Maximal multihomogeneity of algebraic hypersurface singularities

From the degree zero part of logarithmic vector fields along an algebraic hypersurface singularity we indentify the maximal multihomogeneity of a defining equation in form of a maximal algebraic torus in the embedded automorphism group. We show that all such maximal tori are conjugate and in one-to-one correspondence to maxmimal tori in the degree zero jet of the embedded automorphism group. The result is motivated by Kyoji Saito's characterization of quasihomogeneity for isolated hypersurface singularities and extends its formal version and a result of Hauser and Mueller.Comment: 5 page

Altered endocannabinoid signalling after a high-fat diet in Apoe −/− mice: relevance to adipose tissue inflammation, hepatic steatosis and insulin resistance

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Cohomology of bundles on homological Hopf manifold

We discuss the properties of complex manifolds having rational homology of $S^1 \times S^{2n-1}$ including those constructed by Hopf, Kodaira and Brieskorn-van de Ven. We extend certain previously known vanishing properties of cohomology of bundles on such manifolds.As an application we consider degeneration of Hodge-deRham spectral sequence in this non Kahler setting.Comment: To appear in Proceedings of 2007 conference on Several complex variables and Complex Geometry. Xiamen. Chin

Hyperholomorpic connections on coherent sheaves and stability

Let $M$ be a hyperkaehler manifold, and $F$ a torsion-free and reflexive coherent sheaf on $M$. Assume that $F$ (outside of its singularities) admits a connection with a curvature which is invariant under the standard SU(2)-action on 2-forms. If the curvature is square-integrable, then $F$ is stable and its singularities are hyperkaehler subvarieties in $M$. Such sheaves (called hyperholomorphic sheaves) are well understood. In the present paper, we study sheaves admitting a connection with SU(2)-invariant curvature which is not necessarily square-integrable. This situation arises often, for instance, when one deals with higher direct images of holomorphic bundles. We show that such sheaves are stable.Comment: 37 pages, version 11, reference updated, corrected many minor errors and typos found by the refere

Characterizing normal crossing hypersurfaces

The objective of this article is to give an effective algebraic characterization of normal crossing hypersurfaces in complex manifolds. It is shown that a hypersurface has normal crossings if and only if it is a free divisor, has a radical Jacobian ideal and a smooth normalization. Using K. Saito's theory of free divisors, also a characterization in terms of logarithmic differential forms and vector fields is found and and finally another one in terms of the logarithmic residue using recent results of M. Granger and M. Schulze.Comment: v2: typos fixed, final version to appear in Math. Ann.; 24 pages, 2 figure

The Acute Phase Protein Serum Amyloid A Induces Lipolysis and Inflammation in Human Adipocytes through Distinct Pathways

Background: The acute phase response (APR) is characterized by alterations in lipid and glucose metabolism leading to an increased delivery of energy substrates. In adipocytes, there is a coordinated decrease in Free Fatty acids (FFAs) and glucose storage, in addition to an increase in FFAs mobilization. Serum Amyloid A (SAA) is an acute phase protein mainly associated with High Density Lipoproteins (HDL). We hypothesized that enrichment of HDL with SAA, during the APR, could be implicated in the metabolic changes occurring in adipocytes. Methodology/Principal Findings: In vitro differentiated human adipocytes (hMADS) were treated with SAA enriched HDL or recombinant SAA and the metabolic phenotype of the cells analyzed. In hMADS, SAA induces an increased lipolysis through an ERK dependent pathway. At the molecular level, SAA represses PPARc2, C/EBPa and SREBP-1c gene expression, three transcription factors involved in adipocyte differentiation or lipid synthesis. In addition, the activation of the NF-kB pathway by SAA leads to the induction of pro-inflammatory cytokines and chemokines, as in the case of immune cells. These latter findings were replicated in freshly isolated mature human adipocytes. Conclusions/Significance: Besides its well-characterized role in cholesterol metabolism, SAA has direct metabolic effects on human adipocytes. These metabolic changes could be at least partly responsible for alterations of adipocyte metabolism observed during the APR as well as during pathophysiological conditions such as obesity and conditions leading to insuli

Establishment of a Transgenic Mouse Model Specifically Expressing Human Serum Amyloid A in Adipose Tissue

Obesity and obesity co-morbidities are associated with a low grade inflammation and elevated serum levels of acute phase proteins, including serum amyloid A (SAA). In the non-acute phase in humans, adipocytes are major producers of SAA but the function of adipocyte-derived SAA is unknown. To clarify the role of adipocyte-derived SAA, a transgenic mouse model expressing human SAA1 (hSAA) in adipocytes was established. hSAA expression was analysed using real-time PCR analysis. Male animals were challenged with a high fat (HF) diet. Plasma samples were subjected to fast protein liquid chromatography (FPLC) separation. hSAA, cholesterol and triglyceride content were measured in plasma and in FPLC fractions. Real-time PCR analysis confirmed an adipose tissue-specific hSAA gene expression. Moreover, the hSAA gene expression was not influenced by HF diet. However, hSAA plasma levels in HF fed animals (37.7±4.0 µg/mL, n = 7) were increased compared to those in normal chow fed animals (4.8±0.5 µg/mL, n = 10; p<0.001), and plasma levels in the two groups were in the same ranges as in obese and lean human subjects, respectively. In FPLC separated plasma samples, the concentration of hSAA peaked in high-density lipoprotein (HDL) containing fractions. In addition, cholesterol distribution over the different lipoprotein subfractions as assessed by FPLC analysis was similar within the two experimental groups. The established transgenic mouse model demonstrates that adipose tissue produced hSAA enters the circulation, resulting in elevated plasma levels of hSAA. This new model will enable further studies of metabolic effects of adipose tissue-derived SAA

Structure and chromosomal location of the bovine gene for the heart muscle isoform of cytochrome c oxidase subunit VIII

We have isolated the bovine COX8H gene for the heart/muscle isoform of cytochrome c oxidase (COX) subunit VIII from a library of bovine genomic DNA cloned into lambda EMBL3. Primer extension assays on bovine heart mRNA mapped the 5′ ends of COX8H transcripts to a CA dinucleotide 62-bp upstream from the ATG codon. The gene thus spans 1565-bp and comprises two exons and one large intron of 1227 bp. Exon 1 encodes the 5′ untranslated region, a 24-amino acid presequence, and the first 13 amino acids of the mature COX VIII-H protein. Exon 2 encodes the remainder of the cDNA: amino acids 14 to 46 plus the 66-bp 3′ untranslated region. The exon-intron boundaries matched the consensus splice junction sequences. Two protein polymorphisms were seen: an Ala/Val polymorphism at position-6 in the presequence and the previously noted Lys/Arg polymorphism at residue 7 of the mature protein. A Taq I polymorphism occurs in the intron. The COX8H gene was mapped by bovine x rodent somatic cell hybrid mapping panels to bovine (BTA) Chromosome (Chr) 25 with 100% concordancy. BTA25 is conserved relative to the long arm of human (HSA) Chr 11, which contains COX8, the gene for the single human COX VIII subunit that is homologous to the liver isoform.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47018/1/335_2004_Article_BF00303255.pd