Jewish Hospital

About: Jewish Hospital is a healthcare organization based out in Cincinnati, Ohio, United States. It is known for research contribution in the topics: Antigen & Population. The organization has 3881 authors who have published 3414 publications receiving 123044 citations.

Features of the bronchial bacterial microbiome associated with atopy, asthma, and responsiveness to inhaled corticosteroid treatment

Abstract: Background Compositional differences in the bronchial bacterial microbiota have been associated with asthma, but it remains unclear whether the findings are attributable to asthma, to aeroallergen sensitization, or to inhaled corticosteroid treatment. Objectives We sought to compare the bronchial bacterial microbiota in adults with steroid-naive atopic asthma, subjects with atopy but no asthma, and nonatopic healthy control subjects and to determine relationships of the bronchial microbiota to phenotypic features of asthma. Methods Bacterial communities in protected bronchial brushings from 42 atopic asthmatic subjects, 21 subjects with atopy but no asthma, and 21 healthy control subjects were profiled by using 16S rRNA gene sequencing. Bacterial composition and community-level functions inferred from sequence profiles were analyzed for between-group differences. Associations with clinical and inflammatory variables were examined, including markers of type 2–related inflammation and change in airway hyperresponsiveness after 6 weeks of fluticasone treatment. Results The bronchial microbiome differed significantly among the 3 groups. Asthmatic subjects were uniquely enriched in members of the Haemophilus , Neisseria , Fusobacterium , and Porphyromonas species and the Sphingomonodaceae family and depleted in members of the Mogibacteriaceae family and Lactobacillales order. Asthma-associated differences in predicted bacterial functions included involvement of amino acid and short-chain fatty acid metabolism pathways. Subjects with type 2–high asthma harbored significantly lower bronchial bacterial burden. Distinct changes in specific microbiota members were seen after fluticasone treatment. Steroid responsiveness was linked to differences in baseline compositional and functional features of the bacterial microbiome. Conclusion Even in subjects with mild steroid-naive asthma, differences in the bronchial microbiome are associated with immunologic and clinical features of the disease. The specific differences identified suggest possible microbiome targets for future approaches to asthma treatment or prevention.

Relationships of Serum Plant Sterols (Phytosterols) and Cholesterol in 595 Hypercholesterolemic Subjects, and Familial Aggregation of Phytosterols, Cholesterol, and Premature Coronary Heart Disease in Hyperphytosterolemic Probands and Their First-Degree Relatives

Abstract: To assess relationships of serum phytosterols (plant sterols [P]) to serum cholesterol (C), P were measured by gas-liquid chromatography (GLC) in 595 hypercholesterolemics (top C quintile in screening of 3,472 self-referred subjects). A second specific aim was to determine whether high serum P would track over time and whether they would predict familial aggregation of high C, high low-density lipoprotein cholesterol (LDLC), high apolipoprotein (apo) B, and increased premature coronary heart disease (CHD) in hyperphytosterolemic probands and their first-degree relatives. Mean +/- (SD) C was 260 +/- 56 mg/dL, campesterol (CAMP) was 2.10 +/- 1.6 micrograms/mL, stigmasterol (STIG) 1.71 +/- 1.67, sitosterol (SIT) 2.98 +/- 1.61, and total P 6.79 +/- 3.66 micrograms/mL. Serum C correlated with CAMP (r = .15, P less than or equal to .001), STIG (r = .10, P less than or equal to .02), SIT (r = .34, P less than or equal to .0001), and total P (r = .29, P less than or equal to .0001). High serum CAMP and STIG were associated with a personal or family history of CHD in subjects less than or equal to age 55 years (premature CHD). In 21 hyperphytosterolemic probands who initially had at least one P at or above the 95th percentile and a second P at or above the 75th percentile, P were remeasured 2 years later. Initial and 2-year follow-up CAMP, STIG, and SIT did not differ (P greater than .7). Initial and follow-up CAMP were correlated (r = .47, P = .03).(ABSTRACT TRUNCATED AT 250 WORDS)

The Biology of Cancer-Related Fatigue: A Review of the Literature

Abstract: Understanding the etiology of cancer-related fatigue (CRF) is critical to identify targets to develop therapies to reduce CRF burden The goal of this systematic review was to expand on the initial work by the National Cancer Institute CRF Working Group to understand the state of the science related to the biology of CRF and, specifically, to evaluate studies that examined the relationships between biomarkers and CRF and to develop an etiologic model of CRF to guide researchers on pathways to explore or therapeutic targets to investigate This review was completed by the Multinational Association of Supportive Care in Cancer Fatigue Study Group–Biomarker Working Group The initial search used three terms (biomarkers, fatigue, cancer), which yielded 11,129 articles After removing duplicates, 9145 articles remained Titles were assessed for the keywords “cancer” and “fatigue” resulting in 3811 articles Articles published before 2010 and those with samples <50 were excluded, leaving 75 articles for full-text review Of the 75 articles, 28 were further excluded for not investigating the associations of biomarkers and CRF Of the 47 articles reviewed, 25 were cross-sectional and 22 were longitudinal studies More than half (about 70 %) were published recently (2010–2013) Almost half (45 %) enrolled breast cancer participants The majority of studies assessed fatigue using self-report questionnaires, and only two studies used clinical parameters to measure fatigue The findings from this review suggest that CRF is linked to immune/inflammatory, metabolic, neuroendocrine, and genetic biomarkers We also identified gaps in knowledge and made recommendations for future research

Mast cells process bacterial Ags through a phagocytic route for class I MHC presentation to T cells.

Abstract: The pivotal role of mast cells in allergic reactions and inflammatory processes is well established and recent studies have suggested that mast cells may also have a role in specific immune responses. Because mast cells have been shown to phagocytose and kill enterobacteria, we wished to determine whether they could also process bacterial Ags for presentation to T cells. Using a model system in which a well-characterized T cell epitope is expressed within bacteria as a fusion protein, we demonstrate in this paper that mast cells are indeed capable of processing bacterial Ags for presentation through class I MHC molecules to T cell hybridomas after phagocytic uptake of live bacteria. Processing occurs from a number of Gram-negative enterobacteria including Salmonella typhimurium and Escherichia coli. Parallel assays show that processing of the model Ag from enterobacteria by mast cells is similar in efficiency to processing by peritoneal macrophages. Consistent with earlier observations demonstrating a function of the bacterial fimbrial protein FimH in promoting bacterial binding to mast cells, the magnitude of the Ag processing response of E. coli is influenced by bacterial expression of FimH. Taken together, these observations extend the range of cell types capable of the phagocytic pathway of Ag processing and suggest that mast cells may have a previously unrecognized role in the induction of specific immune responses to bacteria.