Legionella Urinary Antigen in Early Disease

1994 ◽  
Vol 26 (6) ◽  
pp. 777-778 ◽  
Author(s):  
Sverker Bernander ◽  
Bengt Gästrin ◽  
Sture Löfgren ◽  
Anne-Marie Olinder-Nielsen
Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 144
Author(s):  
Daniele Focosi ◽  
Marco Tuccori ◽  
Massimo Franchini

Effective treatments specific for COVID-19 are still lacking. In the setting of passive immunotherapies based on neutralizing antibodies (nAbs), randomized controlled trials of COVID-19 convalescent plasma (CCP) anti-SARS-CoV-2 Spike protein monoclonal antibodies (mAb), which have been granted emergency use authorization, have suggested benefit in early disease course (less than 72 hours from symptoms and seronegative). Meanwhile, polyclonal immunoglobulins (i.e., hyperimmune serum), derived either from CCP donations or from animals immunized with SARS-CoV-2 antigens, are likely to become the next nAb-derived candidate. We here discuss the pros and cons of hyperimmune serum versus CCP and mAb, and summarize the ongoing clinical trials of COVID-19 hyperimmune sera.


2021 ◽  
Vol 1 (1) ◽  
pp. 50-62
Author(s):  
Carmelo Scarpignato ◽  
David H. Wang

Gastro-esophageal reflux disease (GERD) and Barrett’s esophagus are risk factors for esophageal adenocarcinoma (EAC). Chemoprevention is an attractive strategy, more effective than identifying early disease. Since acid reflux can lead to increased cell proliferation, decreased apoptosis, production of reactive oxygen species, DNA damage, and esophageal production of proinflammatory and pro-proliferative cytokines, proton pump inhibitors (PPIs) alone, or in combination with COX-inhibition, are the most suitable chemopreventive agents. Other compounds (statins, metformin, and selected nutraceuticals) cannot currently be recommended. Data are strong enough to warrant PPI treatment of virtually all patients with Barrett’s esophagus, although the best regimen has not yet been defined.


2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Ze Peng ◽  
Yanhong He ◽  
Saroj Parajuli ◽  
Qian You ◽  
Weining Wang ◽  
...  

AbstractDowny mildew (DM), caused by obligate parasitic oomycetes, is a destructive disease for a wide range of crops worldwide. Recent outbreaks of impatiens downy mildew (IDM) in many countries have caused huge economic losses. A system to reveal plant–pathogen interactions in the early stage of infection and quickly assess resistance/susceptibility of plants to DM is desired. In this study, we established an early and rapid system to achieve these goals using impatiens as a model. Thirty-two cultivars of Impatiens walleriana and I. hawkeri were evaluated for their responses to IDM at cotyledon, first/second pair of true leaf, and mature plant stages. All I. walleriana cultivars were highly susceptible to IDM. While all I. hawkeri cultivars were resistant to IDM starting at the first true leaf stage, many (14/16) were susceptible to IDM at the cotyledon stage. Two cultivars showed resistance even at the cotyledon stage. Histological characterization showed that the resistance mechanism of the I. hawkeri cultivars resembles that in grapevine and type II resistance in sunflower. By integrating full-length transcriptome sequencing (Iso-Seq) and RNA-Seq, we constructed the first reference transcriptome for Impatiens comprised of 48,758 sequences with an N50 length of 2060 bp. Comparative transcriptome and qRT-PCR analyses revealed strong candidate genes for IDM resistance, including three resistance genes orthologous to the sunflower gene RGC203, a potential candidate associated with DM resistance. Our approach of integrating early disease-resistance phenotyping, histological characterization, and transcriptome analysis lay a solid foundation to improve DM resistance in impatiens and may provide a model for other crops.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 725.2-725
Author(s):  
S. Gulle ◽  
İ. Sari ◽  
E. Durak Ediboglu ◽  
H. Candan ◽  
F. Onen ◽  
...  

