The solar differential rotation in the 18th century

The sunspot drawings of Johann Staudacher of 1749--1799 were used to determine the solar differential rotation in that period. These drawings of the full disk lack any indication of their orientation. We used a Bayesian estimator to obtain the position angles of the drawings, the corresponding heliographic spot positions, a time offset between the drawings and the differential rotation parameter \delta\Omega, assuming the equatorial rotation period is the same as today. The drawings are grouped in pairs, and the resulting marginal distributions for \delta\Omega were multiplied. We obtain \delta\Omega=-0.048 \pm 0.025 d^-1 (-2.75^o/d) for the entire period. There is no significant difference to the value of the present Sun. We find an (insignificant) indication for a change of \delta\Omega throughout the observing period from strong differential rotation, \delta\Omega\approx -0.07 d^-1, to weaker differential rotation, \delta\Omega\approx-0.04 d^-1.Comment: 6 pages, 6 figures, accepted for Astronomy and Astrophysic

Benzo[a]pyrene-induced DNA adducts and gene expression profiles in target and non-target organs for carcinogenesis in mice

Background: Gene expression changes induced by carcinogens may identify differences in molecular function between target and non-target organs. Target organs for benzo[a]pyrene (BaP) carcinogenicity in mice (lung, spleen and forestomach) and three non-target organs (liver, colon and glandular stomach) were investigated for DNA adducts by 32P-postlabelling, for gene expression changes by cDNA microarray and for miRNA expression changes by miRNA microarray after exposure of animals to BaP. Results: BaP-DNA adduct formation occurred in all six organs at levels that did not distinguish between target and non-target. cDNA microarray analysis showed a variety of genes modulated significantly by BaP in the six organs and the overall gene expression patterns were tissue specific. Gene ontology analysis also revealed that BaP-induced bioactivities were tissue specific; eight genes (Tubb5, Fos, Cdh1, Cyp1a1, Apc, Myc, Ctnnb1 and Cav) showed significant expression difference between three target and three non-target organs. Additionally, several gene expression changes, such as in Trp53 activation and Stat3 activity suggested some similarities in molecular mechanisms in two target organs (lung and spleen), which were not found in the other four organs. Changes in miRNA expression were generally tissue specific, involving, in total, 21/54 miRNAs significantly up- or down-regulated. Conclusions: Altogether, these findings showed that DNA adduct levels and early gene expression changes did not fully distinguish target from non-target organs. However, mechanisms related to early changes in p53, Stat3 and Wnt/β-catenin pathways may play roles in defining BaP organotropism

Genotoxicity: damage to DNA and its consequences

A genotoxin is a chemical or agent that can cause DNA or chromosomal damage. Such damage in a germ cell has the potential to cause a heritable altered trait (germline mutation). DNA damage in a somatic cell may result in a somatic mutation, which may lead to malignant transformation (cancer). Many in vitro and in vivo tests for genotoxicity have been developed that, with a range of endpoints, detect DNA damage or its biological consequences in prokaryotic (e.g. bacterial) or eukaryotic (e.g. mammalian, avian or yeast) cells. These assays are used to evaluate the safety of environmental chemicals and consumer products and to explore the mechanism of action of known or suspected carcinogens. Many chemical carcinogens/ mutagens undergo metabolic activation to reactive species that bind covalently to DNA, and the DNA adducts thus formed can be detected in cells and in human tissues by a variety of sensitive techniques. The detection and characterisation of DNA adducts in human tissues provides clues to the aetiology of human cancer. Characterisation of gene mutations in human tumours, in common with the known mutagenic profiles of genotoxins in experimental systems, may provide further insight into the role of environmental mutagens in human cancer

Bose-Einstein condensation in a stiff TOP trap with adjustable geometry

We report on the realisation of a stiff magnetic trap with independently adjustable trap frequencies, $\omega_z$ and $\omega_r$, in the axial and radial directions respectively. This has been achieved by applying an axial modulation to a Time-averaged Orbiting Potential (TOP) trap. The frequency ratio of the trap, $\omega_z / \omega_r$, can be decreased continuously from the original TOP trap value of 2.83 down to 1.6. We have transferred a Bose-Einstein condensate (BEC) into this trap and obtained very good agreement between its observed anisotropic expansion and the hydrodynamic predictions. Our method can be extended to obtain a spherical trapping potential, which has a geometry of particular theoretical interest.Comment: 4 pages, 3 figure

