Raya Kh. Yashooa

Mrs. Raya Kh. Yashooa

orcid

Research Focus & Metrics

Academic Career Length

4Years (2023-Present)

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

Representative Publications

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RYRaya Kh. Yashooa
Raya Kh. Yashooa
Elisa DurantiElisa Duranti
Elisa Duranti
DCDonatella Conconi
Donatella Conconi
MLMarialuisa Lavitrano
Marialuisa Lavitrano
SMSuhad Asad Mustafa
Suhad Asad Mustafa
Chiara VillaChiara Villa
Chiara Villa
MicroRNAs (miRNAs) are a class of small non-coding RNAs (ncRNAs) crucial for regulating gene expression at the post-transcriptional level. Recent evidence has shown that miRNAs are also found in mitochondria, organelles that produce energy in the cell. These mitochondrial miRNAs, also known as mitomiRs, are essential for regulating mitochondrial function and metabolism. MitomiRs can originate from the nucleus, following traditional miRNA biogenesis pathways, or potentially from mitochondrial DNA, allowing them to directly affect gene expression and cellular energy dynamics within the mitochondrion. While miRNAs have been extensively investigated, the function and involvement of mitomiRs in the development of neurodegenerative disorders like Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis remain to be elucidated. This review aims to discuss findings on the role of mitomiRs in such diseases and their potential as therapeutic targets, as well as to highlight future research directions.

25 June 2025 in Neurological Research
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SSshukur smail
shukur smail
AKAzad Hasan Kheder
Azad Hasan Kheder
HMHero Khalid Mustafa
Hero Khalid Mustafa
SAShang Ziyad Abdulqadir
Shang Ziyad Abdulqadir
KJKovan Faidhalla Jalal
Kovan Faidhalla Jalal
MSMudhir Shekha
Mudhir Shekha
Kenpaullone is known for its neuroprotective and anti-inflammatory properties. We explored the potential of a specific intervention to influence cognitive abilities and disease-related brain changes in a mice model replicating key aspects of Alzheimer's disease (AD). We employed 5XFAD transgenic mice, which develop Aβ plaques and cognitive impairments that mirror those observed in individuals with Alzheimer's disease (AD). The animals were treated with Kenpaullone (1 mg/kg, 3 mg/kg, and 5 mg/kg) or a vehicle (DMSO). The study evaluated memory using the Morris water maze (MWM) and the novel object recognition (NOR) task. This study employed immunohistochemistry, ELISA, and Western blot to analyze Aβ plaques and proinflammatory factors, investigating neurodegeneration. In contrast, the expression of genes related to neurodegeneration and apoptosis was evaluated using polymerase chain reaction (PCR). Administration of Kenpaullone yielded significant improvements in cognitive performance in the 5XFAD mice. Mice that received the 5 mg/kg treatment demonstrated the highest improvement in spatial learning and recognition memory. Furthermore, Kenpaullone decreased the burden of amyloid-beta plaques in key brain regions associated with memory (hippocampus and cortex), along with decreased levels of proinflammatory cytokines. Furthermore, Kenpaullone treatment resulted in a downregulation of genes related to neurodegeneration and apoptosis, suggesting a potential therapeutic benefit in mitigating neural apoptosis in AD. Our results suggest that Kenpaullone holds promise for improving cognitive function and mitigating neuropathological changes in AD, warranting further exploration as a potential medicinal substance.

