Prospects for PI3 Kinase Signaling Inhibition in Obstructive Airway Diseases

2016 ◽  
pp. 352-371
Keyword(s):  
Pi3 Kinase ◽  
Kinase Signaling ◽  
Airway Diseases ◽  
Obstructive Airway Diseases

scholarly journals Drosophila Spidey/Kar Regulates Oenocyte Growth via PI3-Kinase Signaling

PLoS Genetics ◽  
2016 ◽  
Vol 12 (8) ◽  
pp. e1006154 ◽  
Author(s):  
Einat Cinnamon ◽  
Rami Makki ◽  
Annick Sawala ◽  
Leah P. Wickenberg ◽  
Gary J. Blomquist ◽  
...  
Keyword(s):  
Pi3 Kinase ◽  
Kinase Signaling

scholarly journals Multimorbidity clusters in patients with chronic obstructive airway diseases in the EpiChron Cohort

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jonás Carmona-Pírez ◽  
Beatriz Poblador-Plou ◽  
Ignatios Ioakeim-Skoufa ◽  
Francisca González-Rubio ◽  
Luis Andrés Gimeno-Feliú ◽  
...  
Keyword(s):  
Substance Use ◽  
Chronic Conditions ◽  
Large Scale ◽  
Mental Health Problems ◽  
Epidemiological Studies ◽  
Chronic Obstructive ◽  
High Morbidity ◽  
Airway Diseases ◽  
Obstructive Sleep ◽  
Obstructive Airway Diseases

AbstractChronic obstructive airway diseases such as chronic obstructive pulmonary disease (COPD), asthma, rhinitis, and obstructive sleep apnea (OSA) are amongst the most common treatable and preventable chronic conditions with high morbidity burden and mortality risk. We aimed to explore the existence of multimorbidity clusters in patients with such diseases and to estimate their prevalence and impact on mortality. We conducted an observational retrospective study in the EpiChron Cohort (Aragon, Spain), selecting all patients with a diagnosis of allergic rhinitis, asthma, COPD, and/or OSA. The study population was stratified by age (i.e., 15–44, 45–64, and ≥ 65 years) and gender. We performed cluster analysis, including all chronic conditions recorded in primary care electronic health records and hospital discharge reports. More than 75% of the patients had multimorbidity (co-existence of two or more chronic conditions). We identified associations of dermatologic diseases with musculoskeletal disorders and anxiety, cardiometabolic diseases with mental health problems, and substance use disorders with neurologic diseases and neoplasms, amongst others. The number and complexity of the multimorbidity clusters increased with age in both genders. The cluster with the highest likelihood of mortality was identified in men aged 45 to 64 years and included associations between substance use disorder, neurologic conditions, and cancer. Large-scale epidemiological studies like ours could be useful when planning healthcare interventions targeting patients with chronic obstructive airway diseases and multimorbidity.

scholarly journals PI3 kinase signaling pathway in hematopoietic cancers: A glance in miRNA's role

2021 ◽  
Vol 35 (4) ◽  
Author(s):  
Elham Roshandel ◽  
Leila Noorazar ◽  
Behrouz Farhadihosseinabadi ◽  
Mahshid Mehdizadeh ◽  
Mohammad Hossein Kazemi ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Pi3 Kinase ◽  
Kinase Signaling ◽  
Kinase Signaling Pathway ◽  
Hematopoietic Cancers

scholarly journals 178 PI3-kinase signaling modulates the induction of MHC molecules by IFN-gamma

2018 ◽  
Vol 138 (5) ◽  
pp. S30
Author(s):  
S. Chandrasekaran ◽  
M. Sasaki ◽  
B. Sapkota ◽  
B. Pollack
Keyword(s):  
Pi3 Kinase ◽  
Kinase Signaling ◽  
Ifn Gamma ◽  
Mhc Molecules

scholarly journals Wiskott-Aldrich Syndrome Interacting Protein Deficiency Uncovers the Role of the Co-receptor CD19 as a Generic Hub for PI3 Kinase Signaling in B Cells

Immunity ◽  
2015 ◽  
Vol 43 (4) ◽  
pp. 660-673 ◽  
Author(s):  
Selina Jessica Keppler ◽  
Francesca Gasparrini ◽  
Marianne Burbage ◽  
Shweta Aggarwal ◽  
Bruno Frederico ◽  
...  
Keyword(s):  
B Cells ◽  
Pi3 Kinase ◽  
Protein Deficiency ◽  
Kinase Signaling ◽  
Interacting Protein ◽  
Wiskott Aldrich Syndrome

scholarly journals IGFs stimulate zebrafish cell proliferation by activating MAP kinase and PI3-kinase-signaling pathways

2001 ◽  
Vol 280 (4) ◽  
pp. R1230-R1239 ◽  
Author(s):  
Kasiani C. Pozios ◽  
Jun Ding ◽  
Brian Degger ◽  
Zee Upton ◽  
Cunming Duan
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase ◽  
Dna Synthesis ◽  
Signaling Pathways ◽  
Kinase Inhibitor ◽  
Pi3 Kinase ◽  
Dependent Manner ◽  
Embryonic Cells ◽  
Kinase Signaling ◽  
Igf I

