Schutz und Instandsetzung von Waschbetonoberflächen

Waschbeton unterscheidet sich von üblichen Stahlbetonoberflächen nur durch die Oberflächenstruktur. Folglich treten auch hier die bekannten Abplatzschäden über korrodierenden Bewehrungsstählen bei unzureichender Betonüberdeckung oder Betonqualität infolge Karbonatisierung auf. Für Schutz und Instandsetzung von Schäden an Stahlbetonoberflächen gelten die Vorgaben und Anforderungen der ZTV-SIB des BMV bzw. der Rili-Sib des DAfStb derzeit als Stand der Technik. In beiden Regelwerken finden sich jedoch keine Vorgaben oder Hinweise für Schutz und Instandsetzung von Waschbetonoberflächen. Unter Berücksichtigung der Verfahren und Werkstoffe der Regelwerke wurden drei im Erscheinungsbild unterschiedliche Verfahrensweisen zur Instandsetzung von Waschbetonoberflächen in umfangreichen Untersuchungen im Labor und am Bauwerk untersucht. Ein weiterer Schwerpunkt lag auf der Messung und statistischen Auswertung der Schichtdicken der OS-Beschichtung zur Sicherstellung der erforderlichen systemspezifischen Mindestschichtdicke. Aufgrund der Ergebnisse der vorliegenden Arbeit kann davon ausgegangen werden, daß Schutz und Instandsetzung von Waschbetonoberflächen auch unter Erhalt bzw. Wiederherstellung der ursprünglichen Oberflächenstruktur mit den hier ermittelten Werkstoffen und Verfahrensweisen unter Anwendung der erforderlichen Sorgfalt entsprechend dem Stand der Technik möglich ist, wobei das Anlegen von Probeflächen am Bauwerk in jedem Falle unerläßlich ist.The well-known concrete surface damages can also be found on structured concrete surfaces for example washed out or stonemasonry treated ones. The existing technical standards give no instructions for protection and repair of such rough surfaces. In place of other rough surface structures, the suitability of proven repair systems is investigated on laboratory specimens and building test areas with different exposed aggregate concrete surfaces. Focus is to guarantee a durable protection, maintaining or restoring the original surface structure, particularly by producing hole-free coatings with defined thickness. It is the result of the investigations, that it's possible to ensure the so called system-specific minimum thickness of the coatings, if the roughness of the surface is reduced with PCC-mortar and the required mass of fluent coating materials is kept through applying additional layers. To proof visual demands and technical standards test areas should always be carried out, at best before starting restoration

Longitudinal associations among relationship factors, partner change, and sexually transmitted infection acquisition in adolescent women

OBJECTIVES: New sex partners put adolescents at increased risk for sexually transmitted infections (STIs), even when these sex partners are nonoverlapping. Although the risk of partner change is well described, little is known about its antecedents. We prospectively examined associations between relationship characteristics, partner change, and subsequent STI during intervals of "serial monogamy." METHODS: As part of a longitudinal study, 332 adolescent women were interviewed and tested for gonorrhea, chlamydia, and trichomonas every 3 months for up to just over 6 years. Interviews covered partner-specific relationship characteristics and sexual behaviors. The quarterly interval, a 3-month period bracketed by interviews and STI testing, was the unit of analysis. We examined associations among relationship factors, partner change, and subsequent STI using a series of mixed regression models, controlling for age, STI at Time 1, and condom nonuse. RESULTS: Age, lower relationship quality, and lower levels of partner closeness to friends and family predicted partner change from Time 1 to Time 2. In turn, partner change was associated with acquisition of a new STI at Time 2. Although relationship factors did not exert a direct effect on STI at Time 2, they improved partner change-STI model fit. Similar patterns were seen with each organism. CONCLUSION: Relationship factors drive partner change, which in turn contributes to STI acquisition. STI prevention research may need to focus on the relationship antecedents to partner change, in addition to the partner change itself

ICOS and B7 costimulatory molecule expression identifies activated cellular subsets in rheumatoid arthritis

To better define important cell subsets expressing activation markers in rheumatoid arthritis (RA), we compared selective lymphocyte and monocyte B7H1, B7H2, B7RP.1, B7RP.2, and inducible costimulatory molecule (ICOS) expression from normal peripheral blood (NL PB), RA PB, and RA synovial fluid (SF) by multicolor flow cytometry and immunohistochemistry. RA SF memory lymphocytes expressed B7RP.1 and B7RP.2, suggesting that T-cells may function as antigen presenting cells (APCs) in RA joints. We found similar results for ICOS expression. RA SF CD14+ monocytes also expressed B7RP.1 (an ICOS ligand) and the homologous ligand B7RP.2, identifying monocytes as potential mediators of antigen processing and lymphocyte activation in RA. Furthermore, we found an increased population of RA SF CD14+ monocytes expressing B7H1 and B7H2. [The FACS analysis was supported by immunohistochemistry, showing intense lymphocyte and APC (macrophages with dendritic morphology) ICOS staining in RA synovial tissue (ST). Overall, these results define elevated populations of memoryT-lymphocytes expressing proinflammatory B7 molecules in RA SF that either stimulate T cells through ICOS (via ICOS ligands B7RP.1 and B7RP.2), or down-regulate RA ST T-lymphocytes through B7H1 and B7H2.] Therefore, in the same joint, there may exist positive and negative influences on the inflammatory response, and perhaps, the negative signals dominate as joint inflammation resolves. © 2007 International Society for Analytical CytologyPeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/56032/1/20383_ftp.pd

