Localization is an important component of autonomous vehicles, as it enables the accomplishment of tasks, such as path planning and navigation. Although vehicle position can be obtained by GNSS ...devices, they are susceptible to errors and satellite signal unavailability in urban scenarios. Several map-aided localization solution methods have been proposed in the literature, but mostly for indoor environments. Maps used for localization store relevant environmental features that are extracted by a detection method. However, many feature detection methods do not consider the presence of dynamic obstacles or occlusions in the environment, which can impair the localization performance. In order to detect curbs even in occluding scenes, we developed a method based on ring compression analysis and least trimmed squares. For road marking detection, we developed a modified version of the Otsu thresholding method to segment road painting from road surfaces. Finally, the feature detection methods were integrated with a Monte Carlo localization method to estimate the vehicle position. Experimental tests in urban streets have been used to validate the proposed approach with favorable results.
Buduneli N, Kinane DF: Host‐derived diagnostic markers related to soft tissue destruction and bone degradation in periodontitis. J Clin Periodontol 2011; 38 (Suppl. 11): 85–105. doi: ...10.1111/j.1600‐051X.2010.01670.x.
Background: A major challenge in clinical periodontics is to find a reliable molecular marker of periodontal tissue destruction with high sensitivity, specificity and utility.
Objectives: The aim of this systematic review is to evaluate available literature on ‘the utility of molecular markers of soft and hard periodontal tissue destruction’.
Materials and Methods: Based on the focused question, ‘What is the utility of molecular markers of soft and hard periodontal tissue destruction’, an electronic and manual search was conducted for human studies presenting clinical data for the potential of molecular markers of tissue destruction in biofluids; gingival crevicular fluid (GCF), saliva, and serum.
Results: Papers fulfilling the inclusion criteria were selected. All relevant data from the selected papers were extracted and recorded in separate tables for molecules in GCF, saliva, and serum.
Conclusion: Within the defined limits of the Problem/Population, Intervention, Comparison, Outcome, the present analysis reveals that (a) no single or combination of markers exists that can disclose periodontal tissue destruction adequately; (b) while the most fruitful source of biomarkers for periodontal destruction appears to be in molecules tightly related to bone and soft tissue destruction, this remains to be objectively demonstrated. Currently, clinical measurements are still the most reliable.
A new periodontitis classification scheme has been adopted, in which forms of the disease previously recognized as “chronic” or “aggressive” are now grouped under a single category (“periodontitis”) ...and are further characterized based on a multi‐dimensional staging and grading system. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management, while grading provides supplemental information about biological features of the disease including a history‐based analysis of the rate of periodontitis progression; assessment of the risk for further progression; analysis of possible poor outcomes of treatment; and assessment of the risk that the disease or its treatment may negatively affect the general health of the patient.
Necrotizing periodontal diseases, whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category.
Endodontic‐periodontal lesions, defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment.
Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination.
A new periodontitis classification scheme has been adopted, in which forms of the disease previously recognized as “chronic” or “aggressive” are now grouped under a single category (“periodontitis”) ...and are further characterized based on a multi‐dimensional staging and grading system. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management, while grading provides supplemental information about biological features of the disease including a history‐based analysis of the rate of periodontitis progression; assessment of the risk for further progression; analysis of possible poor outcomes of treatment; and assessment of the risk that the disease or its treatment may negatively affect the general health of the patient.
Necrotizing periodontal diseases, whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category.
Endodontic‐periodontal lesions, defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment.
Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination.
