9 results on '"Mikaeili H"'
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2. Ultraslow light realization using an interacting Bose–Einstein condensate trapped in a shallow optical lattice
- Author
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Mikaeili, H., Dalafi, A., Ghanaatshoar, M., and Askari, B.
- Published
- 2022
- Full Text
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3. Nanocurcumin modulates Th17 cell responses in moderate and severe COPD patients.
- Author
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Mardi A, Abdolmohammadi-Vahid S, Sadeghi SA, Jafarzadeh S, Abbaspour-Aghdam S, Hazrati A, Mikaeili H, Valizadeh H, Sadeghi A, Ahmadi M, and Nadiri M
- Abstract
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory process in the airways that results in airflow obstruction. It is mainly linked to cigarette smoke exposure. Th17 cells have a role in the pathogenesis of COPD by secreting pro-inflammatory cytokines, which cause hyperinflammation and progression of the disease. This study aimed to assess the potential therapeutic effects of nanocurcumin on the Th17 cell frequency and its responses in moderate and severe COPD patients. This study included 20 patients with severe COPD hospitalized in an intensive care unit (ICU) and 20 patients with moderate COPD. Th17 cell frequency, Th17-related factors gene expression (RAR-related orphan receptor t (RORγt), IL-17, IL-21, IL-23, and granulocyte-macrophage colony-stimulating factor), and serum levels of Th17-related cytokines were assessed before and after treatment in both placebo and nanocurcumin-treated groups using flow cytometry, real-time PCR, and ELISA, respectively. According to our findings, in moderate and severe nanocurcumin-treated COPD patients, there was a substantial reduction in the frequency of Th17 cells, mRNA expression, and cytokines secretion level of Th17-related factors compared to the placebo group. Furthermore, after treatment, the metrics mentioned above were considerably lower in the nanocurcumin-treated group compared to before treatment. Nanocurcumin has been shown to decrease the number of Th17 cells and their related inflammatory cytokines in moderate and severe COPD patients. As a result, it might be used as an immune-modulatory agent to alleviate the patient's inflammatory state., Competing Interests: The authors declare that they have no competing interests.The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Majid Ahmadi reports financial support was provided by 10.13039/501100012155National Institute for Medical Research Development. Majid Ahmadi reports a relationship with 10.13039/501100004366Tabriz University of Medical Sciences that includes: employment. Majid Ahmadi has patent pending to NA. NA If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2024 Published by Elsevier Ltd.)
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- 2024
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4. Molecular basis of FAAH-OUT-associated human pain insensitivity.
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Mikaeili H, Habib AM, Yeung CW, Santana-Varela S, Luiz AP, Panteleeva K, Zuberi S, Athanasiou-Fragkouli A, Houlden H, Wood JN, Okorokov AL, and Cox JJ
- Subjects
- Humans, Pain genetics, Analgesics, Ganglia, Spinal, RNA, Long Noncoding
- Abstract
Chronic pain affects millions of people worldwide and new treatments are needed urgently. One way to identify novel analgesic strategies is to understand the biological dysfunctions that lead to human inherited pain insensitivity disorders. Here we report how the recently discovered brain and dorsal root ganglia-expressed FAAH-OUT long non-coding RNA (lncRNA) gene, which was found from studying a pain-insensitive patient with reduced anxiety and fast wound healing, regulates the adjacent key endocannabinoid system gene FAAH, which encodes the anandamide-degrading fatty acid amide hydrolase enzyme. We demonstrate that the disruption in FAAH-OUT lncRNA transcription leads to DNMT1-dependent DNA methylation within the FAAH promoter. In addition, FAAH-OUT contains a conserved regulatory element, FAAH-AMP, that acts as an enhancer for FAAH expression. Furthermore, using transcriptomic analyses in patient-derived cells we have uncovered a network of genes that are dysregulated from disruption of the FAAH-FAAH-OUT axis, thus providing a coherent mechanistic basis to understand the human phenotype observed. Given that FAAH is a potential target for the treatment of pain, anxiety, depression and other neurological disorders, this new understanding of the regulatory role of the FAAH-OUT gene provides a platform for the development of future gene and small molecule therapies., (© The Author(s) 2023. Published by Oxford University Press on behalf of the Guarantors of Brain.)