Short-Term Rationing of Combination Antiretroviral Therapy: Impact on Morbidity, Mortality, and Loss to Follow-Up in a Large HIV Treatment Program in Western Kenya

Background. There was a 6-month shortage of antiretrovirals (cART) in Kenya. Methods. We assessed morbidity, mortality, and loss to follow-up (LTFU) in this retrospective analysis of adults who were enrolled during the six-month period with restricted cART (cap) or the six months prior (pre-cap) and eligible for cART at enrollment by the pre-cap standard. Cox models were used to adjust for potential confounders. Results. 9009 adults were eligible for analysis: 4,714 pre-cap and 4,295 during the cap. Median number of days from enrollment to cART initiation was 42 pre-cap and 56 for the cap (P < 0.001). After adjustment, individuals in the cap were at higher risk of mortality (HR = 1.21; 95% CI : 1.06–1.39) and LTFU (HR = 1.12; 95% CI : 1.04–1.22). There was no difference between the groups in their risk of developing a new AIDS-defining illness (HR = 0.92 95% CI 0.82–1.03). Conclusions. Rationing of cART, even for a relatively short period of six months, led to clinically adverse outcomes

A type III complement factor D deficiency: Structural insights for inhibition of the alternative pathway.

Abstract Background: Complement factor D (FD) is the rate-limiting enzyme of the alternative complement pathway. Previous reports of FD deficiency featured absent plasma FD (type I deficiency) and susceptibility to meningococcal infection. A new FD mutant, which is non-functional but fully expressed, was identified in a patient with invasive meningococcal disease. Objectives: We sought to investigate the molecular features of this novel FD mutant. Methods: We performed complement haemolytic assays, western blot analysis of serum FD and Sanger sequencing of the CFD gene. Recombinant mutant FD was assessed by in vitro catalytic assays, circular dichroism, thermal shift assays, esterolytic assays and surface plasmon resonance. Molecular dynamics simulation was used to visualise the structural changes in mutant FD. Results: A homozygous single-nucleotide variation of the CFD gene in the patient and their sibling resulted in an arginine to proline (R176P) substitution in FD. While R176P FD was stable and fully expressed in blood, it had minimal catalytic activity. Mutation R176P caused key FD-C3bB binding exosite loop 156-162 to lose its binding-competent conformation and stabilised the inactive conformation of FD. Consequently, R176P FD was unable to bind its natural substrate, C3bB. Neither patient nor sibling demonstrated the glucose homeostasis impairment that occurs in FD-null mice. Conclusions: Here, we report the first genetically confirmed functional, or type III, deficiency of an activating complement serine protease. This novel mechanism of FD inhibition can inform further development of alternative pathway inhibitors to treat common inflammatory diseases such as age-related macular degeneration

The therapeutic potential of the filarial nematode-derived immunodulator, ES-62 in inflammatory disease

The dramatic recent rise in the incidence of allergic or autoimmune inflammatory diseases in the West has been proposed to reflect the lack of appropriate priming of the immune response by infectious agents such as parasitic worms during childhood. Consistent with this, there is increasing evidence supporting an inverse relationship between worm infection and T helper type 1/17 (Th1/17)-based inflammatory disorders such as rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes and multiple sclerosis. Perhaps more surprisingly, given that such worms often induce strong Th2-type immune responses, there also appears to be an inverse correlation between parasite load and atopy. These findings therefore suggest that the co-evolution of helminths with hosts, which has resulted in the ability of worms to modulate inflammatory responses to promote parasite survival, has also produced the benefit of protecting the host from pathological lesions arising from aggressive proinflammatory responses to infection or, indeed, aberrant inflammatory responses underlying autoimmune and allergic disorders. By focusing upon the properties of the filarial nematode-derived immunomodulatory molecule, ES-62, in this review we shall discuss the potential of exploiting the immunomodulatory products of parasitic worms to identify and develop novel therapeutics for inflammation