Insulin-like growth factor (IGF)-I and -II have been cloned from a number of teleost species, but their cellular actions in fish are poorly defined. In this study, we show that both IGF-I and -II stimulated zebrafish embryonic cell proliferation and DNA synthesis in a concentration-dependent manner, whereas insulin had little mitogenic activity. Affinity cross-linking and immunoblotting studies revealed the presence of IGF receptors with the characteristics of the mammalian type I IGF receptor. Competitive binding assay results indicated that the binding affinities of the zebrafish IGF-I receptors to IGF-I, IGF-II, and insulin are 1.9, 2.6, and >190 nM, indicating that IGF-I and -II bind to the IGF-I receptor(s) with approximately equal high affinity. To further investigate the cellular mechanism of IGF actions, we have studied the effects of IGFs on two major signal transduction pathways: mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3 kinase). IGFs activated MAPK in zebrafish embryonic cells in a dose-dependent manner. This activation occurred within 5 min of IGF-I stimulation and disappeared after 1 h. IGF-I also caused a concentration-dependent activation of protein kinase B, a downstream target of PI3 kinase, this activation being sustained for several hours. Inhibition of MAPK activation by the MAPK kinase inhibitor PD-98059 inhibited the IGF-I-stimulated DNA synthesis. Similarly, use of the PI3 kinase inhibitor LY-294002 also inhibited IGF-I-stimulated DNA synthesis. When both the MAPK and PI3 kinase pathways were inhibited using a combination of these compounds, the IGF-I-stimulated DNA synthesis was completely negated. These results indicate that both IGF-I and -II are potent mitogens for zebrafish embryonic cells and that activation of both the MAPK and PI3 kinase-signaling pathways is required for the mitogenic action of IGFs in zebrafish embryonic cells.

scholarly journals Hepcidin and MELD-XI score as markers of multiple organ failure in patients with heart failure with preserved and reduced ejection fraction

2020 ◽  
Vol 19 (3) ◽  
pp. 2529
Author(s):  
V. I. Podzolkov ◽  
N. A. Dragomiretskaya ◽  
S. K. Stolbova ◽  
A. V. Tolmacheva
Keyword(s):  
Heart Failure ◽  
Body Mass Index ◽  
Ejection Fraction ◽  
Cardiac Arrhythmias ◽  
Multiple Organ ◽  
Left Ventricular ◽  
Chronic Obstructive ◽  
Hepcidin Level ◽  
Airway Diseases ◽  
Obstructive Airway Diseases

Data on the changes in hepcidin levels in heart failure (HF) patients are contradictory and do not give an answer about its effect on the progression of multiple organ failure. Since the model of end-stage liver disease excluding INR (MELD-XI) reflects the severity of liver and kidney dysfunction, these markers have been suggested to be associated with decompensated HF.Aim. To assess the MELD-XI score and serum hepcidin levels in patients with decompensated HF with different values of left ventricular ejection fraction (EF).Material and methods. The study included 68 patients (29 women, 39 men; mean age 72,3±11,7 years) hospitalized due to decompensated HF. Patients were divided into three groups: reduced (HFrEF) (n=20), mid-range (HFmrEF) (n=23), and preserved EF (HFpEF) (n=24)). Upon admission, along with standard diagnostic tests, all patients were examined for hepcidin-25 levels by enzyme-linked immunosorbent assay. MELD-XI score was calculated. Statistical processing was carried out using the software package Statistica 8.0.Results. Hepcidin levels in the HFrEF group (31,63 ng/ml [22,0; 71,6]) were significantly higher than in the HFmrEF (23,89 ng/ml [21,1; 27,9]) (p<0,05) and HFpEF (26,91 ng/ml [18,6; 31,1]) (p<0,05) groups. In HFpEF, there was a correlation of hepcidin level with body mass index (r=0,47, p<0,05) and chronic obstructive airway diseases (r=0,44, p<0,05). A correlation of hepcidin level with significant cardiac arrhythmias (r=0,61, p<0,05) was revealed in HFmrEF patients. MELD-XI score were significantly increased from 9,44±3,96 for HFpEF and 11,53±3,82 for HFmrEF to 14,3±4,3 for HFrEF (p<0,005). We also revealed correlation of MELD-XI score with hepcidin levels (r=0,3, p<0,05) and EF (r=-0,43, p<0,0003). Patients with a MELD-XI score of >10,4 were more likely to have NYHA class III-IV HF, HFrEF and significantly higher levels of hepcidin (p<0,05 for all) These patients were also more likely to have chronic kidney disease (p<0,05).Conclusion. Hepcidin level and MELD-XI score in patients with decompensated HF are inversely related to left ventricular EF. There is a direct relationship between hepcidin levels and other clinical parameters: body mass index, the presence of chronic obstructive airway diseases and cardiac arrhythmias.

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