The Use of a Disclosing Agent During Resective Periodontal Surgery for Improved Removal of Biofilm

A total removal of the bacterial deposits is one of the main challenges of periodontal therapy. A surgical approach is sometimes required in order to allow a correct access to the areas not thoroughly reached during the initial therapy. The present study focuses on the surgical scaling effectiveness in root deposits removal; the potential support of a disclosing agent during this procedure is also evaluated. Forty surgical periodontal patients were randomly divided between surgeries where the operator was informed about a final examination of the residual root deposits and surgeries where the operator was not informed. Straight after scaling procedures a supervisor recorded the O’Leary Plaque Index of the exposed roots by mean of a disclosing agent and the percentage of teeth with residual biofilm. After the stained deposits removal, a second chromatic examination was performed and new data were collected. Mann-Whitney U-test and Wilcoxon test for paired samples were used for comparisons respectively between the two surgery groups and the first and the second chromatic examination; one-sided p-value was set at 0.05. At first examination no significant differences between the two groups were observed regarding Plaque Index (p=0.24) and percentages of teeth with residual biofilm (p=0.07). The 100% removal of roots deposits was never achieved during the study but a significant reduction of 80% of root deposits was observed between first and second examination (p=0.0001). Since root deposits removal during periodontal surgery resulted always suboptimal, the use of a disclosing agent during this procedure could be a useful and practical aid

T cell lymphoproliferative disorders associated with anti-tumor necrosis factor alpha antibody therapy for ulcerative colitis: literature summary

The enhanced risk of development of lymphoproliferative disorders in patients with inflammatory bowel disease has been attributed to immunosuppressive/immunomodulatory therapies. Infliximab is a chimeric monoclonal immunoglobulin G1 antibody directed against tumor necrosis factor alpha (TNF-α) that was approved by the Food and Drug Administration (FDA) in 1998 as an effective therapeutic agent against inflammatory bowel disease. Malignant lymphomas of both B and T cell lineage have been described in patients undergoing therapy involving TNF-α blockade. To date, eight cases of Epstein–Barr virus (EBV)-negative hepatosplenic T cell lymphoma associated with infliximab have been reported to the FDA’s Adverse Event Reporting System, as well as several other T cell lymphoproliferative disorders with aggressive clinical outcomes. We present the histologic, immunophenotypic, and molecular features of a T cell lymphoproliferative disorder involving the axillary lymph node of a 33-year-old male following infliximab treatment for ulcerative colitis. These EBV-negative lymphomas suggest that lymphoproliferative disorders following infliximab treatment for inflammatory bowel disease may involve EBV-independent immune dysregulation. The spectrum of lymphoproliferative disorders associated with infliximab and the potential mechanisms by which they occur are discussed

Physics of Neutron Star Crusts

The physics of neutron star crusts is vast, involving many different research fields, from nuclear and condensed matter physics to general relativity. This review summarizes the progress, which has been achieved over the last few years, in modeling neutron star crusts, both at the microscopic and macroscopic levels. The confrontation of these theoretical models with observations is also briefly discussed.Comment: 182 pages, published version available at <http://www.livingreviews.org/lrr-2008-10

Gravitational-wave research as an emerging field in the Max Planck Society. The long roots of GEO600 and of the Albert Einstein Institute

On the occasion of the 50th anniversary since the beginning of the search for gravitational waves at the Max Planck Society, and in coincidence with the 25th anniversary of the foundation of the Albert Einstein Institute, we explore the interplay between the renaissance of general relativity and the advent of relativistic astrophysics following the German early involvement in gravitational-wave research, to the point when gravitational-wave detection became established by the appearance of full-scale detectors and international collaborations. On the background of the spectacular astrophysical discoveries of the 1960s and the growing role of relativistic astrophysics, Ludwig Biermann and his collaborators at the Max Planck Institute for Astrophysics in Munich became deeply involved in research related to such new horizons. At the end of the 1960s, Joseph Weber's announcements claiming detection of gravitational waves sparked the decisive entry of this group into the field, in parallel with the appointment of the renowned relativist Juergen Ehlers. The Munich area group of Max Planck institutes provided the fertile ground for acquiring a leading position in the 1970s, facilitating the experimental transition from resonant bars towards laser interferometry and its innovation at increasingly large scales, eventually moving to a dedicated site in Hannover in the early 1990s. The Hannover group emphasized perfecting experimental systems at pilot scales, and never developed a full-sized detector, rather joining the LIGO Scientific Collaboration at the end of the century. In parallel, the Max Planck Institute for Gravitational Physics (Albert Einstein Institute) had been founded in Potsdam, and both sites, in Hannover and Potsdam, became a unified entity in the early 2000s and were central contributors to the first detection of gravitational waves in 2015.Comment: 94 pages. Enlarged version including new results from further archival research. A previous version appears as a chapter in the volume The Renaissance of General Relativity in Context, edited by A. Blum, R. Lalli and J. Renn (Boston: Birkhauser, 2020

