Frequency of Dental X-ray Diagnostics in Children and Adolescents: What Is the Radiation Exposure?

Children are exposed to ionizing radiation through radiographs during their development for various reasons. At present, there are no officially valid reference values for dental X-rays in children and adolescents for dental X-ray diagnostics. This study retrospectively examined 9680 extraoral dental radiographs in pediatric patients between 2002 and 2020. The aim was to analyze the radiation doses in pediatric patients, which indications were used, and whether there were specific age and gender differences. The evaluation showed that radiation doses were considered low, with dose area products of 2.2 cGy × cm 2 for a lateral cephalogram, 14 cGy × cm 2 for an orthopantomogram (OPG), and 45 cGy × cm 2 for cone beam computer tomography (CBCT). This corresponds to an effective dose of 1.5 μSv for a lateral cephalogram, 7 μSv for an OPG, and 33.8 μSv for CBCT. Of the 9680 images, 78% were orthopantomograms, and only 0.4% were CBCT images. OPG has become more important over the years, as reflected in the indication. Approximately one-third of all extraoral exposures are orthodontic indications. Overall, the indications were similar for both genders. According to the dental indications, boys were X-rayed slightly more frequently than girls (54.5–45.5%). A future publication of dose guide values and corresponding guidelines is of high priority

Evaluation of the post-processing algorithms SimGrid and S-Enhance for paediatric intensive care patients and neonates

Abstract Background Post-processing software can be used in digital radiography to achieve higher image quality, especially in cases of scattered radiation. SimGrid is a grid-like software based on a Convolutional Neuronal Network that estimates the distribution and degree of scattered radiation in radiographs and thus improves image quality by simulating an anti-scatter grid. S-Enhance is an algorithm programmed to improve contrast visibility of foreign material. Objective The objective of this study was to evaluate the SimGrid and S-Enhance digital radiography post-processing methods for neonatology and paediatric intensive care. Materials and Methods Two hundred and ten radiographs from the neonatal ( n  = 101, 0 to 6 months of age) and paediatric ( n  = 109, 6 months to 18 years of age) intensive care units performed in daily clinical routine using a mobile digital radiography system were post-processed with one of the algorithms, anonymized and then evaluated comparatively by two experienced paediatric radiologists. For every radiograph, patient data and exposure data were collected and analysed. Results Analysis of different radiographs showed that SimGrid significantly improves image quality for patients with a weight above 10 kg (range: 10–30 kg: odds ratio [OR] = 6.683, P  < 0.0001), especially regarding the tracheobronchial system, intestinal gas, and bones. Utilizing S-Enhance significantly advances the assessment of foreign material (OR = 136.111, P  < 0.0001) and bones (OR = 34.917, P  < 0.0001) for children of all ages and weight, whereas overall image quality decreases. Conclusion SimGrid offers a differentiated spectrum in image improvement for children beyond the neonatal period whereas S-Enhance especially improves visibility of foreign material and bones for all patients

Adjuvant hyperthermic intraperitoneal chemotherapy (HIPEC) in patients with colon cancer at high risk of peritoneal carcinomatosis; the COLOPEC randomized multicentre trial

