Improvement On Brooks Chromatic Bound For A Class Of Graphs

Brooks' Theorem says that if for a graph G,Δ(G)=n, then G is n-colourable, unless (1) n=2 and G has an odd cycle as a component, or (2) n>2 and Kn+1 is a component of G. In this paper we prove that if a graph G has none of some three graphs (K1,3;K5−e and H) as an induced subgraph and if Δ(G)greater-or-equal, slanted6 and d(G)<Δ(G), then χ(G)<Δ(G). Also we give examples to show that the hypothesis Δ(G)greater-or-equal, slanted6 can not be non-trivially relaxed and the graph K5−e can not be removed from the hypothesis. Moreover, for a graph G with none of K1,3;K5−e and H as an induced subgraph, we verify Borodin and Kostochka's conjecture that if for a graph G,Δ(G)greater-or-equal, slanted9 and d(G)<Δ(G), then χ(G)<Δ(G).

Social-class inequalities in ill health - the contribution of physical workload

Tutkimuksen aiheita olivat yhteiskuntaluokkien väliset erot sairastavuudessa ja alentuneessa toimintakyvyssä, sekä fyysisen työkuormituksen ja joidenkin muiden työolojen vaikutus sairastavuuteen. Empiirisestä työstä on raportoitu myös neljässä kansainvälisissä tieteellisissä aikakauskirjoissa julkaistussa artikkelissa. Tässä julkaistu yhteenveto sisältää tulosten yhteenvedon lisäksi myös tutkimusta koskevien käsitteellisten ja teoreettisten kysymysten sekä tutkimustradition kriittisen katsauksen. Työn päätavoitteita olivat 1) tutkia fyysisesti kuormittavan työn, ja jossain määrin muiden työolojen osuutta yhteiskuntaluokkien välisiin eroihin sairaudessa ja toimintakyvyn alentuneisuudessa; 2) tutkia työn fyysisen kuormittavuuden, työhön liittyvien vaikutusmahdollisuuksien ja hallinnan (decision latitude), luokka-aseman, iän ja sukupuolen yhteisvaikutuksia heikentyneeseen terveydentilaan; sekä 3) tutkia missä määrin mekaanisten työaltisteiden ja tuki- ja liikuntaelinsairastavuuden välinen yhteys voi selittää yhteiskuntaluokkien välisiä eroja heikentyneessä yleisessä terveydentilassa. Tutkittavat olivat keski-ikäisiä Helsingin kaupungin työntekijöitä. Analyysit perustuivat poikittaisasetelmaan, ja käytetty aineisto oli Helsinki Health Studyn vuosien 2000 ja 2002 välillä kerättyä aineistoa. Analyyseihin käytetyssä aineistossa oli 3740:stä 8002:een tutkittavaa. Tulosten perusteella fyysisillä (sekä fysikaalisilla) työoloilla on merkittävä vaikutus yhteiskuntaluokkien välisiin eroihin yleisessä sairastavuudessa, toimintakyvyn heikentymisessä, tuki- ja liikuntaelinsairastavuudessa sekä itsearvioidussa terveydentilassa. Naisilla lähes puolet heikentyneen toimintakyvyn ja koetun terveydentilan luokkaeroista vaikutti olevan selitettävissä fyysisellä työkuormituksella. Hallintamahdollisuuksien ei havaittu merkittävästi muuttavan fyysisen kuormituksen vaikutusta toimintakykyyn. Fyysisen kuormittavuuden terveysvaikutus voimistui kasvavan iän mukaan enemmän naisilla kuin miehillä. Osa, mutta ei koko fyysisen kuormituksen vaikutus yhteiskuntaluokkien eroihin heikentyneessä terveydessä vaikutti välittyvän tuki- ja liikuntaelinsairastavuuden kautta. Terveys ja sairaus eivät ole yhtenäisiä tiloja, ja siksi monet eri sosiaalisesti ja rakenteellisesti määräytyvät olosuhteet todennäköisesti vaikuttavat yhteiskunnallisten terveyserojen syntymiseen. Fyysis-materiaalisten olojen vaikutusta terveyserojen syntyyn nyky-yhteiskunnassa on mahdollisesti aliarvioitu. Yhteiskuntaluokkien väliset erot fyysis-materiaalisissa olosuhteissa eivät ole kadonneet, ja nämä erot todennäköisesti vaikuttavat terveyserojen syntyyn.