31 October 2024 in Journal of Medical Mycology
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KMKarzan A. Mohammad
Karzan A. Mohammad
HIHero M. Ismail
Hero M. Ismail
KSKhattab A.M. Shekhany
Khattab A.M. Shekhany
RYRaya Kh. Yashooa
Raya Kh. Yashooa
DYDelan Ameen Younus
Delan Ameen Younus
DDDavid W. Denning
David W. Denning
The surveillance of serious and superficial skin fungal infections in Iraq has not been conducted. Limited information exists on their incidence and prevalence. This study aimed to analyze, compute and estimate the prevalence and burden of fungal infections, as no previous data is available and no studies has been attempted in Iraq. In the present study the data were collected and reviewed from published data on epidemiology of fungal infections nationally, internationally, from unpublished postgraduate master and PhD theses, hospital records and private clinic records. External sources of data from other countries were used for diseases which lacked sufficient local data. We estimated 985,628 annual serious infections comprising of 2.26 % of the total population. When including superficial fungal infections group of the skin, this rises to 2,075,113 infections at 4.76 % of the total population. The most common serious and skin infections were recurrent Candida vaginitis, fungal rhinosinusitis and tinea capitis comprising 61.5 %, 21.8 %, and 22.4 % of all infections although the total incidence of superficial fungal infections was also high at 1,071,485. Respiratory fungal disease is also common comprising 14.0 % of infections. We predicted the following annual burden per 100,000; oral candidiasis at 247.9, esophageal candidiasis at 6.04, candidemia at 5.0, Candida peritonitis at 0.75, recurrent Candida vaginitis at 5461, allergic bronchopulmonary aspergillosis at 35, severe asthma with fungal sensitisation at 46, invasive aspergillosis at 7.9, chronic pulmonary aspergillosis at 11.7, chronic fungal rhinosinusitis at 496, mucormycosis at 0.99, fungal keratitis at 14.0, and total dermatophytosis at 1631, the most severe being tinea capitis at 366. Many of these estimates were made with data sourced from other nations, so additional data from Iraq is required to validate or modify these estimates. Recurrent Candida vaginitis, fungal rhinosinusitis, and tinea capitis are considered to be the most frequent fungal diseases present in Iraq.

30 June 2023 in BioMed Target Journal
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KMKarzan Abdulmuhsin Mohammad
Karzan Abdulmuhsin Mohammad
RYRaya Kh. Yashooa
Raya Kh. Yashooa
SMSuhad Asad Mustafa
Suhad Asad Mustafa
The oral thrush due to biofilms of Candida species is a common infection for the oral cavity of cancer patients undergoing chemotherapy, leading to oral infections. These biofilms, composed of Candida organisms, pose challenges in terms of diagnosis and treatment due to their increased resistance and ability to persist in the oral environment. This study aimed to determine the frequency of Candida species biofilm colonization in the oral cavity of pediatric cancer patients receiving chemotherapy. By examining the incidence of Candida sp. biofilms, this research provides valuable insights into the oral health challenges specific to children with cancer, emphasizing the need for targeted preventive and management strategies to address these infections effectively. In this study, a total of 100 oral cavity swabs were collected, with 50 swabs obtained from cancer patients undergoing chemotherapy and suspected to have oral candidiasis, and the other 50 swabs collected from non-cancer healthy individuals serving as control. All swabs were cultured on Sabouraud Dextrose agar (SDA) media, followed by microscopic examination of positive samples. The API identification candida system was utilized for the identification of Candida species, along with the implementation of biochemical tests to further study the characteristics of the identified species.The findings demonstrated that out of the 50 cancer patients, approximately 47% (23 patients) exhibited positive yeast growth on SDA agar. Among the 50 non-cancer control cases, approximately 30% (15 cases) showed positive growth on SDA agar. Furthermore, using the API candida system, we confirmed the presence of candida species in 25 cases. Candida albicans was identified as the most prevalent species, followed by Candida parapsilosis, Candida krusei, and Saccharomyces cerevisiae, which were detected less frequently.In conclusion, there were a significant increase in Candida species among cancer patients undergoing chemotherapy treatment in comparison to non-cancer control individuals. This finding highlights the impact of chemotherapy on the prevalence of Candida infections in cancer patients, emphasizing the need for heightened attention and appropriate management strategies in this vulnerable population.