Parallels between Pathogens and Gluten Peptides in Celiac Sprue

Pathogens are exogenous agents capable of causing disease in susceptible organisms. In celiac sprue, a disease triggered by partially hydrolyzed gluten peptides in the small intestine, the offending immunotoxins cannot replicate, but otherwise have many hallmarks of classical pathogens. First, dietary gluten and its peptide metabolites are ubiquitous components of the modern diet, yet only a small, genetically susceptible fraction of the human population contracts celiac sprue. Second, immunotoxic gluten peptides have certain unusual structural features that allow them to survive the harsh proteolytic conditions of the gastrointestinal tract and thereby interact extensively with the mucosal lining of the small intestine. Third, they invade across epithelial barriers intact to access the underlying gut-associated lymphoid tissue. Fourth, they possess recognition sequences for selective modification by an endogenous enzyme, transglutaminase 2, allowing for in situ activation to a more immunotoxic form via host subversion. Fifth, they precipitate a T cell–mediated immune reaction comprising both innate and adaptive responses that causes chronic inflammation of the small intestine. Sixth, complete elimination of immunotoxic gluten peptides from the celiac diet results in remission, whereas reintroduction of gluten in the diet causes relapse. Therefore, in analogy with antibiotics, orally administered proteases that reduce the host's exposure to the immunotoxin by accelerating gluten peptide destruction have considerable therapeutic potential. Last but not least, notwithstanding the power of in vitro methods to reconstitute the essence of the immune response to gluten in a celiac patient, animal models for the disease, while elusive, are likely to yield fundamentally new systems-level insights

Hypertension and renin-angiotensin system blockers are not associated with expression of angiotensin-converting enzyme 2 (ACE2) in the kidney

AIMS: Angiotensin-converting enzyme 2 (ACE2) is the cellular entry point for severe acute respiratory syndrome coronavirus (SARS-CoV-2)-the cause of coronavirus disease 2019 (COVID-19). However, the effect of renin-angiotensin system (RAS)-inhibition on ACE2 expression in human tissues of key relevance to blood pressure regulation and COVID-19 infection has not previously been reported. METHODS AND RESULTS: We examined how hypertension, its major metabolic co-phenotypes, and antihypertensive medications relate to ACE2 renal expression using information from up to 436 patients whose kidney transcriptomes were characterized by RNA-sequencing. We further validated some of the key observations in other human tissues and/or a controlled experimental model. Our data reveal increasing expression of ACE2 with age in both human lungs and the kidney. We show no association between renal expression of ACE2 and either hypertension or common types of RAS inhibiting drugs. We demonstrate that renal abundance of ACE2 is positively associated with a biochemical index of kidney function and show a strong enrichment for genes responsible for kidney health and disease in ACE2 co-expression analysis. CONCLUSION: Our results indicate that neither hypertension nor antihypertensive treatment is likely to alter the expression of the key entry receptor for SARS-CoV-2 in the human kidney. Our data further suggest that in the absence of SARS-CoV-2 infection, kidney ACE2 is most likely nephro-protective but the age-related increase in its expression within lungs and kidneys may be relevant to the risk of SARS-CoV-2 infection

Hypertension and renin-angiotensin system blockers are not associated with expression of angiotensin-converting enzyme 2 (ACE2) in the kidney

AIMS: Angiotensin-converting enzyme 2 (ACE2) is the cellular entry point for severe acute respiratory syndrome coronavirus (SARS-CoV-2)-the cause of coronavirus disease 2019 (COVID-19). However, the effect of renin-angiotensin system (RAS)-inhibition on ACE2 expression in human tissues of key relevance to blood pressure regulation and COVID-19 infection has not previously been reported. METHODS AND RESULTS: We examined how hypertension, its major metabolic co-phenotypes, and antihypertensive medications relate to ACE2 renal expression using information from up to 436 patients whose kidney transcriptomes were characterized by RNA-sequencing. We further validated some of the key observations in other human tissues and/or a controlled experimental model. Our data reveal increasing expression of ACE2 with age in both human lungs and the kidney. We show no association between renal expression of ACE2 and either hypertension or common types of RAS inhibiting drugs. We demonstrate that renal abundance of ACE2 is positively associated with a biochemical index of kidney function and show a strong enrichment for genes responsible for kidney health and disease in ACE2 co-expression analysis. CONCLUSION: Our results indicate that neither hypertension nor antihypertensive treatment is likely to alter the expression of the key entry receptor for SARS-CoV-2 in the human kidney. Our data further suggest that in the absence of SARS-CoV-2 infection, kidney ACE2 is most likely nephro-protective but the age-related increase in its expression within lungs and kidneys may be relevant to the risk of SARS-CoV-2 infection