Jude Alawa

Mr. Jude Alawa

orcid

Research Focus & Metrics

Academic Career Length

8Years (2019-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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11 December 2019 in Science Translational Medicine
Verified
Journal Article
Closed access
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XHXue Han
Xue Han
MVMatthew D. Vesely
Matthew D. Vesely
WYWendy Yang
Wendy Yang
MSMiguel F. Sanmamed
Miguel F. Sanmamed
TBTi Badri
Ti Badri
LCLieping Chen
Lieping Chen
Systemic lupus erythematosus (SLE) and discoid lupus erythematosus (DLE) of the skin are autoimmune diseases characterized by inappropriate immune responses against self-proteins; the key elements that determine disease pathogenesis and progression are largely unknown. Here, we show that mice lacking immune inhibitory receptor VISTA or programmed death-1 homolog (PD-1H KO) on a BALB/c background spontaneously develop cutaneous and systemic autoimmune diseases resembling human lupus. Cutaneous lupus lesions of PD-1H KO mice have clustering of plasmacytoid dendritic cells (pDCs) similar to human DLE. Using mass cytometry, we identified proinflammatory neutrophils as critical early immune infiltrating cells within cutaneous lupus lesions of PD-1H KO mice. We also found that PD-1H is highly expressed on immune cells in human SLE, DLE lesions, and cutaneous lesions of MRL/lpr mice. A PD-1H agonistic monoclonal antibody in MRL/lpr mice reduces cutaneous disease, autoantibodies, inflammatory cytokines, chemokines, and immune cell expansion. Furthermore, PD-1H on both T cells and myeloid cells including neutrophils and pDCs could transmit inhibitory signals, resulting in reduced activation and function, establishing PD-1H as an inhibitory receptor on T cells and myeloid cells. On the basis of these findings, we propose that PD-1H is a critical element in the pathogenesis and progression of lupus, and PD-1H activation could be effective for treatment of systemic and cutaneous lupus.

JAJude Alawa
Jude Alawa
PZParmida Zarei
Parmida Zarei
KKKaveh Khoshnood
Kaveh Khoshnood
Background: While Turkey hosts the largest number of Syrian refugees, the provision of health services for chronic disease among Syrian refugees in Turkey has been inadequate and understudied. This paper explores Turkish healthcare policies surrounding Syrian refugees’ access to health services for chronic diseases. Methods: We conducted a literature review and supplementary stakeholder interviews to evaluate the provision of chronic health services and the most common barriers to healthcare access among Syrian refugees in Turkey. Results: Though access to treatment for displaced Syrians has improved throughout the past five years, five primary barriers persist: registration procedure regulations, navigation of a new health system, language barriers, fear of adverse treatment, and cost. Conclusions: To drive improvements in healthcare for chronic diseases among Syrian refugees in Turkey, we recommend making registration procedures more accessible, developing more healthcare options in patients’ native language, increasing human resources, and advocating for more research surrounding chronic health conditions among refugees.

