ORCID Profile
0000-0002-8980-4616
Current Organisations
UNSW Sydney
,
Amman Arab University
,
University of Jordan
,
Batterjee Medical College for Sciences and Technology
,
The University of Sydney Sydney University Press
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Related Links
Publications
Asthmatic airway smooth muscle CXCL10 production: mitogen-activated protein kinase JNK involvement
Publisher: American Physiological Society
Date: 15-05-2012
DOI: 10.1152/AJPLUNG.00232.2011
Abstract: CXCL10 (IP10) is involved in mast cell migration to airway smooth muscle (ASM) bundles in asthma. We aimed to investigate the role of cytokine-induced MAPK activation in CXCL10 production by ASM cells from people with and without asthma. Confluent growth-arrested ASM cells were treated with inhibitors of the MAPKs ERK, p38, and JNK and transcription factor NF-κB, or vehicle, and stimulated with IL-1β, TNF-α, or IFN-γ, alone or combined (cytomix). CXCL10 mRNA and protein, JNK, NF-κB p65 phosphorylation, and Iκ-Bα protein degradation were assessed using real-time PCR, ELISA, and immunoblotting, respectively. Cytomix, IL-1β, and TNF-α induced CXCL10 mRNA expression more rapidly in asthmatic than nonasthmatic ASM cells. IL-1β and/or TNF-α combined with IFN-γ synergistically increased asthmatic ASM cell CXCL10 release. Inhibitor effects were similar in asthmatic and nonasthmatic cells, but cytomix-induced release was least affected, with only JNK and NF-κB inhibitors halving it. Notably, JNK phosphorylation was markedly less in asthmatic compared with nonasthmatic cells. However, in both, the JNK inhibitor SP600125 reduced JNK phosphorylation and CXCL10 mRNA levels but did not affect CXCL10 mRNA stability or Iκ-Bα degradation. Together, the JNK and NF-κB inhibitors completely inhibited their CXCL10 release. We concluded that, in asthmatic compared with nonasthmatic ASM cells, JNK activation was reduced and CXCL10 gene expression was more rapid following cytomix stimulation. However, in both, JNK activation did not regulate early events leading to NF-κB activation. Thus JNK and NF-κB provide independent therapeutic targets for limiting CXCL10 production and mast cell migration to the ASM in asthma.
Evaluation of the impact of pharmaceutical care service on hospitalized patients with chronic kidney disease in Jordan
Publisher: Springer Science and Business Media LLC
Date: 25-07-2013
DOI: 10.1007/S11096-013-9806-8
Abstract: The primary goal of the present study was to implement and evaluate the impact of pharmaceutical care service for hospitalized chronic kidney disease (CKD) patients in Jordan. Nephrology wards of one of the largest general hospitals in Jordan. All patients who were previously diagnosed with CKD by their physician were eligible for inclusion in the study. Recruited patients were fully assessed for treatment related problems (TRPs) by a clinical pharmacist. Pharmaceutical care service was assessed through a systematic, prospective before-after design. Chi Square test was used to investigate association between categorical variables. P value <0.05 was considered to be statistically significant. Study outcomes included: Process outcomes (prevalence and nature of identified TRPs, clinical significance of TRPs, associated diseases and drugs), General clinical outcomes (Therapeutic outcomes of TRPs) and CKD specific clinical outcomes (Change from baseline in the number of patients receiving appropriate progression modifying therapy and appropriate management of complications). 130 patients were included in the study. The average number of the identified TRPs was 5.31. Eighty-six percent of the recommendations were accepted by physicians. Efficacy related problems were the most common TRP category. Seventeen percent of all TRPs were resolved, 5.5 % were improved, and 37.4 % were prevented through the clinical pharmacist interventions. The current study indicated that hospitalized patients with CKD suffer from multiple TRPs mostly related to efficacy of medications and patients monitoring. Clinical pharmacists substantially contributed towards the care of hospitalized CKD patients through optimizing progression modifying therapies, medications safety and management of CKD complications. Based on this study it is strongly recommended to implement pharmaceutical care services for hospitalized CKD patients.
Airway smooth muscle CXCR3 ligand production: regulation by JAK-STAT1 and intracellular Ca2+
Publisher: American Physiological Society
Date: 12-06-2019
DOI: 10.1152/AJPLUNG.00356.2012
Abstract: In asthma, airway smooth muscle (ASM) chemokine (C-X-C motif) receptor 3 (CXCR3) ligand production may attract mast cells or T lymphocytes to the ASM, where they can modulate ASM functions. In ASM cells (ASMCs) from people with or without asthma, we aimed to investigate JAK-STAT1, JNK, and Ca 2+ involvement in chemokine (C-X-C motif) ligand (CXCL)10 and CXCL11 production stimulated by interferon-γ, IL-1β, and TNF-α combined (cytomix). Confluent, growth-arrested ASMC were treated with inhibitors for pan-JAK (pyridone-6), JAK2 (AG-490), JNK (SP-600125), or the sarco(endo)plasmic reticulum Ca 2+ ATPase (SERCA) pump (thapsigargin), Ca 2+ chelator (BAPTA-AM), or vehicle before and during cytomix stimulation for up to 24 h. Signaling protein activation as well as CXCL10/CXCL11 mRNA and protein production were examined using immunoblot analysis, real-time PCR, and ELISA, respectively. Cytomix-induced STAT1 activation was lower and CXCR3 ligand mRNA production was more sensitive to pyridone-6 and AG-490 in asthmatic than nonasthmatic ASMCs, but CXCL10/CXCL11 release was inhibited by the same proportion. Neither agent caused additional inhibition of release when used in combination with the JNK inhibitor SP-600125. Conversely, p65 NF-κB activation was higher in asthmatic than nonasthmatic ASMCs. BAPTA-AM abolished early CXCL10/CXCL11 mRNA production, whereas thapsigargin reduced it in asthmatic cells and inhibited CXCL10/CXCL11 release by both ASMC types. Despite these inhibitory effects, neither Ca 2+ agent affected early activation of STAT1, JNK, or p65 NF-κB. In conclusion, intracellular Ca 2+ regulated CXCL10/CXCL11 production but not early activation of the signaling molecules involved. In asthma, reduced ASM STAT1-JNK activation, increased NF-κB activation, and altered Ca 2+ handling may contribute to rapid CXCR3 ligand production and enhanced inflammatory cell recruitment.
Ion channel regulation of intracellular calcium and airway smooth muscle function
Publisher: Elsevier BV
Date: 10-2009
Related Organisations
Batterjee Medical College For Sciences And Technology
Location: Saudi Arabia
Related Funding Activities
No related grants have been discovered for Yazan AlRashdan.