30 September 2024 in The Journal of Infection in Developing Countries
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SMSevan O Majed
Sevan O Majed
RDRande Dzay
Rande Dzay
RYRaya Kh. Yashooa
Raya Kh. Yashooa
SMSuhad A Mustafa
Suhad A Mustafa
Introduction: Coronavirus disease 2019 (COVID-19) first appeared in Iraq, including the Iraqi Kurdistan region governorates, in March 2020. Methodology: 48,494 samples were collected from public hospitals in the Kurdish governates from February 2021 to May 2022. Viral RNA was extracted, and real time quantitative polymerase chain reaction (RT-PCR) was used to detect the COVID-19 variants. Statistical analysis of patients’ clinical data was performed. Results: The RT-PCR results identified the Alpha (B.1.1.7), Delta (B.1.617.2), and Omicron (B.1.1.529) variants in the Kurdistan governorates. Young adults (20-39 years) had significantly higher rate of infection than children (1-11 months) and older adults (80-89 years). The Delta wave was more contiguous, spread more easily, and more fatal than the Alpha and Omicron waves. The highest number of COVID-19 cases was reported in Sulaymaniyah and Duhok; and the highest death rate was reported in Sulaymaniyah. The death rate in males was higher than in females, especially among older people. Fatigue, cough, and fever were common symptoms among the three variants. The phylogenetic tree revealed that the L-type of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was a descendant of the S-type at an early stage of evolution. The L-type could spread faster in Kurdistan. Multiple sequence alignment (MSA) confirmed that all L-type variants in different countries were 100% similar in sequence, and all were mutated in the regions 8782: ORF1ab and 28144: ORF8 703. Conclusions: This study described the COVID-19 waves, pathogenesis, and evolution of the virus in the Iraqi Kurdistan region.

7 August 2026 in Pharmaceutics
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SSshukur smail
shukur smail
HHHawro Taha Hamza
Hawro Taha Hamza
Mohammed Awat AliMohammed Awat Ali
Mohammed Awat Ali
RYRaya Kh. Yashooa
Raya Kh. Yashooa
WAWissam Albeer
Wissam Albeer
Christer JansonChrister Janson
Christer Janson
T-cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) emerged as one of the most promising next-generation immune checkpoint targets following the success of programmed cell death protein 1 (PD-1), programmed death-ligand 1 (PD-L1), and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) blockade. TIGIT suppresses antitumor immunity through interaction with cluster of differentiation 155 (CD155), inhibition of CD226-mediated co-stimulation, and promotion of immunosuppressive regulatory T-cell (Treg) activity within the tumor microenvironment (TME). Strong preclinical evidence demonstrated that TIGIT blockade, particularly in combination with PD-1/PD-L1 inhibition, restored T-cell and natural killer (NK) cell function and produced durable antitumor responses in multiple tumor models, leading to rapid clinical development. Despite this compelling biological rationale, most late-stage clinical programs failed to reproduce early success. Although the phase II CITYSCAPE trial showed encouraging activity in PD-L1-high non-small cell lung cancer (NSCLC), subsequent phase III trials, including SKYSCRAPER-01, SKYSCRAPER-02, SKYSCRAPER-03, SKYSCRAPER-14, AdvanTIG-302, KEYVIBE, and STAR-221, failed to improve survival outcomes or meet primary endpoints. The notable exception was SKYSCRAPER-08 in esophageal squamous cell carcinoma, suggesting that TIGIT blockade may be effective only in selected biological contexts. This review critically examines the molecular biology of the TIGIT–CD155–CD226 axis, its role in immune regulation and tumor immune evasion, and the preclinical and clinical evidence supporting TIGIT-targeted therapy. Particular emphasis is placed on understanding the causes of clinical failure, including CD226 loss during T-cell exhaustion, checkpoint network redundancy, Fc-engineering uncertainty, immunosuppressive TMEs, inadequate biomarker-guided patient selection, and tumor-type-specific dependence on the TIGIT pathway. We also present original bioinformatics analyses demonstrating that broader checkpoint network signatures outperform TIGIT expression alone for patient stratification. Finally, we evaluate emerging solutions including biomarker-guided precision immunotherapy, Fc-optimized antibodies, bispecific checkpoint inhibitors, TIGIT-engineered chimeric antigen receptor T-cell (CAR-T) cells, radiotherapy combinations, and multi-checkpoint blockade. Collectively, current evidence suggests that the future of TIGIT-directed therapy lies not in universal checkpoint inhibition but in biologically informed, precision-guided immunotherapy strategies.