Background: The peritoneum is the second most common site of recurrence in colorectal cancer. Early detection of peritoneal carcinomatosis (PC) by imaging is difficult. Patients eventually presenting with clinically apparent PC have a poor prognosis. Median survival is only about five months if untreated and the benefit of palliative systemic chemotherapy is limited. Only a quarter of patients are eligible for curative treatment, consisting of cytoreductive surgery and hyperthermic intraperitoneal chemotherapy (CR/HIPEC). However, the effectiveness depends highly on the extent of disease and the treatment is associated with a considerable complication rate. These clinical problems underline the need for effective adjuvant therapy in high-risk patients to minimize the risk of outgrowth of peritoneal micro metastases. Adjuvant hyperthermic intraperitoneal chemotherapy (HIPEC) seems to be suitable for this purpose. Without the need for cytoreductive surgery, adjuvant HIPEC can be performed with a low complication rate and short hospital stay. Methods/Design: The aim of this study is to determine the effectiveness of adjuvant HIPEC in preventing the development of PC in patients with colon cancer at high risk of peritoneal recurrence. This study will be performed in the nine Dutch HIPEC centres, starting in April 2015. Eligible for inclusion are patients who underwent curative resection for T4 or intra-abdominally perforated cM0 stage colon cancer. After resection of the primary tumour, 176 patients will be randomized to adjuvant HIPEC followed by routine adjuvant systemic chemotherapy in the experimental arm, or to systemic chemotherapy only in the control arm. Adjuvant HIPEC will be performed simultaneously or shortly after the primary resection. Oxaliplatin will be used as chemotherapeutic agent, for 30 min at 42-43 degrees C. Just before HIPEC, 5-fluorouracil and leucovorin will be administered intravenously. Primary endpoint is peritoneal disease-free survival at 18 months. Diagnostic laparoscopy will be performed routinely after 18 months postoperatively in both arms of the study in patients without evidence of disease based on routine follow-up using CT imaging and CEA. Discussion: Adjuvant HIPEC is assumed to reduce the expected 25 % absolute risk of PC in patients with T4 or perforated colon cancer to a risk of 10 %. This reduction is likely to translate into a prolonged overall survival

The James Webb Space Telescope Mission

Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least $4m$. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the $6.5m$ James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

Erhöhung der Genauigkeit bei der Ermittlung des Bremsstrahlungsspektrums klinischer Linearbeschleuniger

Abstract Scheithauer M.: Improvement of the accuracy of determining the bremsstrahlung spectra of clinical linear accelerators. Dissertation, Ilmenau (2004) The present study focuses on the reconstruction of the bremsstrahlung spectra of a clinical linear accelerator from the measured transmission curve with the aim of improving the accuracy of this method. The generation and interaction of bremsstrahlung as well as several methods of determining its spectra has been analysed. The reconstruction of the spectra from simply measured data is possible in clinical routine. The essence of the method is the analytic inverse Laplace transformation of a parameter function fitted to the measured transmission curve. It was tested with known fitting functions, however, they resulted in considerable fitting inaccuracy, leading to inaccuracy of the bremsstrahlung spectra. In order to minimise the fitting errors, a linear combination of n equations with 2n-1 parameters was employed. As a result, the fitting errors are considerably smaller with the new flexible function. The measurement of the transmission function requires that the energy-dependent detector response is taken into account. In this thesis the underlying physical context was analysed resulting in the development of a correction function for the energy-dependent detector response. The factors of this function were experimentally determined or calculated from tabulated values. The energy-distribution of photons for several clinically relevant fields was determined with this new method, e.g. spectra of variable field size, fields with radial distance between centre central axis and fields with fluence-modifying elements. A measuring setup for separating photon-contamination from primary electrons was developed. Thereby it was possible to analyse the spectra of the photon-contamination.Aufgabe dieser Arbeit ist die Rekonstruktion des Bremsstrahlungsspektrums eines klinischen Linearbeschleunigers aus der gemessenen Transmissionsfunktion mit dem Ziel, die Genauigkeit dieser Methode zu erhöhen. Analysiert wurden die Erzeugung und Beeinflussung der Bremsstrahlung sowie verschiedene Methoden zur Ermittlung des Bremsstrahlungsspektrums. Die in der klinischen Routine durchführbare Methode ist die Rekonstruktion des Bremsstrahlungsspektrums aus einfach messbaren Daten. Kern der Rekonstruktion ist die analytische inverse Laplacetransformation einer an die gemessene Transmissionskurve angepassten Parameterfunktion. Die bekannten Anpassungsfunktionen lieferten erhebliche Anpassungsfehler, so dass die Genauigkeit des Bremsstrahlungsspektrums beeinträchtigt wurde. Um die Anpassungsfehler zu minimieren, wurde zur Wiedergabe der Transmissionskurve ein neuer Funktionstyp, eine Linearkombination von n Gleichungen mit 2n-1 freien Parametern, verwendet. Die neue Kurvenanpassung zeigt eine hohe Flexibilität und geringe Anpassungsfehler. Bei der Messung der Transmissionsfunktion muss das energieabhängige Detektoransprechvermögen berücksichtigt werden. Analysiert wurden die zugrundeliegenden physikalischen Zusammenhänge, so dass es möglich war, eine Korrektionsfunktion für das energieabhängige Detektoransprechvermögen aufzustellen, deren Faktoren experimentell bestimmt wurden oder aus Tabellenwerten berechnet werden konnten. Mit der verbesserten Methode konnte die Energieverteilung der Photonen für unterschiedliche klinisch relevante Bestrahlungssituationen ermittelt werden. Bremsstrahlungsspektren in unterschiedlichen radialen Abständen des Mittelpunktes zum Zentralstrahl, bei verschiedenen Feldgrößen und beim Einsatz von fluenzmodifizierenden Elementen wurden bestimmt. Entwickelt wurde ein Messaufbau zur Trennung der Photonenkontamination von primärer Elektronenstrahlung. Dadurch war es möglich, die spektrale Verteilung der Kontaminationsphotonen zu bestimmen