- Published
- 2023
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5. Immunomodulatory role of Nanocurcumin in COVID-19 patients with dropped natural killer cells frequency and function.
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Abbaspour-Aghdam S, Hazrati A, Abdolmohammadi-Vahid S, Tahmasebi S, Mohseni J, Valizadeh H, Nadiri M, Mikaeili H, Sadeghi A, Yousefi M, Roshangar L, Nikzad B, Jadidi-Niaragh F, Kafil HS, Malekpour K, and Ahmadi M
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- Case-Control Studies, Chemotactic Factors pharmacology, Cytokines metabolism, Humans, Immunity, Inflammation Mediators pharmacology, Interleukin-6, Killer Cells, Natural, Pandemics, Tumor Necrosis Factor-alpha metabolism, COVID-19 Drug Treatment
- Abstract
The ongoing COVID-19 pandemic is still a challenging problem in the case of infection treatment. The immunomodulatory effect of Nanocurcumin was investigated in the present study in an attempt to counterbalance the immune response and improve the patients' clinical symptoms. 60 confirmed COVID-19 patients and 60 healthy controls enrolled in the study. COVID-19 patients were divided into Nanocurcumin and placebo received groups. Due to the importance of the role of NK cells in this disease, the frequency, cytotoxicity, receptor gene expression of NK cells, and serum secretion levels of inflammatory cytokines IL-1β, IL-6, TNF-α, as well as circulating C5a as a chemotactic factor an inflammatory mediator was evaluated by flow cytometry, real-time PCR and enzyme-linked immunosorbent assay in both experimental groups before and after the intervention. Given the role of measured factors in the progression and pathogenesis of COVID-19 disease, the results can help find appropriate treatments. The results of this study indicated that the Nanocurcumin could significantly increase the frequency and function of NK cells compared to the placebo-treated group. As an immunomodulatory agent, Nanocurcumin may be a helpful choice to improve NK cell function in COVID-19 patients and improve the clinical outcome of patients., Competing Interests: Declaration of competing interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be considered as a potential conflict of interest., (Copyright © 2022. Published by Elsevier B.V.)
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- 2022
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6. Tissue plasminogen activator for the treatment of adults with critical COVID-19: A pilot randomized clinical trial.
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Rashidi F, Barco S, Rezaeifar P, Sadeghipour P, Ghodrati S, Bakhshandeh H, Mousavi-Aghdas SA, Sadeghi A, Sharifi A, Valizadeh H, Mikaeili H, Rafiee F, Navarbaf Z, Farajian G, Mahmoodpoor A, Bikdeli B, and Ansarin K
- Subjects
- Adult, Fibrinolysis, Fibrinolytic Agents therapeutic use, Humans, Pilot Projects, SARS-CoV-2, Tissue Plasminogen Activator pharmacology, Tissue Plasminogen Activator therapeutic use, COVID-19 Drug Treatment
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- 2022
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7. Etiopathogenesis of Psoriasis from Genetic Perspective: An updated Review.
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Babaie F, Omraninava M, Gorabi AM, Khosrojerdi A, Aslani S, Yazdchi A, Torkamandi S, Mikaeili H, Sathyapalan T, and Sahebkar A
- Abstract
Psoriasis is an organ-specific autoimmune disease characterized by the aberrant proliferation and differentiation of keratinocytes, leading to skin lesions. Abnormal immune responses mediated by T cells and dendritic cells and increased production of inflammatory cytokines have been suggested as underlying mechanisms in the pathogenesis of psoriasis. Emerging evidence suggests that there is a heritable basis for psoriatic disorders. Moreover, numerous gene variations have been associated with the disease risk, particularly those in innate and adaptive immune responses and antigen presentation pathways. Herein, this article discusses the genetic implications of psoriatic diseases' etiopathogenesis to develop novel investigative and management options., (© 2022 Bentham Science Publishers.)