Background:Treatment options for axial spondyloarthritis (axSpA) is currently limited, and up to 40% of the patients require biologic therapies to control symptoms. Early commencement of biologics suggested to have higher response rates but data regarding this subject is limited.Objectives:The primary aim was to investigate tumor necrosis factor inhibitor (TNFi) response and retention rates in axSpA patients who were treated in the early disease period (symptom duration (≤5 years). Our secondary aim was to identify factors predicting response to TNFi.Methods:Adult axial SpA patients who started TNFi treatments within the five years of their symptoms were identified and defined as “Group 1”. Patients whose TNFi treatments started five years after their initial symptoms served as a control group (Group 2: 5-10 years and Group3: ≥10 years). Response and survival rates at 6, 12, and 24 months were calculated. Predictors of response on TNFi survival at 24 months were also analyzed.Results:There was a total of 364 axiSpA (Group 1: 95, Group 2: 82 and Group 3: 187) patients in the study (69.8% male, 46.8±12.6 years). Group 1 patients tended to be younger, with a lower baseline CRP titers and lower HLA–B27 rate compared to the other groups. Drug survival rates were similar between the groups. This finding also remained similar when AS and nraxSpA patients analyzed separately. However, regardless of symptom duration, the drug retention rates were significantly higher in the AS group than in nraxSpA (Table 2). ASAS40 responses were higher in Group 1 than in Group 3 both at 12 and 24 months. Predictors of response based on ASAS40 at 24 months were treatment within the five years of the symptoms (OR:2.2) and age at baseline (OR:0.97) in univariate analysis. However, baseline ASDAS (OR:1.4) was the only factor in multiple regression.Conclusion:In this study we showed the following: 1) TNFi started in the early disease course resulted in a better ASAS40 response at both 12 and 24 months, 2) TNFi timing (started in the early or late disease period) seems not affecting drug retention rates, and 3) baseline disease activity is the most important predictor in achieving ASAS40 response at 24 months.Disclosure of Interests:None declared


2021 ◽  
Vol 22 (4) ◽  
pp. 1996 ◽  
Author(s):  
Christine M. Khella ◽  
Rojiar Asgarian ◽  
Judith M. Horvath ◽  
Bernd Rolauffs ◽  
Melanie L. Hart

Understanding the causality of the post-traumatic osteoarthritis (PTOA) disease process of the knee joint is important for diagnosing early disease and developing new and effective preventions or treatments. The aim of this review was to provide detailed clinical data on inflammatory and other biomarkers obtained from patients after acute knee trauma in order to (i) present a timeline of events that occur in the acute, subacute, and chronic post-traumatic phases and in PTOA, and (ii) to identify key factors present in the synovial fluid, serum/plasma and urine, leading to PTOA of the knee in 23–50% of individuals who had acute knee trauma. In this context, we additionally discuss methods of simulating knee trauma and inflammation in in vivo, ex vivo articular cartilage explant and in vitro chondrocyte models, and answer whether these models are representative of the clinical inflammatory stages following knee trauma. Moreover, we compare the pro-inflammatory cytokine concentrations used in such models and demonstrate that, compared to concentrations in the synovial fluid after knee trauma, they are exceedingly high. We then used the Bradford Hill Framework to present evidence that TNF-α and IL-6 cytokines are causal factors, while IL-1β and IL-17 are credible factors in inducing knee PTOA disease progresssion. Lastly, we discuss beneficial infrastructure for future studies to dissect the role of local vs. systemic inflammation in PTOA progression with an emphasis on early disease.


Author(s):  
Joshua M Thiede ◽  
Abigail R Gress ◽  
Samuel D Libby ◽  
Christine E Ronayne ◽  
William E Matchett ◽  
...  

Abstract COVID-19 outcomes are linked to host immune responses and may be impacted by antiviral therapy. We investigated antibody and cytokine responses in ACTT-1 study participants enrolled at our center. We studied serum specimens from 19 hospitalized adults with COVID-19 randomized to treatment with remdesivir or placebo. We assessed SARS-CoV-2 antibody responses and identified cytokine signatures using hierarchical clustering. We identified no clear immunologic trends attributable to remdesivir treatment. Seven subjects were initially seronegative at study enrollment, and all four deaths occurred in this group with more recent symptom onset. We identified three dominant cytokine signatures, demonstrating different disease trajectories.


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