The gut microbiota: A driver of Type 2 diabetes

The studies described in this thesis investigated how changes in the gut microbiota relate to alterations in the immune system and the development of beta-cell dysfunction. Moreover, we addressed the interrelation between intestinal immunoglobulins and gut microbiota in individuals with metabolic diseases. Chapter 1 provides a general introduction to the gut microbiota, the pathogenesis of T2D, and the function of IgA. Chapter 2 summarizes the current literature on gut microbiota, obesity, and T2D. A western diet leads to changes in gut microbial composition and intestinal physiology. Altered intestinal microbial composition promotes obesity by increasing energy harvest and gut permeability that may facilitate the translocation of bacteria or bacterial components into the circulation. Thereby, the gut microbiota can impact the function of metabolic organs. Interventions aiming to restore gut microbial homeostasis, such as ingestion of fibers or therapeutic microbes, are novel strategies to reduce metabolic abnormalities. Inflammation in the pancreas can lead to beta-cell dysfunction with the driving inflammatory triggers yet to be identified. The gut microbiota provides a plausible source of pro-inflammatory molecules. Chapter 3 shows that a high-fat diet significantly altered the gut and pancreatic bacterial signature in mice. Importantly, our findings could not be traced back to contamination, a well-known factor disturbing microbial signal identification in low-abundance samples. Our data point out that the pancreas comprises bacterial DNA. This underscores similar speculations and observations in the field implying that gut microbial components translocate and act on distal organs and tissue. Chapter 4 summarizes the current literature on gut microbiota and metabolic inflammation. T2D is characterized by a chronic state of low-grade inflammation, which has been linked to the development of insulin resistance. Intestinal microbiota drive the development of insulin resistance in obesity and T2D, possibly by initiating an inflammatory response. Overall, there is strong evidence for the tripartite interaction between the gut microbiota and the host’s immune system as well as metabolism. Chapter 5 explores how a (dysbiotic) gut microbiota can influence beta-cell dysfunction. Enterobacteriaceae, which harbors several pro-inflammatory bacteria such as Enterobacter cloacae, was more abundant in the gut of individuals with T2D. These bacteria can express flagellin, an integral part of the locomotive function of bacteria. Flagellin induced a pro-inflammatory response in pancreatic islets, which was at least partly mediated by toll-like receptor (TLR)-5 on resident islet macrophages. This inflammatory response was associated with beta-cell dysfunction, characterized by reduced insulin gene expression, impaired proinsulin processing, and stress-induced insulin hypersecretion. We postulate that increased systemically disseminated flagellin is a contributing factor to beta-cell failure and hence to T2D development in time. Chapter 6 addresses the effect of antibiotics-induced alterations in the gut microbiota on the intestinal antibody response. Individuals with or without metabolic syndrome received oral vancomycin for seven days. Coinciding with a surge in Gram-negative bacteria, fecal levels of the immunogenic bacterial components LPS and flagellin in- creased. Intestinal antibodies significantly increased, whereas peripheral antibodies were mostly unaffected by vancomycin treatment. Typical pro-inflammatory bacteria were mostly coated with IgA after antibiotic treatment. We suggest that the intestinal antibody response after antibiotic treatment prevents systemic inflammation. Chapter 7 addresses the intestinal antibody response after bariatric surgery, an 8-weight-loss surgery with significant consequences for gut microbiota composition. Body weight, fasting glucose, and inflammatory parameters decreased after bariatric surgery, whereas pro-inflammatory bacterial species, LPS, and flagellin increased. Simultaneously, concentrations of LPS- and flagellin-specific intestinal IgA levels increased. Serum antibodies decreased in both groups, along with a lower inflammatory tone. We concluded that intestinal rearrangement by bariatric surgery expands typical pro-inflammatory bacteria, which might be compensated by an improved antibody response. Chapter 8 summarizes the findings and gives future perspectives