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- 2022
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8. NK cells - Dr. Jekyll and Mr. Hyde in autoimmune rheumatic diseases.
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Hojjatipour T, Aslani S, Salimifard S, Mikaeili H, Hemmatzadeh M, Gholizadeh Navashenaq J, Ahangar Parvin E, Jadidi-Niaragh F, and Mohammadi H
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- Cytotoxicity, Immunologic, Humans, Killer Cells, Natural, Arthritis, Rheumatoid, Autoimmune Diseases, Lupus Erythematosus, Systemic, Rheumatic Diseases
- Abstract
Natural killer (NK) cells belong to innate immune system that are large granular lymphocytes differentiating from the common lymphoid progenitors. These cells were first identified by their functional response against tumor cells and virus-infected cells. That notwithstanding, NK cells are able to affect both adaptive and innate immune arms and modulate a wide range of immune cells. As a consequence, NK cells are capable of bridging between the innate and adaptive immune responses. The effector cytokines as well as direct cell-cell cytotoxicity by NK cells have been shown to be involved in the regulation of the immune responses and might participate in the etiopathogenesis of several disorders, particularly autoimmune rheumatic diseases (AIRDs), such as Ankylosing spondylitis (AS), Rheumatoid arthritis (RA), Systemic lupus erythematosus (SLE), Behcet's disease (BD), Systemic sclerosis (SSc), and psoriasis. Nonetheless, NK cells demonstrate both harmful and protective functions during autoimmune diseases pathogenesis based on the subset of NK cell as well as disease microenvironment and disease phase or genetic/environmental stimuli. Here in this review, we intend to go through the recent findings in the etiology and pathogenesis of AIRDs and discuss about their clinical potential to be utilized as targets for the sake of therapy in the context of such disorders., (Copyright © 2022 Elsevier B.V. All rights reserved.)
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- 2022
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9. The early start of hemoperfusion decreases the mortality rate among severe COVID-19 patients: A preliminary study.
- Author
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Mikaeili H, Taghizadieh A, Nazemiyeh M, Rezaeifar P, Zununi Vahed S, Safiri S, Ardalan M, and Ansarin K
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- Humans, Renal Dialysis, Respiration, Artificial, SARS-CoV-2, COVID-19 therapy, Hemoperfusion
- Abstract
Background: Coronavirus disease-2019 (COVID-19)-related organ failure is partly related to a sepsis-like syndrome and extreme pro-inflammatory cytokine release, named cytokine storm. Therapeutic strategies that prevent the production of or remove the pro-inflammatory cytokines could potentially be an effective therapy in critically afflicted COVID-19 patients., Methods: In this clinical trial study, from April until June 2020, 68 COVID-19 patients (35 vs. 33 controls) with severe critical symptoms, and PaO
2 /FiO2 (P/F) ratio less than 200 mmHg either received a single standard therapy or a combination of standard treatment for COVID-19 combined with hemoperfusion (hemofilter, HA330 D Javfron) for 4 h, in 3 consecutive days. The length of hospital stay and mechanical ventilation, the resolution of radiologic abnormalities, and the mortality rate were defined as the primary outcomes., Results: Demographic characteristics, the acute physiology, and chronic health evaluation score of both groups were similar (p > 0.05). Importantly, we noticed a significant mortality rate reduction in the perfused group compared with controls (37.1% vs. 63.6%, p = 0.02), this positive effect was stronger among those with a P/F ratio higher than 75 (mortality rate of 84.7% for P/F ratio < 75 vs. 15.4% for P/F ratio ≥ 75, p = 0.02)., Conclusions: The results imply that early start of hemoperfusion could be more effective and significantly reduce the mortality rate among COVID-19 patients with critical diseases., (© 2021 International Society for Hemodialysis.)- Published
- 2022
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