Reactive and clonal neutrophil expansion has been associated with thrombosis, suggesting that neutrophils play a role in this process. However, although there is no doubt that activated monocytes ...trigger coagulation in a tissue factor-dependent manner, it remains uncertain whether stimulated neutrophils can also directly activate coagulation. After more than a decade of debate, it is now largely accepted that normal human neutrophils do not synthetize tissue factor, the initiator of the extrinsic pathway of coagulation. However, neutrophils may passively acquire tissue factor from monocytes. Recently, the contact system, which initiates coagulation via the intrinsic pathway, has been implicated in the pathogenesis of thrombosis. After the recent description of neutrophil extracellular trap (NET) release by activated neutrophils, some animal models of thrombosis have demonstrated that coagulation may be enhanced by direct NET-dependent activation of the contact system. However, there is currently no consensus on how to assess or quantify NETosis in vivo, and other experimental animal models have failed to demonstrate a role for neutrophils in thrombogenesis. Nevertheless, it is likely that NETs can serve to localize other circulating coagulation components and can also promote vessel occlusion independent of fibrin formation. This article provides a critical appraisal of the possible roles of neutrophils in thrombosis and highlights some existing knowledge gaps regarding the procoagulant activities of neutrophil-derived extracellular chromatin and its molecular components. A better understanding of these mechanisms could guide future approaches to prevent and/or treat thrombosis.
Periodontal diseases comprise a wide range of inflammatory conditions that affect the supporting structures of the teeth (the gingiva, bone and periodontal ligament), which could lead to tooth loss ...and contribute to systemic inflammation. Chronic periodontitis predominantly affects adults, but aggressive periodontitis may occasionally occur in children. Periodontal disease initiation and propagation is through a dysbiosis of the commensal oral microbiota (dental plaque), which then interacts with the immune defences of the host, leading to inflammation and disease. This pathophysiological situation persists through bouts of activity and quiescence, until the affected tooth is extracted or the microbial biofilm is therapeutically removed and the inflammation subsides. The severity of the periodontal disease depends on environmental and host risk factors, both modifiable (for example, smoking) and non-modifiable (for example, genetic susceptibility). Prevention is achieved with daily self-performed oral hygiene and professional removal of the microbial biofilm on a quarterly or bi-annual basis. New treatment modalities that are actively explored include antimicrobial therapy, host modulation therapy, laser therapy and tissue engineering for tissue repair and regeneration.
Background
The coronavirus disease-19 (COVID-19) is characterized with intense inflammatory response, cardiac involvement, and coagulopathy. Fibrinogen, as a biomarker for inflammation, ...cardiovascular disease, and coagulation, has not been fully investigated yet. The aim of this study was to assess the clinical application of fibrinogen in COVID-19 patients.
Methods
We retrospectively analyzed the demographic and laboratory characteristics of 119 COVID-19 patients in the University of Alabama of Birmingham Medical Center. Correlations of fibrinogen on admission with intensive care unit (ICU) admission, disease severity, and laboratory parameters were analyzed.
Results
Among the 119 COVID-19 patients, 77.3% (92/119) had severe disease, and 59.5% (71/119) patients were admitted to the ICU. Elevated fibrinogen was detected in 67.2% (80/119) of the patients. Fibrinogen levels were significantly associated with inflammatory markers and disease severity, but not with cardiac injury biomarker high sensitivity troponin I. Patients with severe disease had increased fibrinogen levels upon admission compared to patients with non-severe disease (
P
= 0.001). Fibrinogen level at 528.0 mg/dl was the optimal cutoff to predict disease severity, with a sensitivity and specificity of 66.7% and 70.3% (area undty -60er the curve AUC 0.72,
P
= 0.0006).
Conclusions
Fibrinogen is commonly elevated in COVID-19 patients, especially in those with severe disease. Elevated fibrinogen correlates with excessive inflammation, disease severity, and ICU admission in COVID-19 patients.