The gut microbiota: A driver of Type 2 diabetes

The studies described in this thesis investigated how changes in the gut microbiota relate to alterations in the immune system and the development of beta-cell dysfunction. Moreover, we addressed the interrelation between intestinal immunoglobulins and gut microbiota in individuals with metabolic diseases. Chapter 1 provides a general introduction to the gut microbiota, the pathogenesis of T2D, and the function of IgA. Chapter 2 summarizes the current literature on gut microbiota, obesity, and T2D. A western diet leads to changes in gut microbial composition and intestinal physiology. Altered intestinal microbial composition promotes obesity by increasing energy harvest and gut permeability that may facilitate the translocation of bacteria or bacterial components into the circulation. Thereby, the gut microbiota can impact the function of metabolic organs. Interventions aiming to restore gut microbial homeostasis, such as ingestion of fibers or therapeutic microbes, are novel strategies to reduce metabolic abnormalities. Inflammation in the pancreas can lead to beta-cell dysfunction with the driving inflammatory triggers yet to be identified. The gut microbiota provides a plausible source of pro-inflammatory molecules. Chapter 3 shows that a high-fat diet significantly altered the gut and pancreatic bacterial signature in mice. Importantly, our findings could not be traced back to contamination, a well-known factor disturbing microbial signal identification in low-abundance samples. Our data point out that the pancreas comprises bacterial DNA. This underscores similar speculations and observations in the field implying that gut microbial components translocate and act on distal organs and tissue. Chapter 4 summarizes the current literature on gut microbiota and metabolic inflammation. T2D is characterized by a chronic state of low-grade inflammation, which has been linked to the development of insulin resistance. Intestinal microbiota drive the development of insulin resistance in obesity and T2D, possibly by initiating an inflammatory response. Overall, there is strong evidence for the tripartite interaction between the gut microbiota and the host’s immune system as well as metabolism. Chapter 5 explores how a (dysbiotic) gut microbiota can influence beta-cell dysfunction. Enterobacteriaceae, which harbors several pro-inflammatory bacteria such as Enterobacter cloacae, was more abundant in the gut of individuals with T2D. These bacteria can express flagellin, an integral part of the locomotive function of bacteria. Flagellin induced a pro-inflammatory response in pancreatic islets, which was at least partly mediated by toll-like receptor (TLR)-5 on resident islet macrophages. This inflammatory response was associated with beta-cell dysfunction, characterized by reduced insulin gene expression, impaired proinsulin processing, and stress-induced insulin hypersecretion. We postulate that increased systemically disseminated flagellin is a contributing factor to beta-cell failure and hence to T2D development in time. Chapter 6 addresses the effect of antibiotics-induced alterations in the gut microbiota on the intestinal antibody response. Individuals with or without metabolic syndrome received oral vancomycin for seven days. Coinciding with a surge in Gram-negative bacteria, fecal levels of the immunogenic bacterial components LPS and flagellin in- creased. Intestinal antibodies significantly increased, whereas peripheral antibodies were mostly unaffected by vancomycin treatment. Typical pro-inflammatory bacteria were mostly coated with IgA after antibiotic treatment. We suggest that the intestinal antibody response after antibiotic treatment prevents systemic inflammation. Chapter 7 addresses the intestinal antibody response after bariatric surgery, an 8-weight-loss surgery with significant consequences for gut microbiota composition. Body weight, fasting glucose, and inflammatory parameters decreased after bariatric surgery, whereas pro-inflammatory bacterial species, LPS, and flagellin increased. Simultaneously, concentrations of LPS- and flagellin-specific intestinal IgA levels increased. Serum antibodies decreased in both groups, along with a lower inflammatory tone. We concluded that intestinal rearrangement by bariatric surgery expands typical pro-inflammatory bacteria, which might be compensated by an improved antibody response. Chapter 8 summarizes the findings and gives future perspectives