22 December 2020 in BMJ Open
Verified
Journal Article
Open access
PDF file
YAYazan A Al-Ajlouni
Yazan A Al-Ajlouni
Su Hyun ParkSu Hyun Park
Su Hyun Park
JAJude Alawa
Jude Alawa
GSGhaith Shamaileh
Ghaith Shamaileh
ABAziz Bawab
Aziz Bawab
DDDustin T Duncan
Dustin T Duncan
Background Jordan, a Middle Eastern country, declared a state of national emergency due to COVID-19 and a strict nationwide lockdown on 17 March 2020, banning all travel and movement around the country, potentially impacting mental health. This study sought to investigate the association between mental health (eg, anxiety and depressive symptoms) and sleep health among a sample of Jordanians living through a state of COVID-19-induced nationwide lockdown. Methods Using Facebook, participants (n=1240) in Jordan in March 2020 were recruited and direct to a web-based survey measuring anxiety (items from General Anxiety Disorder 7-item (GAD-7) scale instrument), depressive symptoms (items from Center for Epidemiologic Studies Depression Scale), sleep health (items from the Pittsburgh Sleep Quality Index) and sociodemographic. A modified Poisson regression model with robust error variance. Adjusted prevalence ratios (aPRs) and 95% CIs were estimated to examine how anxiety and depressive symptoms may affect different dimensions of sleep health: (1) poor sleep quality, (2) short sleep duration, (3) encountering sleep problems. Results The majority of participants reported having experienced mild (33.8%), moderate (12.9%) or severe (6.3%) levels of anxiety during lockdown, and nearly half of respondents reported depressive symptoms during lockdown. Similarly, over 60% of participants reported having experienced at least one sleep problem in the last week, and nearly half reported having had short sleep duration. Importantly, anxiety was associated with poor sleep health outcomes. For example, corresponding to the dose–response relationship between anxiety and sleep health outcomes, those reporting severe anxiety were the most likely to experience poor sleep quality (aPR =8.95; 95% CI=6.12 to 13.08), short sleep duration (aPR =2.23; 95% CI=1.91 to 2.61) and at least one problem sleep problem (aPR=1.73; 95% CI=1.54 to 1.95). Moreover, depressive symptoms were also associated with poor sleep health outcomes. As compared with scoring in the first quartile, scoring fourth quartile was associated with poor sleep quality (aPR=11.82; 95% CI=6.64 to 21.04), short sleep duration (aPR=1.87; 95% CI=1.58 to 2.22), and experiencing at least one sleep problem (aPR=1.90; 95% CI=1.66 to 2.18). Conclusions Increased levels of anxiety and depressive symptoms can negatively influence sleep health among a sample of Jordanian adults living in a state of COVID-19-induced nationwide lockdown.

10 September 2020 in Conflict and Health
Verified
Journal Article
Open access
PDF file
JAJude Alawa
Jude Alawa
NANawara Alawa
Nawara Alawa
ACAdam Coutts
Adam Coutts
RSRichard Sullivan
Richard Sullivan
KKKaveh Khoshnood
Kaveh Khoshnood
FFFouad M. Fouad
Fouad M. Fouad
Refugees and internally displaced persons in humanitarian settings are particularly susceptible to the spread of infectious illnesses such as COVID-19 due to overcrowding and inadequate access to clean water, sanitation, and hygiene facilities. Countries facing conflict or humanitarian emergencies often have damaged or fragmented health systems and little to no capacity to test, isolate, and treat COVID-19 cases. Without a plan to address COVID-19 in humanitarian settings, host governments, aid agencies, and international organizations risk prolonging the spread of the virus across borders, threatening global health security, and devastating vulnerable populations. Stakeholders must coordinate a multifaceted response to address COVID-19 in humanitarian settings that incorporates appropriate communication of risks, sets forth resource-stratified guidelines for the use of limited testing, provides resources to treat affected patients, and engages displaced populations.

28 March 2019 in Journal of Cancer Education
Verified
Journal Article
Closed access
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JAJude Alawa
Jude Alawa
OHOmar Hamade
Omar Hamade
AAAmin Alayleh
Amin Alayleh
LFLuna Fayad
Luna Fayad
KKKaveh Khoshnood
Kaveh Khoshnood

1 February 2024 in Journal of Clinical Investigation
Verified
Journal Article
Open access
PDF file
TKTae Kon Kim
Tae Kon Kim
XHXue Han
Xue Han
QHQianni Hu
Qianni Hu
EVEsten N. Vandsemb
Esten N. Vandsemb
CFCarly M. Fielder
Carly M. Fielder
LCLieping Chen
Lieping Chen
Acute myeloid leukemia (AML) presents a pressing medical need in that it is largely resistant to standard chemotherapy as well as modern therapeutics, such as targeted therapy and immunotherapy, including anti–programmed cell death protein (anti-PD) therapy. We demonstrate that programmed death-1 homolog (PD-1H), an immune coinhibitory molecule, is highly expressed in blasts from the bone marrow of AML patients, while normal myeloid cell subsets and T cells express PD-1H. In studies employing syngeneic and humanized AML mouse models, overexpression of PD-1H promoted the growth of AML cells, mainly by evading T cell–mediated immune responses. Importantly, ablation of AML cell-surface PD-1H by antibody blockade or genetic knockout significantly inhibited AML progression by promoting T cell activity. In addition, the genetic deletion of PD-1H from host normal myeloid cells inhibited AML progression, and the combination of PD-1H blockade with anti-PD therapy conferred a synergistic antileukemia effect. Our findings provide the basis for PD-1H as a potential therapeutic target for treating human AML.