Understanding temporal regulation of development remains an important challenge. Whereas average, species-typical timing of many developmental processes has been established, less is known about ...inter-individual variability and correlations in timing of specific events. We addressed these questions in the context of postembryonic development in Caenorhabditis elegans. Based on patterns of locomotor activity of freely moving animals, we inferred durations of four larval stages (L1-L4) in over 100 individuals. Analysis of these data supports several conclusions. Individuals have consistently faster or slower rates of development because durations of L1 through L3 stages are positively correlated. The last larval stage, the L4, is less variable than the earlier stages and its duration is largely independent of the rate of early larval development, implying existence of two distinct larval epochs. We describe characteristic patterns of variation and correlation, as well as the fact that stage durations tend to scale relative to total developmental time. This scaling relationship suggests that each larval stage is not limited by an absolute duration, but is instead terminated when a subset of events that must occur prior to adulthood have been completed. The approach described here offers a scalable platform that will facilitate the study of temporal regulation of postembryonic development.
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•Behavioral tracking data reveal rates of development in individual C. elegans.•Correlations among larval stage durations result in faster or slower development.•Individual rates of development are decoupled from behavioral activity.•Durations of larval stages scale as a fraction of total time to adulthood.
It is critical to understand the underlying host responses in aggressive periodontitis to provide a better appreciation of the risk and susceptibility to this disease. Such knowledge may elucidate ...the etiology and susceptibility to aggressive periodontitis and directly influence treatment decisions and aid diagnosis. This review is timely in that several widely held tenets are now considered unsupportable, namely the concept that Aggregatibacter actinomycetemycomitans is the key pathogen and that chemotactic defects in polymorphonuclear leukocytes are part of the etiopathology. This review also serves to put into context key elements of the host response that may be implicated in the genetic background of aggressive periodontitis. Furthermore, key molecules unique to the host response in aggressive periodontitis may have diagnostic utility and be used in chairside clinical activity tests or as population screening markers. It is becoming increasingly appreciated that the microbial etiology of aggressive periodontitis and the histopathology of this disease are more similar to than different from that of chronic periodontitis. An important therapeutic consideration from the lack of support for A. actinomycetemycomitans as a critical pathogen here is that the widely held belief that tetracycline had a role in aggressive periodontitis therapy is now not supported and that antibiotics such as those used effectively in chronic periodontitis (metronidazole and amoxicillin) are not contraindicated. Furthermore, A. actinomycetemycomitans‐related molecules, such as cytolethal distending toxin and leukotoxin, are less likely to have utility as diagnosis agents or as therapeutic targets.
NETosis is a physiologic process in which neutrophils release their nuclear material in the form of neutrophil extracellular traps (NETs). NETs have been reported to directly promote thrombosis in ...animal models. Although the effects of purified NET components including DNA, histone proteins, and neutrophil enzymes on coagulation have been characterized, the mechanism by which intact NETs promote thrombosis is largely unknown. In this study, human neutrophils were stimulated to produce NETs in platelet-free plasma (PFP) or in buffer using phorbol myristate actetate or calcium ionophore. DNA and histone proteins were also separately purified from normal human neutrophils and used to reconstitute chromatin using a salt-gradient dialysis method. Neutrophil stimulation resulted in robust NET release. In recalcified PFP, purified DNA triggered contact-dependent thrombin generation (TG) and amplified TG initiated by low concentrations of tissue factor. Similarly, in a buffer milieu, DNA initiated the contact pathway and amplified thrombin-dependent factor XI activation. Recombinant human histones H3 and H4 triggered TG in recalcified human plasma in a platelet-dependent manner. In contrast, neither intact NETs, reconstituted chromatin, individual nucleosome particles, nor octameric core histones reproduced any of these procoagulant effects. We conclude that unlike DNA or individual histone proteins, human intact NETs do not directly initiate or amplify coagulation in vitro. This difference is likely explained by the complex histone-histone and histone-DNA interactions within the nucleosome unit and higher-order supercoiled chromatin leading to neutralization of the negative charges on polyanionic DNA and modification of the binding properties of individual histone proteins.
•Individual histone proteins and DNA purified from normal human neutrophils promote coagulation activation.•Neither intact NETs nor nucleosomes directly promote coagulation activation in plasma in vitro.
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