The gut microbiota

The studies described in this thesis investigated how changes in the gut microbiota relate to alterations in the immune system and the development of beta-cell dysfunction. Moreover, we addressed the interrelation between intestinal immunoglobulins and gut microbiota in individuals with metabolic diseases. Chapter 1 provides a general introduction to the gut microbiota, the pathogenesis of T2D, and the function of IgA. Chapter 2 summarizes the current literature on gut microbiota, obesity, and T2D. A western diet leads to changes in gut microbial composition and intestinal physiology. Altered intestinal microbial composition promotes obesity by increasing energy harvest and gut permeability that may facilitate the translocation of bacteria or bacterial components into the circulation. Thereby, the gut microbiota can impact the function of metabolic organs. Interventions aiming to restore gut microbial homeostasis, such as ingestion of fibers or therapeutic microbes, are novel strategies to reduce metabolic abnormalities. Inflammation in the pancreas can lead to beta-cell dysfunction with the driving inflammatory triggers yet to be identified. The gut microbiota provides a plausible source of pro-inflammatory molecules. Chapter 3 shows that a high-fat diet significantly altered the gut and pancreatic bacterial signature in mice. Importantly, our findings could not be traced back to contamination, a well-known factor disturbing microbial signal identification in low-abundance samples. Our data point out that the pancreas comprises bacterial DNA. This underscores similar speculations and observations in the field implying that gut microbial components translocate and act on distal organs and tissue. Chapter 4 summarizes the current literature on gut microbiota and metabolic inflammation. T2D is characterized by a chronic state of low-grade inflammation, which has been linked to the development of insulin resistance. Intestinal microbiota drive the development of insulin resistance in obesity and T2D, possibly by initiating an inflammatory response. Overall, there is strong evidence for the tripartite interaction between the gut microbiota and the host’s immune system as well as metabolism. Chapter 5 explores how a (dysbiotic) gut microbiota can influence beta-cell dysfunction. Enterobacteriaceae, which harbors several pro-inflammatory bacteria such as Enterobacter cloacae, was more abundant in the gut of individuals with T2D. These bacteria can express flagellin, an integral part of the locomotive function of bacteria. Flagellin induced a pro-inflammatory response in pancreatic islets, which was at least partly mediated by toll-like receptor (TLR)-5 on resident islet macrophages. This inflammatory response was associated with beta-cell dysfunction, characterized by reduced insulin gene expression, impaired proinsulin processing, and stress-induced insulin hypersecretion. We postulate that increased systemically disseminated flagellin is a contributing factor to beta-cell failure and hence to T2D development in time. Chapter 6 addresses the effect of antibiotics-induced alterations in the gut microbiota on the intestinal antibody response. Individuals with or without metabolic syndrome received oral vancomycin for seven days. Coinciding with a surge in Gram-negative bacteria, fecal levels of the immunogenic bacterial components LPS and flagellin in- creased. Intestinal antibodies significantly increased, whereas peripheral antibodies were mostly unaffected by vancomycin treatment. Typical pro-inflammatory bacteria were mostly coated with IgA after antibiotic treatment. We suggest that the intestinal antibody response after antibiotic treatment prevents systemic inflammation. Chapter 7 addresses the intestinal antibody response after bariatric surgery, an 8-weight-loss surgery with significant consequences for gut microbiota composition. Body weight, fasting glucose, and inflammatory parameters decreased after bariatric surgery, whereas pro-inflammatory bacterial species, LPS, and flagellin increased. Simultaneously, concentrations of LPS- and flagellin-specific intestinal IgA levels increased. Serum antibodies decreased in both groups, along with a lower inflammatory tone. We concluded that intestinal rearrangement by bariatric surgery expands typical pro-inflammatory bacteria, which might be compensated by an improved antibody response. Chapter 8 summarizes the findings and gives future perspectives.</jats:p