenoic acid induced by ultraviolet radiation.

To reveal the underlying mechanisms in the therapeutic effectiveness of ultraviolet (UBV)- and psoralen plus UVA phototherapy, the photostability of leukotriene B4 (LTB4), 12-hydroxyeicosatetraenoic acid (12-HETE) and 5-HETE was investigated in the presence and absence of photosensitizers (8-methoxypsoralen and 5-methoxypsoralen). Arachidonic lipoxygenase products were irradiated with doses of narrow-band UVB (311 nm) ranging from 0.5-3.2 J/cm2, UVB and UVA (305-400 nm) ranging from 0.6-6.3 J/cm2 and UVA ranging from 5.0-60.0 J/cm2, respectively. High-performance liquid chromatography demonstrated a dose-dependent decrease of LTB4, 12-HETE, and 5-HETE. The photostability of 12-HETE was much higher than that of LTB4 and 5-HETE. Two products of transformation of LTB4 were identified as 5(S), 12(R)-dihydroxy-(6E, 8E, 10E, 14Z)-eicosatetraenoic acid [6-trans-LTB4] and 5(S), 12(R)-dihydroxy-(6E, 8Z, 10E, 14Z)-eicosatetraenoic acid [5(S), 12(R)-DiHETE]. There was no significant increase in photodegradation after addition of photosensitizing psoralens.

[Influence of endotoxin on the synthesis of lipoxygenase products formed from arachidonic acid by rat alveolar macrophages]. / Zum Einfluss von Endotoxin auf die Synthese von Lipoxygenaseprodukten der Arachidonsäure in Alveolarmakrophagen der Ratte.

Alveolar macrophages of normal and endotoxin--treated rats were stimulated in suspension by calcium ionophore A 23187. After solid phase extraction and isocratic separation by HPLC the lipoxygenase products (Leukotriene B4, 5-hydroxyeicosatetraenoic acid and 12-hydroxyeicosatetraenioc acid) were quantified. Unlike alveolar macrophages of control animals, alveolar macrophages of endotoxin treated rats showed an increased synthesis of lipoxygenase products (Leukotriene B4: 1.6fold; 5-hydroxyeicosatetraenoic acid: 2.1fold; 12-hydroxyeicosatetraenoic acid: 1.3fold). Our results suggest that in vivo endotoxin disturbs the mechanisms of arachidonic acid liberation in alveolar macrophages.

Synthetic inhibitors of Escherichia coli, calf thymus, and Ehrlich ascites tumor thymidylate synthetase.

In a study of active site binding the inhibition of thymidylate synthetase derived from Escherichia coli, calf thymus, and Ehrlich ascites tumor was examined using eight inhibitors. 5-Substituted 2'-deoxyuridine 5'-phosphate analogues used in this study are the hydroxymethyl, methoxymethyl, benzyloxymethyl, formyl, acetyl, allyl, and two potential active site alkylating substituents: 2,3-oxypropyl and the azidomethyl analogues. All compounds were competitive with the substrate, 2'-deoxyuridine 5'-phosphate; the most potent inhibitor was 5-formyl-dUMP (Ki = 0.1, 0.09, and 0.08 muM for the respective enzyme). The 5-hydroxymethyl, 5-benzyloxymethyl, and 5-azidomethyl derivatives of dUMP showed some differential inhibition; these compounds were two to three times more active against the ascites tumor enzyme than against the thymus enzyme.

Synthesis of 5-substituted 2'-deoxyuridines.

A series of thymidylate synthetase inhibitors was synthesized, some of which were potential irreversible inhibitors. 5-Formyl-2'-deoxyuridine (9) and its dithiolane derivative 11 were prepared by condensation of the bis(trimethylsilyl) derivative of 5-formyluracil dimethyl acetal and the protected chloro sugar followed by saponification of the protective groups. 5-Acetyl-2'-deoxyuridine (15) was prepared in the same way from 5-acetyluracil. Treatment of the diester of 5-allyl-2'-deoxyuridine (17 or 22) with m-chloroperbenzoic acid gave the corresponding epoxide. Dimethylamine removed the ester groups and opened the epoxide to give the amino alcohol 24. The diester of 5-chloromethyl-2'-deoxyuridine (27) treated with methanol or sodium azide gave 5-methoxymethyl- (29) and 5-azidomethyl- (31) 2'-deoxyuridines. Compound 27 also was converted to 5-iodoacetamidomethyl-2'-deoxyuridine by treatment with ammonia, chloroacetyl chloride, base saponification, and finally sodium iodide.