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

Time-resolved spectroscopy of the primary photosynthetic processes of membrane-bound reaction centers from an antenna-deficient mutant of Rhodobacter capsulatus

The primary photosynthetic reactions in whole membranes of the antenna-deficient mutant strain U43 (pTXA6–10) of Rhodobacter capsulatus are studied by transient absorption and emission spectroscopy with subpicosecond time resolution. Extensive similarities between the transient absorption data on whole membranes and on isolated reaction centers support the idea that the primary processes in isolated reaction centers are not modified by the isolation procedure

IEX-1 directly interferes with RelA/p65 dependent transactivation and regulation of apoptosis

The early response gene IEX-1 plays a complex role in the regulation of apoptosis. Depending on the cellular context and the apoptotic stimulus, IEX-1 is capable to either enhance or suppress apoptosis. To further dissect the molecular mechanisms involved in the modulation of apoptosis by IEX-1, we analysed the molecular crosstalk between IEX-1 and the NF-kappa B pathway. Using GST-pulldown assays, a direct interaction of IEX-1 with the C-terminal region of the subunit RelA/p65 harbouring the transactivation domain of the NF-kappa B transcription factor was shown. This interaction negatively regulates RelA/p65 dependent transactivation as shown by GAL4-and luciferase assay and was confirmed for the endogenous proteins by co-immunoprecipitation experiments. Using deletion constructs, we were able to map the C-terminal region of IEX-1 as the critical determinant of the interaction with RelA/p65. We could further show, that IEX-1 mediated NF-kappa B inhibition accounts for the reduced expression of the anti-apoptotic NF-kappa B target genes Bc1-2, Bcl-xL, cIAP1 and cIAP2, thereby sensitizing cells for apoptotic stimuli. Finally, ChIP-assays revealed that IEX-1 associates with the promoter of these genes. Altogether, our findings suggest a critical role of IEX-1 in the NF-kappa B dependent regulation of apoptotic responses. (C) 2007 Elsevier B.V All rights reserved

Guidelines for the management of glucocorticoids during the peri-operative period for patients with adrenal insufficiency: Guidelines from the Association of Anaesthetists, the Royal College of Physicians and the Society for Endocrinology UK

These guidelines aim to ensure that patients with adrenal insufficiency are identified and adequately supplemented with glucocorticoids during the peri-operative period. There are two major categories of adrenal insufficiency. Primary adrenal insufficiency is due to diseases of the adrenal gland (failure of the hormone-producing gland), and secondary adrenal insufficiency is due to deficient adrenocorticotropin hormone secretion by the pituitary gland, or deficient corticotropin-releasing hormone secretion by the hypothalamus (failure of the regulatory centres). Patients taking physiological replacement doses of corticosteroids for either primary or secondary adrenal insufficiency are at significant risk of adrenal crisis and must be given stress doses of hydrocortisone during the peri-operative period. Many more patients other than those with adrenal and hypothalamic-pituitary causes of adrenal failure are receiving glucocorticoids as treatment for other medical conditions. Daily doses of prednisolone of 5 mg or greater in adults and 10-15 mg.m-2 hydrocortisone equivalent or greater in children may result in hypothalamo-pituitary-adrenal axis suppression if administered for 1 month or more by oral, inhaled, intranasal, intra-articular or topical routes; this chronic administration of glucocorticoids is the most common cause of secondary adrenal suppression, sometimes referred to as tertiary adrenal insufficiency. A pragmatic approach to adrenal replacement during major stress is required; considering the evidence available, blanket recommendations would not be appropriate, and it is essential for the clinician to remember that adrenal replacement dosing following surgical stress or illness is in addition to usual steroid treatment. Patients with previously undiagnosed adrenal insufficiency sometimes present for the first time following the stress of surgery. Anaesthetists must be familiar with the symptoms and signs of acute adrenal insufficiency so that inadequate supplementation or undiagnosed adrenal insufficiency can be detected and treated promptly. Delays may prove fatal

Behandlung des metastasierten Nebennierenkarzinoms mit Suramin

Bei einem 45jährigen Patienten wurde im April 1986 ein rechtsseitiges Nebennierenrindenkarzinom (978 g) entfernt und das Tumorbett postoperativ mit 40 Gy bestrahlt. Wegen multipler Lungenmetastasen wurde im Januar und im Juni 1987 eine Polychemotherapie mit Cisplatin, Etoposid und Bleomycin durchgeführt, ohne daß eine Befundbesserung erreicht wurde. Auch eine Therapie mit Mitotan (Lysodren®) blieb wirkungslos und mußte wegen schwerer Nebenwirkungen beendet werden. Im August 1987 wurde eine Therapie mit Suramin (Germanin®) begonnen. Nach einer Aufsättigungsdosis von 10,7 g über 6 Wochen kam es zu einer nahezu vollständigen Rückbildung der Lungenmetastasen. Während einer niedrig dosierten Erhaltungstherapie mit Suramin wurden im Januar 1988 erneut Lungenmetastasen nachweisbar. Eine Dosissteigerung führte zu Wachstumsstillstand, nicht jedoch zur Rückbildung der Metastasen. Der Patient starb im April 1988 überraschend an akutem Kreislaufversagen. Die Suramin-Therapie war 6 Wochen zuvor bei Bronchopneumonie und verschlechtertem Allgemeinzustand beendet worden. Nebenwirkungen der Suramin-Therapie waren Thrombozytopenie, Gerinnungsstörungen und eine mäßiggradige Proteinurie