Правове регулювання безоплатної приватизації земель запасу

Досліджуються правові підстави безоплатної приватизації земель запасу. Автор виокремлює два її різновиди – гарантовану і негарантовану. Розкриваються особли­вості багатоетапної процедури реалізації права на безоплатну приватизацію земель запасу в Україні.Исследуются правовые основания бесплатной приватизации земель запаса. Автор разделяет два ее разновидности – гарантированную и негарантированную. Раскрыва­ются особенности многоэтапной процедуры реализации права на бесплатную прива­тизацию земель в Украине.Legal rules about free of payment land privatization are investigated. The author pro­poses dividing free of payment land privatization into two varieties: guaranteed and non­guaranteed ones. Legal peculiarities of multistoried procedure of free of payment land priva­tization in Ukraine are disclosed

A novel inhibitor of the alternative pathway of complement reverses inflammation and bone destruction in experimental arthritis

Complement is an important component of the innate and adaptive immune response, yet complement split products generated through activation of each of the three complement pathways (classical, alternative, and lectin) can cause inflammation and tissue destruction. Previous studies have shown that complement activation through the alternative, but not classical, pathway is required to initiate antibody-induced arthritis in mice, but it is unclear if the alternative pathway (AP) plays a role in established disease. Previously, we have shown that human complement receptor of the immunoglobulin superfamily (CRIg) is a selective inhibitor of the AP of complement. Here, we present the crystal structure of murine CRIg and, using mutants, provide evidence that the structural requirements for inhibition of the AP are conserved in human and mouse. A soluble form of CRIg reversed inflammation and bone loss in two experimental models of arthritis by inhibiting the AP of complement in the joint. Our data indicate that the AP of complement is not only required for disease induction, but also disease progression. The extracellular domain of CRIg thus provides a novel tool to study the effects of inhibiting the AP of complement in established disease and constitutes a promising therapeutic with selectivity for a single complement pathway

CXCL16-mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway

Objective Rheumatoid arthritis (RA) is characterized by profound mononuclear cell (MNC) recruitment into synovial tissue (ST), thought to be due in part to tumor necrosis factor Α (TNFΑ), a therapeutic target for RA. Although chemokines may also be involved, the mechanisms remain unclear. We undertook this study to examine the participation of CXCL16, a novel chemokine, in recruitment of MNCs to RA ST in vivo and to determine the signal transduction pathways mediating this process. Methods Using a human RA ST–SCID mouse chimera, immunohistochemistry, enzyme-linked immunosorbent assay, real-time reverse transcription–polymerase chain reaction, flow cytometry, and in vitro chemotaxis assays, we defined the expression and function of CXCL16 and its receptor, CXCR6, as well as the signal transduction pathways utilized by them for MNC homing in vitro and in vivo. Results CXCL16 was markedly elevated in RA synovial fluid (SF) samples, being as high as 145 ng/ml. Intense macrophage and lining cell staining for CXCL16 in RA ST correlated with increased CXCL16 messenger RNA levels in RA ST compared with those in osteoarthritis and normal ST. By fluorescence-activated cell sorting analysis, one-half of RA SF monocytes and one-third of memory lymphocytes expressed CXCR6. In vivo recruitment of human MNCs to RA ST implanted in SCID mice occurred in response to intragraft injection of human CXCL16, a response similar to that induced by TNFΑ. Lipofection of MNCs with antisense oligodeoxynucleotides for ERK-1/2 resulted in a 50% decline in recruitment to engrafted RA ST and a 5-fold decline in recruitment to regional lymph nodes. Interestingly, RA ST fibroblasts did not produce CXCL16 in response to TNFΑ in vitro, suggesting that CXCL16 protein may function in large part independently of TNFΑ. Conclusion Taken together, these results point to a unique role for CXCL16 as a premier MNC recruiter in RA and suggest additional therapeutic possibilities, targeting CXCL16, its receptor, or its signaling pathways.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/49514/1/21662_ftp.pd

Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1

Multiple sclerosis and its preclinical model, experimental autoimmune encephalomyelitis, are marked by perivascular inflammation and demyelination. Myeloid cells, derived from circulating progenitors, are a prominent component of the inflammatory infiltrate and are believed to directly contribute to demyelination and axonal damage. How the cytotoxic activity of these myeloid cells is regulated is poorly understood. We identify CMRF-35–like molecule-1 (CLM-1) as a negative regulator of autoimmune demyelination. CLM-1 is expressed on inflammatory myeloid cells present in demyelinating areas of the spinal cord after immunization of mice with MOG35-55 (myelin oligodendrocyte glycoprotein) peptide. Absence of CLM-1 resulted in significantly increased nitric oxide and proinflammatory cytokine production, along with increased demyelination and worsened clinical scores, whereas T cell responses in the periphery or in the spinal cord remained unaffected. This study thus identifies CLM-1 as a negative regulator of myeloid effector cells in autoimmune demyelination