Chryseobacterium indologenes infection in a newborn: a case report

<p>Abstract</p> <p>Introduction</p> <p><it>Chryseobacterium indologenes </it>is an uncommon human pathogen. Most infections have been detected in hospitalized patients with severe underlying diseases who had indwelling devices implanted. Infection caused by <it>C. indologenes </it>in a newborn has not been previously reported.</p> <p>Case presentation</p> <p>We present a case of ventilator-associated pneumonia caused by <it>C. indologenes </it>in a full-term Caucasian newborn baby boy with congenital heart disease who was successfully treated with piperacillin-tazobactam.</p> <p>Conclusion</p> <p><it>C. indologenes </it>should be considered as a potential pathogen in newborns in the presence of invasive equipment or treatment with long-term broad-spectrum antibiotics. Appropriate choice of effective antimicrobial agents for treatment is difficult because of the unpredictability and breadth of antimicrobial resistance of these organisms, which often involves resistance to many of the antibiotics chosen empirically for serious Gram-negative infections.</p

Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk.

Lung-function impairment underlies chronic obstructive pulmonary disease (COPD) and predicts mortality. In the largest multi-ancestry genome-wide association meta-analysis of lung function to date, comprising 580,869 participants, we identified 1,020 independent association signals implicating 559 genes supported by ≥2 criteria from a systematic variant-to-gene mapping framework. These genes were enriched in 29 pathways. Individual variants showed heterogeneity across ancestries, age and smoking groups, and collectively as a genetic risk score showed strong association with COPD across ancestry groups. We undertook phenome-wide association studies for selected associated variants as well as trait and pathway-specific genetic risk scores to infer possible consequences of intervening in pathways underlying lung function. We highlight new putative causal variants, genes, proteins and pathways, including those targeted by existing drugs. These findings bring us closer to understanding the mechanisms underlying lung function and COPD, and should inform functional genomics experiments and potentially future COPD therapies

Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk

Lung-function impairment underlies chronic obstructive pulmonary disease (COPD) and predicts mortality. In the largest multi-ancestry genome-wide association meta-analysis of lung function to date, comprising 580,869 participants, we identified 1,020 independent association signals implicating 559 genes supported by ≥2 criteria from a systematic variant-to-gene mapping framework. These genes were enriched in 29 pathways. Individual variants showed heterogeneity across ancestries, age and smoking groups, and collectively as a genetic risk score showed strong association with COPD across ancestry groups. We undertook phenome-wide association studies for selected associated variants as well as trait and pathway-specific genetic risk scores to infer possible consequences of intervening in pathways underlying lung function. We highlight new putative causal variants, genes, proteins and pathways, including those targeted by existing drugs. These findings bring us closer to understanding the mechanisms underlying lung function and COPD, and should inform functional genomics experiments and potentially future COPD therapies

Evaluation of Conditional Transit Signal Priority Technology for Regional Implementation

This research evaluated the implementation of transit signal priority (TSP) on a test corridor along International Drive in Orlando, Florida, to see whether the implementation was successful and justified expansion to a regional implementation of TSP for bus tie-ins to the new regional SunRail commuter rail in Central Florida. TSP is a technology that provides preferential treatment to buses at signalized intersections. This research demonstrated the effectiveness of TSP in improving bus corridor travel time in a simulated environment by using real-world data for the International Drive corridor. Evaluation was conducted with microsimulation to compare unconditional and conditional TSP with the no TSP scenario. This evaluation looked at performance metrics (for buses and all vehicles), including average speed profiles, average travel times, average number of stops, and crossing street delay. Different conditional TSP scenarios of activating TSP when a bus is 3 or 5 min behind schedule were considered. The simulation demonstrated that conditional TSP significantly improved bus travel times with little effect on crossing street delays. Unconditional TSP resulted in significant crossing street delays at some intersections with only minor improvement to bus travel time compared with both conditional TSP scenarios. The results also showed that using TSP technology reduced the environmental emissions in the International Drive corridor. With a benefit–cost ratio of 7.92 in the International Drive corridor, conditional TSP 3 min behind schedule was determined to be the most beneficial and practical TSP scenario for real-world implementation at corridor and regional levels

CD4+ Th1 cells promote CD8+ Tc1 cell survival, memory response, tumor localization and therapy by targeted delivery of interleukin 2 via acquired pMHC I complexes

The cooperative role of CD4+ helper T (Th) cells has been reported for CD8+ cytotoxic T (Tc) cells in tumor eradication. However, its molecular mechanisms have not been well elucidated. We have recently demonstrated that CD4+ Th cells can acquire major histocompatibility complex/peptide I (pMHC I) complexes and costimulatory molecules by dendritic cell (DC) activation, and further stimulate naïve CD8+ T cell proliferation and activation. In this study, we used CD4+ Th1 and CD8+ Tc1 cells derived from ovalbumin (OVA)-specific T cell receptor (TCR) transgenic OT II and OT I mice to study CD4+ Th1 cell's help effects on active CD8+ Tc1 cells and the molecular mechanisms involved in CD8+ Tc1-cell immunotherapy of OVA-expressing EG7 tumors. Our data showed that CD4+ Th1 cells with acquired pMHC I by OVA-pulsed DC (DCOVA) stimulation are capable of prolonging survival and reducing apoptosis formation of active CD8+ Tc1 cells in vitro, and promoting CD8+ Tc1 cell tumor localization and memory responses in vivo by 3-folds. A combined adoptive T-cell therapy of CD8+ Tc1 with CD4+ Th1 cells resulted in regression of well-established EG7 tumors (5 mm in diameter) in all 10/10 mice. The CD4+ Th1’s help effect is mediated via the helper cytokine IL-2 specifically targeted to CD8+ Tc1 cells in vivo by acquired pMHC I complexes. Taken together, these results will have important implications for designing adoptive T-cell immunotherapy protocols in treatment of solid tumors

Primary spinal hydatid cyst in a patient with acquired immunodeficiency syndrome

Spinal hydatid cyst is a serious and unusual infectious disease. There is little information on infections caused by cestodes in patients with human immunodeficiency virus (HIV) infection. Although infrequent, infections by cestodes constitute a cause of disease in HIV-infected patients, especially in endemic areas. This report presents, for the first time in the literature, primary spinal cyst hydatid in a patient with acquired immunodeficiency syndrome