Ilse Baum's class portrait Portraits Family

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Palladin, a novel microfilament protein

Palladin is a novel actin microfilament associated protein, which together with myotilin and myopalladin forms a novel cytoskeletal IgC2 domain protein family. Whereas the expression of myotilin and myopalladin is limited mainly to striated muscle, palladin is widely expressed in both epithelial and mesenchymal tissues, including heart and the nervous system. Palladin has a complex genetic structure and it is expressed as several different sized and structured splice variants, which also display differences in their expression pattern and interactions. In muscle cells, all the family members localize to the sarcomeric Z-disc, and in non-muscle cells palladin also localizes to the stress-fiber-dense regions, lamellipodia, podosomes and focal adhesions. A common feature of this protein family is the binding to α-actinin, but other interactions are mostly unique to each member. Palladin has been shown to interact with several proteins, including VASP, profilin, Eps8, LASP-1 and LPP. Its domain structure, lack of enzymatic activity and multiple interactions define it as a molecular scaffolding protein, which links together proteins with different functional modalities into large complexes. Palladin has an important role in cytoskeletal regulation, particularly in stress fiber formation and stabilization. This assumption is supported by several experimental results. First, over-expression of palladin in non-muscle cells results in rapid reorganization of the actin cytoskeleton and formation of thick actin bundles. Second, the knock-down of palladin with anti-sense and siRNA techniques or knock-out by genetic methods leads to defective stress fiber formation. Furthermore, palladin is usually up-regulated in situations requiring a highly organized cytoskeleton, such as differentiation of dendritic cells, trophoblasts and myofibroblasts, and activation of astrocytes during glial scar formation. The protein family members have also direct disease linkages; myotilin missense mutations are the cause of LGMD1A and myofibrillar myopathy. Palladin mutations and polymorphisms, on the other hand, have been linked to hereditary pancreatic cancer and myocardial infarction, respectively. In this study we set out to characterize human palladin. We identified several palladin isoforms, studied their tissue distribution and sub-cellular localization. Four novel interaction partners were identified; ezrin, ArgBP2, SPIN90 and Src-kinase.The previously identified interaction between palladin and α-actinin was also characterized in detail. All the identified new binding partners are actin cytoskeleton associated proteins; ezrin links the plasma membrane to the cytoskeleton, ArgBP2 and SPIN90 localize, among other structures, to the lamellipodia and in cardiomyocytes to the Z-disc. Src is a transforming tyrosine kinase, which besides its role in oncogenesis has also important cytoskeletal associations. We also studied palladin in myofibroblasts, which are specialized cells involved in diverse physiological and pathological processes, such as wound healing and tissue fibrosis. We demonstrated that palladin is up-regulated during the differentiation of myofibroblasts in an isoform specific manner, and that this up-regulation is induced by TGF-β via activation of both the SMAD and MAPK signalling cascades. In summary, the results presented here describe the initial characterization of human palladin and offer a basis for further studies.

Reproduction of grammar school class portrait including Ella, Beatrice and Rose Herz (circled l-r).

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Reproduction of grammar school class portrait including Fred Herz (front center).

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Class portrait to remember the trip to Kablau(?).

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p53 and little brother p53/47: linking IRES activities with protein functions

The tumor suppressor p53 represents a paradigm for gene regulation. Its rapid induction in response to DNA damage conditions has been attributed to both increased half-life of p53 protein and also increased translation of p53 mRNA. Recent advances in our understanding of the post-transcriptional regulation of p53 include the discovery of internal ribosome entry sites (IRESs) within the p53 mRNA. These IRES elements regulate the translation of the full length as well as the N-terminally truncated isoform, p53/47. The p53/47 isoform is generated by alternative initiation at an internal AUG codon present within the p53 ORF. The aim of this review is to summarize the role of translational control mechanisms in regulating p53 functions. We discuss here in detail how diverse cellular stress pathways trigger alterations in the cap-dependent and cap-independent translation of p53 mRNA and how changes in the relative expression levels of p53 isoforms result in more differentiated p53 activity.

Unterprima (eleventh grade) boys school class portrait Portraits Groups Men

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Probing into the role of conserved N-glycosylation sites in the Tyrosinase glycoprotein family

N-linked glycosylation has a profound effect on the proper folding, oligomerization and stability of glycoproteins. These glycans impart many properties to proteins that may be important for their proper functioning, besides having a tendency to exert a chaperone-like effect on them. Certain glycosylation sites in a protein however, are more important than other sites for their function and stability. It has been observed that some N-glycosylation sites are conserved over families of glycoproteins over evolution, one such being the tyrosinase related protein family. The role of these conserved N-glycosylation sites in their trafficking, sorting, stability and activity has been examined here. By scrutinizing the different glycosylation sites on this family of glycoproteins it was inferred that different sites in the same family of polypeptides can perform distinct functions and conserved sites across the paralogues may perform diverse functions.