Ureasil organic-inorganic hybrids as photoactive waveguides for conjugated polyelectrolyte luminescent solar concentrators

We test the potential of resonance energy transfer to enhance the performance of conjugated copolyelectrolyte donor–acceptor luminescent solar concentrators immobilised within a photoactive organic–inorganic ureasil waveguide.</p

Highly anisotropic Bose-Einstein condensates: crossover to lower dimensionality

We develop a simple analytical model based on a variational method to explain the properties of trapped cylindrically symmetric Bose-Einstein condensates (BEC) of varying degrees of anisotropy well into regimes of effective one dimension (1D) and effective two dimension (2D). Our results are accurate in regimes where the Thomas-Fermi approximation breaks down and they are shown to be in agreement with recent experimental data.Comment: 4 pages, 2 figures; significantly more new material added; title and author-list changed due to changes in conten

Gene Expression Profiles Distinguish the Carcinogenic Effects of Aristolochic Acid in Target (Kidney) and Non-target (Liver) Tissues in Rats

BACKGROUND: Aristolochic acid (AA) is the active component of herbal drugs derived from Aristolochia species that have been used for medicinal purposes since antiquity. AA, however, induced nephropathy and urothelial cancer in people and malignant tumors in the kidney and urinary tract of rodents. Although AA is bioactivated in both kidney and liver, it only induces tumors in kidney. To evaluate whether microarray analysis can be used for distinguishing the tissue-specific carcinogenicity of AA, we examined gene expression profiles in kidney and liver of rats treated with carcinogenic doses of AA. RESULTS: Microarray analysis was performed using the Rat Genome Survey Microarray and data analysis was carried out within ArrayTrack software. Principal components analysis and hierarchical cluster analysis of the expression profiles showed that samples were grouped together according to the tissues and treatments. The gene expression profiles were significantly altered by AA treatment in both kidney and liver (p < 0.01; fold change > 1.5). Functional analysis with Ingenuity Pathways Analysis showed that there were many more significantly altered genes involved in cancer-related pathways in kidney than in liver. Also, analysis with Gene Ontology for Functional Analysis (GOFFA) software indicated that the biological processes related to defense response, apoptosis and immune response were significantly altered by AA exposure in kidney, but not in liver. CONCLUSION: Our results suggest that microarray analysis is a useful tool for detecting AA exposure; that analysis of the gene expression profiles can define the differential responses to toxicity and carcinogenicity of AA from kidney and liver; and that significant alteration of genes associated with defense response, apoptosis and immune response in kidney, but not in liver, may be responsible for the tissue-specific toxicity and carcinogenicity of AA

A SULT2A1 genetic variant identified by GWAS as associated with low serum DHEAS does not impact on the actual DHEA/DHEAS ratio

DHEA is the major precursor of human sex steroid synthesis and is inactivated via sulfonation to DHEAS. A previous genome-wide association study related the single nucleotide polymorphism (SNP) rs2637125, located near the coding region of DHEA sulfotransferase, SULT2A1, to serum DHEAS concentrations. However, the functional relevance of this SNP with regard to DHEA sulfonation is unknown. Using data from 3300 participants of the population-based cohort Study of Health in Pomerania, we identified 43 individuals being homozygote for the minor allele of the SNP rs2637125 (AA) and selected two sex- and age-matched individuals with AG and GG genotype (n=172) respectively. Steroid analysis including measurement of serum DHEA and DHEAS was carried out by liquid chromatography/mass spectrometry, employing steroid oxime analysis for enhancing the sensitivity of DHEA detection. We applied quantile regression models to compare median hormone levels across SULT2A1 genotypes. Median comparisons by SULT2A1 genotype (AA vs AG and GG genotypes respectively) showed no differences in the considered hormones including DHEAS, DHEA, androstenedione, as well as cortisol and cortisone concentrations. SULT2A1 genotype also had no effect on the DHEA/DHEAS ratio. Sex-stratified analyses, as well as alternative use of the SULT2A1 SNP rs182420, yielded similar negative results. Genetic variants of SULT2A1 do not appear to have an effect on individual DHEA and DHEAS concentrations or the DHEA/DHEAS ratio as a marker of DHEA sulfonation capacity