Chemical and molecular basis of the carcinogenicity of Aristolochia plants

The herbal drug aristolochic acid (AA), which is derived from the Aristolochia species, has been associated with the development of a novel nephropathy, designated as aristolochic acid nephropathy (AAN), and with human urothelial cancer. The major components of the plant extract AA are nitrophenanthrene carboxylic acids, which, after metabolic activation, are genotoxic mutagens. The major activation pathway of AA involves reduction of the nitro group, primarily catalyzed by NAD(P) H: quinone oxidoreductase (NQO1), to an electrophilic cyclic N-acylnitrenium ion that reacts preferentially with purine bases to form covalent DNA adducts. These specific AA-DNA adducts have been identified and detected in experimental animals exposed to AA or botanical products containing AA, and in urothelial tissues from AAN patients. In rodent tumors induced by AA the predominantly formed DNA adduct 7-(deoxyadenosin-N-6-yl) aristolactam I has been associated with the activation of ras oncogenes through the characteristic transversion mutation AT -> TA. This mutation has been identified in the p53 gene of urothelial tumors of a patient with AAN (induced by use of a herbal product) and in several patients suffering from Balkan endemic nephropathy (BEN) with specific AA-DNA adducts. This is a rare example of a human cancer causally linked to a distinct environmental exposure (ie, use of a herbal product), where the carcinogenic process of initiation is well established, linking formation of carcinogen-specific exposure (specific DNA adduct formation) with the presence of characteristic human tumor mutations

Width of Sunspot Generating Zone and Reconstruction of Butterfly Diagram

Based on the extended Greenwich-NOAA/USAF catalogue of sunspot groups it is demonstrated that the parameters describing the latitudinal width of the sunspot generating zone (SGZ) are closely related to the current level of solar activity, and the growth of the activity leads to the expansion of SGZ. The ratio of the sunspot number to the width of SGZ shows saturation at a certain level of the sunspot number, and above this level the increase of the activity takes place mostly due to the expansion of SGZ. It is shown that the mean latitudes of sunspots can be reconstructed from the amplitudes of solar activity. Using the obtained relations and the group sunspot numbers by Hoyt and Schatten (1998), the latitude distribution of sunspot groups ("the Maunder butterfly diagram") for the 18th and the first half of the 19th centuries is reconstructed and compared with historical sunspot observations.Comment: 16 pages, 11 figures; accepted by Solar Physics; the final publication will be available at www.springerlink.co

Metabolic activation of carcinogenic aristolochic acid, a risk factor for Balkan endemic nephropathy

Aristolochic acid (AA), a naturally occurring nephrotoxin and carcinogen, is associated with tumor development in patients suffering from Chinese herbs nephropathy (now termed aristolochic acid nephropathy, AAN) and may also be a cause for the development of a similar type of nephropathy, the Balkan endemic nephropathy (BEN). Major DNA adducts [7-(deoxyadenosin-N-6-yl)-aristolactam and 7-(deoxyguanosin-N-2-yl)aristolactam] formed from AA after reductive metabolic activation were found in renal tissues of patients with both diseases. Understanding which human enzymes are involved in AA activation and/or detoxication is important in the assessment of an individual's susceptibility to this plant carcinogen. This paper reviews major hepatic and renal enzymes responsible for AA-DNA adduct formation in humans. Phase I biotransformation enzymes play a crucial role in the metabolic activation of AA to species forming DNA adducts, while a role of phase II enzymes in this process is questionable. Most of the activation of AA in human hepatic microsomes is mediated by cytochrome P450 (CYP) 1A2 and, to a lower extent, by CYP1A1; NADPH:CYP reductase plays a minor role. In human renal microsomes NADPH:CYP reductase is more effective in AA activation. Prostaglandin H synthase (cyclooxygenase, COX) is another enzyme activating AA in human renal microsomes. Among the cytosolic reductases, NAD(P)H:quinone oxidoreductase (NQO I) is the most efficient in the activation of AA in human liver and kidney. Studies with purified enzymes confirmed the importance of CYPs, NADPH:CYP reductase, COX and NQO1 in the AA activation. The orientation of AA in the active sites of human CYP1A1, -1A2 and NQO1 was predicted from molecular modeling and explains the strong reductive potential of these enzymes for AA detected experimentally. We hypothesized that inter-individual variations in expressions and activities of enzymes activating AA may be one of the causes responsible for the different susceptibilities to this carcinogen reflected in the development of AA-induced nephropathies and associated urothelial cancer. (c) 2007 Elsevier B.V. All rights reserved

Energetics of the primary electron transfer reaction revealed by ultrafast spectroscopy on modified bacterial reaction centers

The modification of reaction centers from Rhodobacter sphaeroides by the introduction of pheophytins instead of bacteriopheophytins leads to interesting changes in the primary photosynthetic reaction: long-living populations of the excited electronic state of the special pair P* and the bacteriochlorophyll anion B−A show up. The data allow the determination of the energetics in the reaction center. The free energy of the first intermediate P+B−A, where the electron has reached the accessory bacteriochlorophyll BA lies ≈ 450 cm−1 below the initially excited special pair P*

Dynamics of F=2 Spinor Bose-Einstein Condensates

We experimentally investigate and analyze the rich dynamics in F=2 spinor Bose-Einstein condensates of Rb87. An interplay between mean-field driven spin dynamics and hyperfine-changing losses in addition to interactions with the thermal component is observed. In particular we measure conversion rates in the range of 10^-12 cm^3/s for spin changing collisions within the F=2 manifold and spin-dependent loss rates in the range of 10^-13 cm^3/s for hyperfine-changing collisions. From our data we observe a polar behavior in the F=2 ground state of Rb87, while we measure the F=1 ground state to be ferromagnetic. Furthermore we see a magnetization for condensates prepared with non-zero total spin.Comment: 4 pages, 2 figures, RevTe