Class picture of Gisela Kleinermann Portraits Group

The photograph shows Gisela Kleinermann (standing at the right end of the line) with her class at the ‘Juedische Schule’ in Dresden, late summer of 1938, as she and her mother were preparing for her immigration to the USA. Most other children were deported in October 1938 and perished in the Holocaust. The teacher, Jacob Blum (center back) emigrated to Palestine.

Rab8 and Rab8-interacting proteins as players in cell polarization

Rab8 and its interacting proteins as regulators of cell polarization During the development of a multi-cellular organism, progenitor cells have to divide and migrate appropriately as well as organize their differentiation with one another, in order to produce a viable embryo. To divide, differentiate and migrate cells have to undergo polarization, a process where internal and external components such as actin, microtubules and adhesion receptors are reorganized to produce a cell that is asymmetric, with functionally different surfaces. Also in the adult organism there is a continuous need for these processes, as cells need to migrate in response to tissue damage and to fight infection. Improper regulation of cell proliferation and migration can conversely lead to disease such as cancer. GTP-binding proteins function as molecular switches by cycling between a GTP-bound (active) conformation and a GDP-bound (inactive) conformation. The Ras super-family of small GTPases are found in all eukaryotic cells. They can be functionally divided into five subfamilies. The Ras family members mainly regulate gene expression, controlling cell proliferation and differentiation. Ras was in fact the first human oncogene to be characterized, and as much as 30% of all human tumors may be directly or indirectly caused by mutations of Ras molecules The Rho family members mainly regulate cytoskeletal reorganization. Arf proteins are known to regulate vesicle budding and Rab proteins regulate vesicular transport. Ran regulates nuclear transport as well as microtubule organization during mitosis. The focus of the thesis of Katarina Hattula, is on Rab8, a small GTPase of the Rab family. Activated Rab8 has previously been shown to induce the formation of new surface extensions, reorganizing both actin and microtubules, and to have a role in directed membrane transport to cell surfaces. However, the exact membrane route it regulates has remained elusive. In the thesis three novel interactors of Rab8 are presented. Rabin8 is a Rab8-specific GEF that localizes to vesicles where it presumably recruits and activates its target Rab8. Its expression in cells leads to remodelling of actin and the formation of polarized cell surface domains. Optineurin, known to be associated with a leading cause of blindness in humans (open-angle glaucoma), is shown to interact specifically with GTP-bound Rab8. Rab8 binds to an amino-terminal region and interestingly, the Huntingtin protein binds a carboxy-terminal region of optineurin. (Aberrant Huntingtin protein is known to be the cause Huntington s disease in humans.) Co-expression of Huntingtin and optineurin enhanced the recruitment of Huntingtin to Rab8-positive vesicular structures. Furthermore, optineurin promoted cell polarization in a similar way to Rab8. A third novel interactor of Rab8 presented in this thesis is JFC1, a member of the synaptogamin-like protein (Slp) family. JFC1 interacts with Rab8 specifically in its GTP-bound form, co-localizes with endogenous Rab8 on tubular and vesicular structures, and is probably involved in controlling Rab8 membrane dynamics. Rab8 is in this thesis work clearly shown to have a strong effect on cell shape. Blocking Rab8 activity by expression of Rab8 RNAi, or by expressing the dominant negative Rab8 (T22N) mutant leads to loss of cell polarity. Conversely, cells expressing the constitutively active Rab8 (Q67L) mutant exhibit a strongly polarized phenotype. Experiments in live cells show that Rab8 is associated with macropinosomes generated at ruffling areas of the membrane. These macropinosomes fuse with or transform into tubules that move toward the cell centre, from where they are recycled back to the leading edge to participate in protrusion formation. The biogenesis of these tubules is shown to be dependent on both actin and microtubule dynamics. The Rab8-specific membrane route studied contained several markers known to be internalized and recycled (1 integrin, transferrin, transferrin receptor, cholera toxin B subunit (CTxB), and major histocompatibility complex class I protein (MHCI)). Co-expression studies revealed that Rab8 localization overlaps with that of Rab11 and Arf6. Rab8 is furthermore clearly functionally linked to Arf6. The data presented in this thesis strongly suggests a role for Rab8 as a regulator for a recycling compartment, which is involved in providing structural and regulatory components to the leading edge to participate in protrusion formation.